徳島大学 / 教育研究者総覧 --- 瀬川博子

個人のホームページ

https://researchmap.jp/read0194433 (researchmap)

https://orcid.org/0000-0002-0905-246X (ORCID)

専門分野

○	保健学 (Health Studies)
○	栄養学 (Nutrition)

研究テーマ

○
○	分子腎臓栄養学 (リン酸 (phosphoric acid), トランスポーター, 腎臓, 骨ミネラル代謝 (bone and mineral metabolism))

著書・論文

著書:

1.	瀬川博子, 小池萌, 塩﨑雄治, 宮本賢一 : 抗老化因子を制御するミネラル栄養学-リン代謝恒常制御の重要性., 2022年4月.
2.	辰巳佐和子, 金子一郎, 瀬川博子, 宮本賢一 : 生体におけるリン代謝調節:多臓器連関について, 2018年10月.
3.	佐々木すみれ, 花崎愛, 瀬川博子 : 正常時のカルシウム/リン代謝調節【カルシウム/リン代謝の互角関係】, 株式会社東京医学社, 2018年9月.
4.	瀬川博子 : 第3章タンパク質・アミノ酸，糖，リンの吸収, 株式会社建帛社, 2018年5月.
5.	瀬川博子, 宮本賢一 : Na+非依存性糖トランスポーターGLUT群の概要と糖輸送メカニズム., 先端医学社, 2017年1月.
6.	瀬川博子, 宮本賢一 : 腎臓とトランスポーター., 医薬ジャーナル社, 2016年11月.
7.	金子一郎, 瀬川博子, 辰巳佐和子, 宮本賢一 : 尿細管リン再吸収障害によるくる病/骨軟化症., 株式会社東京医学社, 2016年6月.
8.	金子一郎, 瀬川博子, 辰巳佐和子, 宮本賢一 : FGF23, 科学評論社, 2015年12月.
9.	生田かよ, 瀬川博子, 宮本賢一 : りん吸収阻害薬の展望., 株式会社東京医学社, 2015年9月.
10.	瀬川博子, 生田かよ, 宮本賢一 : リンの吸収と排泄の分子機構, 医薬ジャーナル社, 2014年11月.
11.	辰巳佐和子, 金子一郎, 瀬川博子, 宮本賢一 : 生体内リン恒常性維持機構―多臓器関連制御, 日本DDS学会, 2014年11月.
12.	瀬川博子 : リン，カルシウム，PTH，ビタミンDはどのように作用し合うの?, 株式会社メディカ出版, 2014年7月.
13.	瀬川博子 : リンには，どのようなはたらきがあるの?, 株式会社メディカ出版, 2014年7月.
14.	辰巳佐和子, 瀬川博子, 宮本賢一 : 骨のリン利尿因子, 医薬ジャーナル社, 2014年6月.
15.	瀬川博子, 大西沙織, 塩崎雄治, 佐々木祥平, 宮本賢一 : リン輸送と疾患, 日本メディカルセンター, 2013年7月.
16.	瀬川博子, 宮本賢一 : リンの吸収と排泄, 日本メディカルセンター, 2013年6月.
17.	桑原頌治, 大井彰子, 野村憲吾, 辰巳佐和子, 木戸慎介, 瀬川博子, 宮本賢一 : 消化と吸収Degestion&Absortion, 日本消化吸収学会, 2012年4月.
18.	辰巳佐和子, 野村憲吾, 宮川淳美, 木戸慎介, 瀬川博子 : リンセンシングと腸管, 医薬ジャーナル社, 大阪, 2012年.
19.	宮本賢一, 竹谷豊, 辰巳佐和子, 伊藤美紀子, 瀬川博子 : 無機リン酸イオンとトランスポーター, 京都廣川書店, 2011年3月.
20.	瀬川博子 : リン代謝調節機構 up to date, 2011年1月.
21.	宮本賢一, 瀬川博子 : リントランスポーター, 2010年4月.
22.	伊藤美紀子, 瀬川博子, 桑波田雅士, 宮本賢一 : 無機リン酸トランスポーターファミリー, 株式会社中外医学社, 2002年1月. (キーワード) Renal Phosphate Transporter / Parathyroid Hormone / Endocytosis / PDZ Domain / Brush Border Membrane
23.	宮本賢一, 伊藤美紀子, 瀬川博子, 徳永栄子 : ビタミンD輸送システムと結合蛋白, 2001年.

学術論文(審査論文):

1.	Megumi Koike, Tetsuhiko Sato, Yuji Shiozaki, Aoi Komiya, Mizuki Miura, Ayami Higashi, Akane Ishikawa, Kaori Takayanagi, Minori Uga, Ken-ichi Miyamoto and Hiroko Segawa : Involvement of α-klotho in growth hormone (GH) signaling, Journal of Clinical Biochemistry and Nutrition, Vol.74, No.3, 221-229, 2024. (キーワード) growth hormone / α-klotho / kidney / CKD / GH-resistant (徳島大学機関リポジトリ) ● Metadata: 119161 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.23-127 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390581468909331072 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.23-127 (徳島大学機関リポジトリ: 119161, DOI: 10.3164/jcbn.23-127, CiNii: 1390581468909331072)
2.	Kazuya Tanifuji, Yuji Shiozaki, Megumi Koike, Minori Uga, Mizuki Miura, Ayami Higashi, Takaaki Shimohata, Akira Takahashi, Hisayoshi Hayashi, Noriko Ishizuka, Yasuhiro Ichida, Shuichi Ohtomo, Naoshi Horiba, Ken-ichi Miyamoto and Hiroko Segawa : Effects of EOS789, a novel pan-phosphate transporter inhibitor, on phosphate metabolism : Comparison with a conventional phosphate binder, The Journal of Medical Investigation : JMI, Vol.70, No.1,2, 260-270, 2023. (要約) Inorganic phosphate (Pi) binders are the only pharmacologic treatment approved for hyperphosphatemia. However, Pi binders induce the expression of intestinal Pi transporters and have limited effects on the inhibition of Pi transport. EOS789, a novel pan-Pi transporter inhibitor, reportedly has potent efficacy in treating hyperphosphatemia. We investigated the properties of EOS789 with comparison to a conventional Pi binder. Protein and mRNA expression levels of Pi transporters were measured in intestinal and kidney tissues from male Wistar rats fed diets supplemented with EOS789 or lanthanum carbonate (LC). 32Pi permeability was measured in intestinal tissues from normal rats using a chamber. Increased protein levels of NaPi-2b, an intestinal Pi transporter, and luminal Pi removal were observed in rats treated with LC but not in rats treated with EOS789. EOS789 but not LC suppressed intestinal protein levels of the Pi transporter Pit-1 and sodium/hydrogen exchanger isoform 3. 32Pi flux experiments using small intestine tissues from rats demonstrated that EOS789 may affect transcellular Pi transport in addition to paracellular Pi transport. EOS789 has differing regulatory effects on Pi metabolism compared to LC. The properties of EOS789 may compensate for the limitations of LC therapy. The combined or selective use of EOS789 and conventional Pi binders may allow tighter control of hyperphosphatemia. J. Med. Invest. 70 : 260-270, February, 2023. (キーワード) Rats / Male / Animals / Phosphate Transport Proteins / Rats, Wistar / Hyperphosphatemia / Intestinal Absorption / Phosphates (徳島大学機関リポジトリ) ● Metadata: 118209 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.70.260 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37164731 ● Search Scopus @ Elsevier (PMID): 37164731 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.70.260 (徳島大学機関リポジトリ: 118209, DOI: 10.2152/jmi.70.260, PubMed: 37164731)
3.	Sumire Sasaki, Yuji Shiozaki, Ai Hanazaki, Megumi Koike, Kazuya Tanifuji, Minori Uga, Kota Kawahara, Ichiro Kaneko, Yasuharu Kawamoto, Pattama Wiriyasermkul, Tomoka Hasegawa, Norio Amizuka, Ken-ichi Miyamoto, Shushi Nagamori, Yoshikatsu Kanai and Hiroko Segawa : Tmem174, a regulator of phosphate transporter prevents hyperphosphatemia., Scientific Reports, Vol.12, No.1, 2022. (要約) Renal type II sodium-dependent inorganic phosphate (Pi) transporters NaPi2a and NaPi2c cooperate with other organs to strictly regulate the plasma Pi concentration. A high Pi load induces expression and secretion of the phosphaturic hormones parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) that enhance urinary Pi excretion and prevent the onset of hyperphosphatemia. How FGF23 secretion from bone is increased by a high Pi load and the setpoint of the plasma Pi concentration, however, are unclear. Here, we investigated the role of Transmembrane protein 174 (Tmem174) and observed evidence for gene co-expression networks in NaPi2a and NaPi2c function. Tmem174 is localized in the renal proximal tubules and interacts with NaPi2a, but not NaPi2c. In Tmem174-knockout (KO) mice, the serum FGF23 concentration was markedly increased but increased Pi excretion and hypophosphatemia were not observed. In addition, Tmem174-KO mice exhibit reduced NaPi2a responsiveness to FGF23 and PTH administration. Furthermore, a dietary Pi load causes marked hyperphosphatemia and abnormal NaPi2a regulation in Tmem174-KO mice. Thus, Tmem174 is thought to be associated with FGF23 induction in bones and the regulation of NaPi2a to prevent an increase in the plasma Pi concentration due to a high Pi load and kidney injury. (キーワード) Animals / Fibroblast Growth Factors / 高リン血症 (hyperphosphatemia) / 低リン血症 (hypophosphatemia) / Membrane Proteins / ノックアウトマウス (knockout mice) / Parathyroid Hormone / Phosphate Transport Proteins / Phosphates (出版サイトへのリンク) ● Publication site (DOI): 10.1038/s41598-022-10409-3 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35428804 ● Search Scopus @ Elsevier (PMID): 35428804 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-022-10409-3 (DOI: 10.1038/s41598-022-10409-3, PubMed: 35428804)
4.	Sumire Sasaki, Megumi Koike, Kazuya Tanifuji, Minori Uga, Kota Kawahara, Aoi Komiya, Mizuki Miura, Yamato Harada, Yuki Hamaguchi, Shohei Sasaki, Yuji Shiozaki, Ichiro Kaneko, Ken-ichi Miyamoto and Hiroko Segawa : Dietary polyphosphate has a greater effect on renal damage and FGF23 secretion than dietary monophosphate, The Journal of Medical Investigation : JMI, Vol.69, No.3, 173-179, 2022. (要約) Phosphate (Pi)-containing food additives are used in several forms. Polyphosphate (PPi) salt has more harmful effects than monophosphate (MPi) salt on bone physiology and renal function. This study aimed to analyze the levels of parathyroid hormone PTH and fibroblast growth factor 23 (FGF23) and the expression of renal / intestinal Pi transport-related molecules in mice fed with an MPi or PPi diet. There were no significant differences in plasma Pi concentration and fecal Pi excretion levels between mice fed with the high-MPi and PPi diet. However, more severe tubular dilatation, interstitial fibrosis, and calcification were observed in the kidneys of mice fed with the high PPi diet versus the MPi diet. Furthermore, there was a significant increase in serum FGF23 levels and a decrease in renal phosphate transporter protein expression in mice fed with the PPi diet versus the MPi diet. Furthermore, the high MPi diet was associated with significantly suppressed expression and activity of intestinal alkaline phosphatase protein. In summary, PPi has a more severe effect on renal damage than MPi, as well as induces more FGF23 secretion. Excess FGF23 may be more involved in inflammation, fibrosis, and calcification in the kidney. J. Med. Invest. 69 : 173-179, August, 2022. (キーワード) Animals / Mice / Alkaline Phosphatase / Diet / Fibroblast Growth Factors / Fibrosis / Food Additives / Kidney / Parathyroid Hormone / Phosphate Transport Proteins / Phosphates / Polyphosphates (徳島大学機関リポジトリ) ● Metadata: 117148 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.69.173 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36244766 ● Summary page in Scopus @ Elsevier: 2-s2.0-85139886601 (徳島大学機関リポジトリ: 117148, DOI: 10.2152/jmi.69.173, PubMed: 36244766, Elsevier: Scopus)
5.	Toru Fujii, Hiroko Segawa, Ai Hanazaki, Shiori Nishiguchi, Sakura Minoshima, Akiko Ohi, Rieko Tominaga, Sumire Sasaki, Kazuya Tanifuji, Megumi Koike, Yuki Arima, Yuji Shiozaki, Ichiro Kaneko, Mikiko Ito, Sawako Tatsumi and Ken-ichi Miyamoto : Role of the putative PKC phosphorylation sites of the type IIc sodium-dependent phosphate transporter in parathyroid hormone regulation., Clinical and Experimental Nephrology, Vol.23, No.7, 898-907, 2019. (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s10157-019-01725-6 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30895530 ● Search Scopus @ Elsevier (PMID): 30895530 ● Search Scopus @ Elsevier (DOI): 10.1007/s10157-019-01725-6 (DOI: 10.1007/s10157-019-01725-6, PubMed: 30895530)
6.	Kayo Ikuta, Hiroko Segawa, Ai Hanazaki, Toru Fujii, Ichiro Kaneko, Yuji Shiozaki, Sawako Tatsumi, Yasuko Ishikawa and Ken-ichi Miyamoto : Systemic network for dietary inorganic phosphate adaptation among three organs., Pflügers Archiv : European Journal of Physiology, Vol.471, No.1, 123-136, 2018. (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s00424-018-2242-9 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30523405 ● Search Scopus @ Elsevier (PMID): 30523405 ● Search Scopus @ Elsevier (DOI): 10.1007/s00424-018-2242-9 (DOI: 10.1007/s00424-018-2242-9, PubMed: 30523405)
7.	Toru Fujii, Yuji Shiozaki, Hiroko Segawa, Shiori Nishiguchi, Ai Hanazaki, Miwa Noguchi, Ruri Kirino, Sumire Sasaki, Kazuya Tanifuji, Megumi Koike, Mizuki Yokoyama, Yuki Arima, Ichiro Kaneko, Sawako Tatsumi, Mikiko Ito and Ken-ichi Miyamoto : Analysis of opossum kidney NaPi-IIc sodium-dependent phosphate transporter to understand Pi handling in human kidney., Clinical and Experimental Nephrology, Vol.23, No.3, 313-324, 2018. (キーワード) Animals / Cells, Cultured / Familial Hypophosphatemic Rickets / Humans / Hypercalciuria / Kidney / Mice / Opossums / Phosphate Transport Proteins / Phosphates / RNA, Small Interfering / Sodium-Phosphate Cotransporter Proteins, Type IIc / Xenopus laevis (徳島大学機関リポジトリ) ● Metadata: 113363 (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s10157-018-1653-4 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30317447 ● Search Scopus @ Elsevier (PMID): 30317447 ● Search Scopus @ Elsevier (DOI): 10.1007/s10157-018-1653-4 (徳島大学機関リポジトリ: 113363, DOI: 10.1007/s10157-018-1653-4, PubMed: 30317447)
8.	Shohei Sasaki, Hiroko Segawa, Ai Hanazaki, Ruri Kirino, Toru Fujii, Kayo Ikuta, Miwa Noguchi, Sumire Sasaki, Megumi Koike, Kazuya Tanifuji, Yuji Shiozaki, Ichiro Kaneko, Sawako Tatsumi, Takaaki Shimohata, Yoshichika Kawai, Sonoko Narisawa, Luis José Millán and Ken-ichi Miyamoto : A Role of Intestinal Alkaline Phosphatase 3 (Akp3) in Inorganic Phosphate Homeostasis., Kidney & Blood Pressure Research, Vol.43, No.5, 1409-1424, 2018. (キーワード) Alkaline Phosphatase / Animals / Biological Transport / Disease Models, Animal / Homeostasis / Intestinal Mucosa / Mice / Mice, Knockout / Phosphates / Renal Insufficiency / Sodium-Phosphate Cotransporter Proteins, Type IIb (徳島大学機関リポジトリ) ● Metadata: 112882 (出版サイトへのリンク) ● Publication site (DOI): 10.1159/000493379 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30212831 ● Search Scopus @ Elsevier (PMID): 30212831 ● Search Scopus @ Elsevier (DOI): 10.1159/000493379 (徳島大学機関リポジトリ: 112882, DOI: 10.1159/000493379, PubMed: 30212831)
9.	Ichiro Kaneko, Hiroko Segawa, Ikuta Kayo, Hanazaki Ai, Fujii Toru, Sawako Tatsumi, Kido Shinsuke, Hasegawa Tomoka, Amizuka Norio, Saito Hitoshi and Ken-ichi Miyamoto : Eldecalcitol Causes FGF23 Resistance for Pi Reabsorption and Improves Rachitic Bone Phenotypes in the Male Hyp Mouse., Endocrinology, Vol.159, No.7, 2741-2758, 2018. (要約) X-linked hypophosphatemia (XLH), the most common form of inheritable rickets, is caused by inactivation of phosphate-regulating gene with homologies to endopeptidases on the X chromosome (PHEX) and leads to fibroblast growth factor (FGF) 23-dependent renal inorganic phosphate (Pi) wasting. In the present study, we investigated whether maintaining Pi homeostasis with a potent vitamin D3 analog, eldecalcitol [1α,25-dihydroxy-2β-(3-hydroxypropyloxy) vitamin D3; ED71], could improve hypophosphatemic rickets in a murine model of XLH, the Hyp mouse. Vehicle, ED71, or 1,25-dihydroxyvitamin D was subcutaneously injected five times weekly in wild-type (WT) and Hyp mice for 4 weeks, from 4 to 8 weeks of age. Injection of ED71 into WT mice suppressed the synthesis of renal 1,25-dihydroxyvitamin D and promoted phosphaturic activity. In contrast, administration of ED71 to Hyp mice completely restored renal Pi transport and NaPi-2a protein levels, although the plasma-intact FGF23 levels were further increased. In addition, ED71 markedly increased the levels of the scaffold proteins, renal sodium-hydrogen exchanger regulatory factor 1, and ezrin in the Hyp mouse kidney. Treatment with ED71 increased the body weight and improved hypophosphatemia, the bone volume/total volume, bone mineral content, and growth plate structure in Hyp mice. Thus, ED71 causes FGF23 resistance for phosphate reabsorption and improves rachitic bone phenotypes in Hyp mice. In conclusion, ED71 has opposite effects on phosphate homeostasis in WT and Hyp mice. Analysis of Hyp mice treated with ED71 could result in an additional model for elucidating PHEX abnormalities. (出版サイトへのリンク) ● Publication site (DOI): 10.1210/en.2018-00109 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29878089 ● Search Scopus @ Elsevier (PMID): 29878089 ● Search Scopus @ Elsevier (DOI): 10.1210/en.2018-00109 (DOI: 10.1210/en.2018-00109, PubMed: 29878089)
10.	Atsumi Miyagawa, Sawako Tatsumi, Wako Takahama, Osamu Fujii, Kenta Nagamoto, Emi Kinoshita, Kengo Nomura, Kayo Ikuta, Toru Fujii, Ai Hanazaki, Ichiro Kaneko, Hiroko Segawa and Ken-ichi Miyamoto : The sodium phosphate cotransporter family and nicotinamide phosphoribosyltransferase contribute to the daily oscillation of plasma inorganic phosphate concentration., Kidney International, Vol.93, No.5, 1073-1085, 2018. (要約) system for Npt2 regulation and cellular shifts to tissues such as the liver play an important role in generating daily oscillation of plasma inorganic phosphate levels. (徳島大学機関リポジトリ) ● Metadata: 111600 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.kint.2017.11.022 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29398136 ● Search Scopus @ Elsevier (PMID): 29398136 ● Search Scopus @ Elsevier (DOI): 10.1016/j.kint.2017.11.022 (徳島大学機関リポジトリ: 111600, DOI: 10.1016/j.kint.2017.11.022, PubMed: 29398136)
11.	Osamu Fujii, Sawako Tatsumi, Mao Ogata, Tomohiro Arakaki, Haruna Sakaguchi, Kengo Nomura, Atsumi Miyagawa, Kayo Ikuta, Ai Hanazaki, Ichiro Kaneko, Hiroko Segawa and Ken-ichi Miyamoto : Effect of Osteocyte-Ablation on Inorganic Phosphate Metabolism: Analysis of Bone-Kidney-Gut Axis., Frontiers in Endocrinology, Vol.8, 2017. (要約) < 0.01), thus suggesting that increased intestinal Pi absorption stimulates renal Pi excretion in OCL mice. In addition, the ablation of osteocytes and feeding of a high Pi diet affected FGF15/bile acid metabolism and controlled Npt2b expression. In conclusion, OCL mice exhibited increased renal Pi excretion due to enhanced intestinal Pi absorption. We discuss the role of FGF23-Klotho on renal and intestinal Pi metabolism in OCL mice. (徳島大学機関リポジトリ) ● Metadata: 112958 (出版サイトへのリンク) ● Publication site (DOI): 10.3389/fendo.2017.00359 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29312149 ● Search Scopus @ Elsevier (PMID): 29312149 ● Search Scopus @ Elsevier (DOI): 10.3389/fendo.2017.00359 (徳島大学機関リポジトリ: 112958, DOI: 10.3389/fendo.2017.00359, PubMed: 29312149)
12.	Kayo Ikuta, Hiroko Segawa, Shohei Sasaki, Ai Hanazaki, Toru Fujii, Aoi Kushi, Yuka Kawabata, Ruri Kirino, Sumire Sasaki, Miwa Noguchi, Ichiro Kaneko, Sawako Tatsumi, Otoya Ueda, Naoko Wada, Hiromi Tateishi, Mami Kakefuda, Yosuke Kawase, Shuichi Ohtomo, Yasuhiro Ichida, Akira Maeda, Kou-Ichi Jishage, Naoshi Horiba and Ken-ichi Miyamoto : Effect of Npt2b deletion on intestinal and renal inorganic phosphate (Pi) handling., Clinical and Experimental Nephrology, Vol.22, No.3, 517-528, 2017. (要約) -dependent Pi transport in brush-border membrane vesicle uptake levels was significantly decreased in the distal intestine of Npt2b CKO mice compared with control mice, plasma Pi and fecal Pi excretion levels were not significantly different. Data obtained using the intestinal loop technique showed that Pi uptake in Npt2b CKO mice was not affected at a Pi concentration of 4 mM, which is considered the typical luminal Pi concentration after meals in mice. Claudin, which may be involved in paracellular pathways, as well as claudin-2, 12, and 15 protein levels were significantly decreased in the Npt2b CKO mice. Thus, Npt2b deficiency did not affect Pi absorption within the range of Pi concentrations that normally occurs after meals. (徳島大学機関リポジトリ) ● Metadata: 111601 (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s10157-017-1497-3 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29128884 ● Search Scopus @ Elsevier (PMID): 29128884 ● Search Scopus @ Elsevier (DOI): 10.1007/s10157-017-1497-3 (徳島大学機関リポジトリ: 111601, DOI: 10.1007/s10157-017-1497-3, PubMed: 29128884)
13.	Sawako Tatsumi, A Miyagawa, Ichiro Kaneko, Y Shiozaki, Hiroko Segawa and Ken-ichi Miyamoto : Regulation of renal phosphate handling: inter-organ communication in health and disease., Journal of Bone and Mineral Metabolism, Vol.34, No.1, 1-10, 2016. (要約) In this review, we focus on the interconnection of inorganic phosphate (Pi) homeostasis in the network of the bone-kidney, parathyroid-kidney, intestine-kidney, and liver-kidney axes. Such a network of organ communication is important for body Pi homeostasis. Normalization of serum Pi levels is a clinical target in patients with chronic kidney disease (CKD). Particularly, disorders of the fibroblast growth factor 23/klotho system are observed in early CKD. Identification of phosphaturic factors from the intestine and liver may enhance our understanding of body Pi homeostasis and Pi metabolism disturbances in CKD patients. (キーワード) Bone and Bones / Homeostasis / Humans / Intestines / Kidney / Liver / Parathyroid Glands / Phosphates / Renal Insufficiency, Chronic (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s00774-015-0705-z (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26296817 ● Search Scopus @ Elsevier (PMID): 26296817 ● Search Scopus @ Elsevier (DOI): 10.1007/s00774-015-0705-z (DOI: 10.1007/s00774-015-0705-z, PubMed: 26296817)
14.	Yuji Shiozaki, Hiroko Segawa, Saori Ohnishi, Akiko Ohi, Mikiko Ito, Ichiro Kaneko, Shinsuke Kido, Sawako Tatsumi and Ken-ichi Miyamoto : Relationship between sodium-dependent phosphate transporter (NaPi-IIc) function and cellular vacuole formation in opossum kidney cells., The Journal of Medical Investigation : JMI, Vol.62, No.3-4, 209-218, 2015. (要約) NaPi-IIc/SLC34A3 is a sodium-dependent inorganic phosphate (Pi) transporter in the renal proximal tubules and its mutations cause hereditary hypophosphatemic rickets with hypercalciuria (HHRH). In the present study, we created a specific antibody for opossum SLC34A3, NaPi-IIc (oNaPi-IIc), and analyzed its localization and regulation in opossum kidney cells (a tissue culture model of proximal tubular cells). Immunoreactive oNaPi-IIc protein levels increased during the proliferative phase and decreased during differentiation. Moreover, stimulating cell growth upregulated oNaPi-IIc protein levels, whereas suppressing cell proliferation downregulated oNaPi-IIc protein levels. Immunocytochemistry revealed that endogenous and exogenous oNaPi-IIc proteins localized at the protrusion of the plasma membrane, which is a phosphatidylinositol 4,5-bisphosphate (PIP2) rich-membrane, and at the intracellular vacuolar membrane. Exogenous NaPi-IIc also induced cellular vacuoles and localized in the plasma membrane. The ability to form vacuoles is specific to electroneutral NaPi-IIc, and not electrogenic NaPi-IIa or NaPi-IIb. In addition, mutations of NaPi-IIc (S138F and R468W) in HHRH did not cause cellular PIP2-rich vacuoles. In conclusion, our data anticipate that NaPi-IIc may regulate PIP2 production at the plasma membrane and cellular vesicle formation. (徳島大学機関リポジトリ) ● Metadata: 111281 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.62.209 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26399350 ● Summary page in Scopus @ Elsevier: 2-s2.0-84942042069 (徳島大学機関リポジトリ: 111281, DOI: 10.2152/jmi.62.209, PubMed: 26399350, Elsevier: Scopus)
15.	Yutaka Taketani, Masashi Masuda, Hisami Okumura, Sawako Tatsumi, Hiroko Segawa, Ken-ichi Miyamoto, Eiji Takeda and Hironori Yamamoto : Niacin and Chronic Kidney Disease., Journal of Nutritional Science and Vitaminology, Vol.61 Suppl, S173-5, 2015. (要約) Chronic kidney disease (CKD) is an increasing problem worldwide. The number of end-stage renal disease patients requiring treatment by dialysis is estimated to be increasing by 10,000 patients per year in Japan. Furthermore, an estimated 13 million people are living with CKD in Japan. Various complications are associated with CKD, including cardiovascular disease (CVD). More than one-third of CKD patients die from CVD. Thus, prevention of CVD is a primary concern for the treatment of CKD patients. CKD-mineral and bone disorder (CKD-MBD) is a serious complication that typically leads to CVD. Hyperphosphatemia is thought to be a central-risk factor for CKD-MBD. Therefore, managing hyperphosphatemia is crucial to prevent CKD-MBD and CVD. It is difficult to achieve the target serum phosphate level through dietary modifications alone in patients with hyperphosphatemia, because most foods contain phosphate. Thus, phosphate binders such as calcium carbonate are commonly prescribed to CKD patients with hyperphosphatemia, but these have undesirable side effects. Inhibition of intestinal phosphate transport activity has also been investigated as an alternative approach for controlling serum phosphate levels in CKD patients. Nicotinamide, which is the amide of niacin, can inhibit intestinal phosphate transport. Niacin and related compounds have also been developed as drugs for hyperlipidemia conditions, especially hypertriglyceridemia with low high-density lipoprotein. This type of dyslipidemia is frequently observed in CKD patients and is a modifiable risk factor for CVD. Thus, niacin and related compounds may have utility for the treatment of both hyperphosphatemia and dyslipidemia in CKD patients to prevent CVD. (出版サイトへのリンク) ● Publication site (DOI): 10.3177/jnsv.61.S173 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26598845 ● Summary page in Scopus @ Elsevier: 2-s2.0-84950314636 (DOI: 10.3177/jnsv.61.S173, PubMed: 26598845, Elsevier: Scopus)
16.	Kengo Nomura, Sawako Tatsumi, Atsumi Miyagawa, Yuji Shiozaki, Shohei Sasaki, Ichiro Kaneko, Mikiko Ito, Shinsuke Kido, Hiroko Segawa, Mitsue Sano, Tsutomu Fukuwatari, Katsumi Shibata and Ken-ichi Miyamoto : Hepatectomy-related hypophosphatemia: a novel phosphaturic factor in the liver-kidney axis., Journal of the American Society of Nephrology, Vol.25, No.4, 761-772, 2014. (要約) Marked hypophosphatemia is common after major hepatic resection, but the pathophysiologic mechanism remains unknown. We used a partial hepatectomy (PH) rat model to investigate the molecular basis of hypophosphatemia. PH rats exhibited hypophosphatemia and hyperphosphaturia. In renal and intestinal brush-border membrane vesicles isolated from PH rats, Na(+)-dependent phosphate (Pi) uptake decreased by 50%-60%. PH rats also exhibited significantly decreased levels of renal and intestinal Na(+)-dependent Pi transporter proteins (NaPi-IIa [NaPi-4], NaPi-IIb, and NaPi-IIc). Parathyroid hormone was elevated at 6 hours after PH. Hyperphosphaturia persisted, however, even after thyroparathyroidectomy in PH rats. Moreover, DNA microarray data revealed elevated levels of nicotinamide phosphoribosyltransferase (Nampt) mRNA in the kidney after PH, and Nampt protein levels and total NAD concentration increased significantly in the proximal tubules. PH rats also exhibited markedly increased levels of the Nampt substrate, urinary nicotinamide (NAM), and NAM catabolites. In vitro analyses using opossum kidney cells revealed that NAM alone did not affect endogenous NaPi-4 levels. However, in cells overexpressing Nampt, the addition of NAM led to a marked decrease in cell surface expression of NaPi-4 that was blocked by treatment with FK866, a specific Nampt inhibitor. Furthermore, FK866-treated mice showed elevated renal Pi reabsorption and hypophosphaturia. These findings indicate that hepatectomy-induced hypophosphatemia is due to abnormal NAM metabolism, including Nampt activation in renal proximal tubular cells. (キーワード) Acrylamides / Animals / Hepatectomy / Hypophosphatemia / Kidney / Male / Mice / Mice, Inbred C57BL / NAD / Niacinamide / Nicotinamide Phosphoribosyltransferase / Parathyroidectomy / Piperidines / Rats / Rats, Wistar / Sodium-Phosphate Cotransporter Proteins / Sodium-Phosphate Cotransporter Proteins, Type IIa (徳島大学機関リポジトリ) ● Metadata: 106156 (出版サイトへのリンク) ● Publication site (DOI): 10.1681/ASN.2013060569 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24262791 ● Search Scopus @ Elsevier (PMID): 24262791 ● Search Scopus @ Elsevier (DOI): 10.1681/ASN.2013060569 (徳島大学機関リポジトリ: 106156, DOI: 10.1681/ASN.2013060569, PubMed: 24262791)
17.	Shinsuke Kido, Marina Fujihara, Kengo Nomura, Shohei Sasaki, Rie Mukai, Ritsuko Ohnishi, Ichiro Kaneko, Hiroko Segawa, Sawako Tatsumi, Hiroto Izumi, Kimitoshi Kohno and Ken-ichi Miyamoto : Molecular mechanisms of cadmium-induced fibroblast growth factor 23 upregulation in osteoblast-like cells., Toxicological Sciences, Vol.139, No.2, 301-316, 2014. (要約) Itai-itai disease is thought to be the result of chronic cadmium (Cd) intoxication. Renal proximal tubules are a major target of Cd toxicity. The whole mechanism of the adverse effects of Cd remains unresolved, especially how renal damage is related to the development of bone lesions. Fibroblast growth factor 23 (FGF23) is a bone-derived phosphaturic factor that regulates vitamin D and inorganic phosphate metabolism in the kidney. To clarify the role of FGF23 on Cd toxicity, we investigated the mechanisms of Cd-induced FGF23 production in the bone. Cd injection into mice significantly increased plasma FGF23 concentrations, but did not change FGF23 mRNA expression in bone. GalNAc-T3 is involved in secreting intact FGF23. To determine potential roles of GalNAc-T3 in Cd-induced FGF23 production, we examined the effect of Cd on GalNAc-T3 mRNA expression in vivo and in vitro. GalNAc-T3 gene expression was significantly increased in the bones of Cd-injected mice. Cd also enhanced the expression of GalNAc-T3 in cultured osteosarcoma UMR106 cells and primary osteocytes. Cd activated aryl hydrocarbon receptors (AhR) and AhR were required for GalNAc-T3 gene expression induced by Cd. In addition, Cd-dependent FGF23 production was completely inhibited by an AhR antagonist. AhR siRNA markedly suppressed the stimulation of transcriptional activity by Cd. Furthermore, Cd induced AhR activation via phosphorylation of Ser-68 by p38 kinase in the nuclear export signal of AhR. Thus, Cd stimulated GalNAc-T3 gene transcription via enhanced AhR binding to the GalNAc-T3 promoter. These findings suggest that the Cd-induced increase in GalNAc-T3 suppresses proteolytic processing of FGF23 and increases serum FGF23 concentrations. (キーワード) Animals / Cadmium Chloride / Cell Culture Techniques / Cell Line, Tumor / Female / Femur / Fibroblast Growth Factors / Gene Expression / Mice, Inbred C57BL / Mice, Inbred ICR / N-Acetylgalactosaminyltransferases / Osteoblasts / Osteocytes / Phosphorylation / Receptors, Aryl Hydrocarbon / Up-Regulation / p38 Mitogen-Activated Protein Kinases (出版サイトへのリンク) ● Publication site (DOI): 10.1093/toxsci/kfu043 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24614234 ● Summary page in Scopus @ Elsevier: 2-s2.0-84899983795 (DOI: 10.1093/toxsci/kfu043, PubMed: 24614234, Elsevier: Scopus)
18.	Shoko Ikeda, Hironori Yamamoto, Masashi Masuda, Yuichiro Takei, Otoki Nakahashi, Mina Kozai, Sarasa Tanaka, Mari Nakao, Yutaka Taketani, Hiroko Segawa, Masayuki Iwano, Ken-ichi Miyamoto and Eiji Takeda : Downregulation of renal type IIa sodium-dependent phosphate cotransporter during lipopolysaccharide-induced acute inflammation., American Journal of Physiology, Renal Physiology, Vol.306, No.7, F744-50, 2014. (要約) The type IIa sodium-dependent phosphate cotransporter (Npt2a) plays a critical role in reabsorption of inorganic phosphate (Pi) by renal proximal tubular cells. Pi abnormalities during early stages of sepsis have been reported, but the mechanisms regulating Pi homeostasis during acute inflammation are poorly understood. We examined the regulation of Pi metabolism and renal Npt2a expression during lipopolysaccharide (LPS)-induced inflammation in mice. Dose-response and time-course studies with LPS showed significant increases of plasma Pi and intact parathyroid hormone (iPTH) levels and renal Pi excretion, while renal calcium excretion was significantly decreased. There was no difference in plasma 1,25-dihydroxyvitamin D levels, but the induction of plasma intact fibroblast growth factor 23 levels peaked 3 h after LPS treatment. Western blotting, immunostaining, and quantitative real-time PCR showed that LPS administration significantly decreased Npt2a protein expression in the brush border membrane (BBM) 3 h after injection, but there was no change in renal Npt2a mRNA levels. Moreover, tumor necrosis factor- injection also increased plasma iPTH and decreased renal BBM Npt2a expression. Importantly, we revealed that parathyroidectomized rats had impaired renal Pi excretion and BBM Npt2a expression in response to LPS. These results suggest that the downregulation of Npt2a expression in renal BBM through induction of plasma iPTH levels alter Pi homeostasis during LPS-induced acute inflammation. (キーワード) Acute Disease / Animals / Calcium / Disease Models, Animal / Down-Regulation / Fibroblast Growth Factors / Inflammation / Injections, Intraperitoneal / Kidney / Lipopolysaccharides / Male / Mice / Mice, Inbred C3H / Mice, Inbred C57BL / Microvilli / Parathyroid Hormone / Parathyroidectomy / Phosphates / RNA, Messenger / Rats / Rats, Wistar / Sodium-Phosphate Cotransporter Proteins, Type IIa / Time Factors / Tumor Necrosis Factor-alpha / Vitamin D (徳島大学機関リポジトリ) ● Metadata: 106168 (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajprenal.00474.2013 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24500689 ● Search Scopus @ Elsevier (PMID): 24500689 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00474.2013 (徳島大学機関リポジトリ: 106168, DOI: 10.1152/ajprenal.00474.2013, PubMed: 24500689)
19.	Ritsuko Ohnishi, Hiroko Segawa, Tomoyo Ohmoto, Shohei Sasaki, Ai Hanazaki, Ayaka Mori, Kayo Ikuta, Junya Furutani, Eri Kawakami, Sawako Tatsumi, Yasuhiro Hamada and Ken-ichi Miyamoto : Effect of dietary components on renal inorganic phosphate (Pi) excretion induced by a Pi-depleted diet., The Journal of Medical Investigation : JMI, Vol.61, No.1-2, 162-170, 2014. (要約) Dietary inorganic phosphate (Pi) is the most important factor in the regulation of renal Pi excretion. Recent studies suggest the presence of an enteric-renal signaling axis for dietary Pi as well as the existence of a mechanism by which the intestine detects changes in luminal Pi concentrations. The mechanisms of intestinal Pi sensing, however, are unknown. In the present study, we focused on Pi depletion signals and investigated the effects of dietary components on intestinal Pi sensing. After feeding rats experimental diets for 3 days, we investigated urinary Pi excretion and plasma biochemical parameters. Renal Pi excretion was suppressed in rats fed a low-Pi diet (0.02% Pi). Elimination of dietary calcium (Ca) completely blocked the suppression of Pi excretion, suggesting that the presence of Ca is essential for the Pi depletion signal. Furthermore, a minimum Ca content of more than 0.02% was necessary for the Pi depletion signal. Magnesium, lanthanum, and strontium, which are agonists of calcium sensing receptor, instead of Ca, reduced Pi excretion. Therefore, dietary Ca appears to be important for the Pi depletion-sensing mechanism in the gastrointestinal tract. In addition, the calcium sensing receptor may be involved in the Pi depletion signal. (キーワード) dietary phosphate / sensing / calcium / phosphate excretion (徳島大学機関リポジトリ) ● Metadata: 109545 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.61.162 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24705762 ● CiNii @ 国立情報学研究所 (CRID): 1390001204244658176 ● Summary page in Scopus @ Elsevier: 2-s2.0-84897932982 (徳島大学機関リポジトリ: 109545, DOI: 10.2152/jmi.61.162, PubMed: 24705762, CiNii: 1390001204244658176, Elsevier: Scopus)
20.	木戸慎介, 桑原頌治, 野村憲吾, 大井彰子, 辰巳佐和子, 瀬川博子, 宮本賢一 : FGF23の作用と作用機序., 25-31, 2012年.
21.	Shoji Kuwahara, Fumito Aranami, Hiroko Segawa, Akemi Onitsuka, Naoko Honda, Rieko Tominaga, Etsuyo Hanabusa, Ichiro Kaneko, Setsuko Yamanaka, Shohei Sasaki, Akiko Ohi, Kengo Nomura, Sawako Tatsumi, Shinsuke Kido, Mikiko Ito and Ken-ichi Miyamoto : Identification and functional analysis of a splice variant of mouse sodium-dependent phosphate transporter Npt2c., The Journal of Medical Investigation : JMI, Vol.59, No.1-2, 116-126, 2012. (要約) Mutations in the SLC34A3 gene, a sodium-dependent inorganic phosphate (Pi) cotransporter, also referred to as NaPi IIc, causes hereditary hypophosphatemic rickets with hypercalciuria (HHRH), an autosomal recessive disorder. In human and rodent, NaPi IIc is mainly localized in the apical membrane of renal proximal tubular cells. In this study, we identified mouse NaPi IIc variant (Npt2c-v1) that lacks the part of the exon 3 sequence that includes the assumed translation initiation site of Npt2c. Microinjection of mouse Npt2c-v1 cRNA into Xenopus oocytes demonstrated that Npt2c-v1 showed sodium-dependent Pi cotransport activity. The characterization of pH dependency showed activation at extracellular alkaline-pH. Furthermore, Npt2c-v1 mediated Pi transport activity was significantly higher at any pH value than those of Npt2c. In an in vitro study, the localization of the Npt2c-v1 protein was detected in the apical membrane in opossum kidney cells. The expression of Npt2c-v1 mRNA was detected in the heart, spleen, testis, uterus, placenta, femur, cerebellum, hippocampus, diencephalon and brain stem of mouse. Using mouse bone primary cultured cells, we showed the expression of Npt2c-v1 mRNA. In addition, the Npt2c protein was detected in the spermatozoa head. Thus, Npt2c-v1 was expressed in extra-renal tissues such as epididymal spermatozoa and may function as a sodium-dependent phosphate transporter. (キーワード) Alternative Splicing / Animals / COS Cells / Cercopithecus aethiops / Female / Kidney / Male / Mice / Mice, Inbred C57BL / Opossums / Osteoblasts / Osteocytes / Primary Cell Culture / Sodium-Phosphate Cotransporter Proteins, Type IIc (徳島大学機関リポジトリ) ● Metadata: 106008 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.59.116 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22450000 ● Search Scopus @ Elsevier (PMID): 22450000 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.59.116 (徳島大学機関リポジトリ: 106008, DOI: 10.2152/jmi.59.116, PubMed: 22450000)
22.	Sakiko Haito-Sugino, Mikiko Ito, Akiko Ohi, Yuji Shiozaki, Natsumi Kangawa, Takashi Nishiyama, Fumito Aranami, Shohei Sasaki, Ayaka Mori, Shinsuke Kido, Sawako Tatsumi, Hiroko Segawa and Ken-ichi Miyamoto : Processing and stability of type IIc sodium-dependent phosphate cotransporter mutations in patients with hereditary hypophosphatemic rickets with hypercalciuria., American Journal of Physiology, Cell Physiology, Vol.302, No.9, C1316-30, 2011. (要約) Mutations in the apically located Na(+)-dependent phosphate (NaPi) cotransporter, SLC34A3 (NaPi-IIc), are a cause of hereditary hypophosphatemic rickets with hypercalciuria (HHRH). We have characterized the impact of several HHRH mutations on the processing and stability of human NaPi-IIc. Mutations S138F, G196R, R468W, R564C, and c.228delC in human NaPi-IIc significantly decreased the levels of NaPi cotransport activities in Xenopus oocytes. In S138F and R564C mutant proteins, this reduction is a result of a decrease in the V(max) for P(i), but not the K(m). G196R, R468W, and c.228delC mutants were not localized to oocyte membranes. In opossum kidney (OK) cells, cell surface labeling, microscopic confocal imaging, and pulse-chase experiments showed that G196R and R468W mutations resulted in an absence of cell surface expression owing to endoplasmic reticulum (ER) retention. G196R and R468W mutants could be partially stabilized by low temperature. In blue native-polyacrylamide gel electrophoresis analysis, G196R and R468W mutants were either denatured or present in an aggregation complex. In contrast, S138F and R564C mutants were trafficked to the cell surface, but more rapidly degraded than WT protein. The c.228delC mutant did not affect endogenous NaPi uptake in OK cells. Thus, G196R and R468W mutations cause ER retention, while S138F and R564C mutations stimulate degradation of human NaPi-IIc in renal epithelial cells. Together, these data suggest that the NaPi-IIc mutants in HHRH show defective processing and stability. (キーワード) Animals / Blotting, Western / Humans / Hypercalciuria / Hypophosphatemic Rickets, X-Linked Dominant / Immunoprecipitation / Microscopy, Confocal / Mutagenesis, Site-Directed / Mutation / Polymerase Chain Reaction / Protein Stability / Sodium-Phosphate Cotransporter Proteins, Type IIc / Transfection / Xenopus laevis (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajpcell.00314.2011 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22159077 ● Search Scopus @ Elsevier (PMID): 22159077 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpcell.00314.2011 (DOI: 10.1152/ajpcell.00314.2011, PubMed: 22159077)
23.	Akiko Ohi, Etsuyo Hanabusa, Otoya Ueda, Hiroko Segawa, Naoshi Horiba, Ichiro Kaneko, Shoji Kuwahara, Tomo Mukai, Shohei Sasaki, Rieko Tominaga, Junya Furutani, Fumito Aranami, Shuichi Ohtomo, Yumiko Oikawa, Yousuke Kawase, A Naoko Wada, Takanori Tachibe, Mami Kakefuda, Hiromi Tateishi, Kaoru Matsumoto, Sawako Tatsumi, Shinsuke Kido, Naoshi Fukushima, Kou-Ichi Jishage and Ken-ichi Miyamoto : Inorganic phosphate homeostasis in sodium-dependent phosphate cotransporter Npt2b^+/- mice., American Journal of Physiology, Renal Physiology, Vol.301, No.5, F1105-13, 2011. (要約) An inorganic phosphate (P(i))-restricted diet is important for patients with chronic kidney disease and patients on hemodialysis. Phosphate binders are essential for preventing hyperphosphatemia and ectopic calcification. The sodium-dependent P(i) (Na/P(i)) transport system is involved in intestinal P(i) absorption and is regulated by several factors. The type II sodium-dependent P(i) transporter Npt2b is expressed in the brush-border membrane in intestinal epithelial cells and transports P(i). In the present study, we analyzed the phenotype of Npt2b(-/-) and hetero(+/-) mice. Npt2b(-/-) mice died in utero soon after implantation, indicating that Npt2b is essential for early embryonic development. At 4 wk of age, Npt2b(+/-) mice showed hypophosphatemia and low urinary P(i) excretion. Plasma fibroblast growth factor 23 levels were significantly decreased and 1,25(OH)(2)D(3) levels were significantly increased in Npt2b(+/-) mice compared with Npt2b(+/+) mice. Npt2b mRNA levels were reduced to 50% that in Npt2b(+/+) mice. In contrast, renal Npt2a and Npt2c transporter protein levels were significantly increased in Npt2b(+/-) mice. At 20 wk of age, Npt2b(+/-) mice showed hypophosphaturia and reduced Na/P(i) cotransport activity in the distal intestine. Npt2b(+/+) mice with adenine-induced renal failure had hyperphosphatemia and high plasma creatinine levels. Npt2b(+/-) mice treated with adenine had significantly reduced plasma P(i) levels compared with Npt2b(+/+) mice. Intestinal Npt2b protein and Na(+)/P(i) transport activity levels were significantly lower in Npt2b(+/-) mice than in the Npt2b(+/+) mice. The findings of the present studies suggest that Npt2b is an important target for the prevention of hyperphosphatemia. (キーワード) Adenine / Animals / Blotting, Western / Body Weight / Chromosomes, Artificial, Bacterial / DNA / Diet / Female / Genetic Vectors / Genotype / Homeostasis / Intestines / Mice / Mice, Inbred C57BL / Mice, Knockout / Microvilli / Phosphates / Polymerase Chain Reaction / Pregnancy / Renal Insufficiency / Sodium / Sodium-Phosphate Cotransporter Proteins, Type IIb (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajprenal.00663.2010 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21816756 ● Search Scopus @ Elsevier (PMID): 21816756 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00663.2010 (DOI: 10.1152/ajprenal.00663.2010, PubMed: 21816756)
24.	Mariko Ishiguro, Hironori Yamamoto, Masashi Masuda, Mina Kozai, Yuichiro Takei, Sarasa Tanaka, Tadatoshi Sato, Hiroko Segawa, Yutaka Taketani, Hidekazu Arai, Ken-ichi Miyamoto and Eiji Takeda : Thyroid hormones regulate phosphate homoeostasis through transcriptional control of the renal type IIa sodium-dependent phosphate co-transporter (Npt2a) gene., The Biochemical Journal, Vol.427, No.1, 161-169, 2010. (要約) The type IIa renal sodium-dependent phosphate (Na/Pi) co-transporter Npt2a is implicated in the control of serum phosphate levels. It has been demonstrated previously that renal Npt2a protein and its mRNA expression are both up-regulated by the thyroid hormone T3 (3,3',5-tri-iodothyronine) in rats. However, it has never been established whether the induction was mediated by a direct effect of thyroid hormones on the Npt2a promoter. To address the role of Npt2a in T3-dependent regulation of phosphate homoeostasis and to identify the molecular mechanisms by which thyroid hormones modulate Npt2a gene expression, mice were rendered pharmacologically hypo- and hyper-thyroid. Hypothyroid mice showed low levels of serum phosphate and a marked decrease in renal Npt2a protein abundance. Importantly, we also showed that Npt2a-deficient mice had impaired serum phosphate responsiveness to T3 compared with wild-type mice. Promoter analysis with a luciferase assay revealed that the transcriptional activity of a reporter gene containing the Npt2a promoter and intron 1 was dependent upon TRs (thyroid hormone receptors) and specifically increased by T3 in renal cells. Deletion analysis and EMSAs (electrophoretic mobility-shift assays) determined that there were unique TREs (thyroid-hormone-responsive elements) within intron 1 of the Npt2a gene. These results suggest that Npt2a plays a critical role as a T3-target gene, to control phosphate homoeostasis, and that T3 transcriptionally activates the Npt2a gene via TRs in a renal cell-specific manner. (キーワード) Animals / COS Cells / Cercopithecus aethiops / Dogs / Electrophoretic Mobility Shift Assay / Female / Gene Expression Regulation / Hela Cells / 生体恒常性 (homeostasis) / Humans / Kidney / Luciferases / Male / Mice / Mice, Knockout / Phosphates / Promoter Regions, Genetic / Rats / Receptors, Thyroid Hormone / Response Elements / Sodium-Phosphate Cotransporter Proteins, Type IIa / Transcription, Genetic / Transcriptional Activation / Triiodothyronine (出版サイトへのリンク) ● Publication site (DOI): 10.1042/BJ20090671 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20088828 ● Summary page in Scopus @ Elsevier: 2-s2.0-77950874525 (DOI: 10.1042/BJ20090671, PubMed: 20088828, Elsevier: Scopus)
25.	hua Yin, Nagakatsu Harada, Kazuaki Mawatari, Yasui Sonoko, Hiroko Segawa, Akira Takahashi, Shuzo Oshita and Yutaka Nakaya : L-DOPA inhibits nitric oxide-dependent vasorelaxation via production of reactive ozygen species in rat aorta, The Journal of Medical Investigation : JMI, Vol.56, No.3,4, 120-129, 2009. (要約) To clarify the underlying mechanisms of L-DOPA induced vasoconstriction in rat aorta. Methods: The effect of L-DOPA on phenylephrine-induced contractile force of blood vessels was examined in vitro using rat aortic ring preparations by isometric tension experiment. Involvement of nitric oxide (NO) in the effect of L-DOPA on vascular smooth muscle was studied by using N(omega)-Nitro-L-arginine (L-NNA), Sodium nitroprusside (SNP) in endothelium-intact and endothelium-denuded aortic rings. L-DOPA potentiated alpha-adrenergic receptor- and depolarization-induced vascular contraction and inhibited acetylcholine-induced vasorelaxation. This effect was diminished by pretreatment of the aortic rings with L-NNA, an inhibitor of NO synthesis, or by removing the endothelium from the ring preparations. In endothelium-denuded rings, L-DOPA inhibited exogenous NO-dependent but not cGMP-mediated vasorelaxation. Increases in cGMP levels in response to an NO donor were attenuated by L-DOPA in cultured rat aortic smooth muscle cells. L-DOPA could not contract rings (without endothelium) pretreated with 3-(5'-hydroxymethyl- 2'-furyl)-1-benzyl indazole (YC-1), an activator of guanylyl cyclase, but SOD (150 U/ml) pretreatment of rings with endothelium inhibited contraction by L-DOPA. These results suggest that L-DOPA inhibits nitric-dependent vasorelaxation on vascular smooth muscle cells via production of reactive oxygen species. (キーワード) Animals / Aorta, Thoracic / Cells, Cultured / Cyclic GMP / Drug Synergism / Endothelium, Vascular / Guanylate Cyclase / Levodopa / Male / Myocytes, Smooth Muscle / Nitric Oxide / Phenylephrine / Rats / Rats, Wistar / Reactive Oxygen Species / Receptors, Cytoplasmic and Nuclear / Vasodilation (徳島大学機関リポジトリ) ● Metadata: 111318 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.56.120 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19763024 ● Search Scopus @ Elsevier (PMID): 19763024 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.56.120 (徳島大学機関リポジトリ: 111318, DOI: 10.2152/jmi.56.120, PubMed: 19763024)
26.	Naoki Sawada, Yutaka Taketani, Norio Amizuka, Masako Ichikawa, Chiharu Ogawa, Kaori Nomoto, Kunitaka Nashiki, Tadatoshi Sato, Hidekazu Arai, Masashi Isshiki, Hiroko Segawa, Hironori Yamamoto, Ken-ichi Miyamoto and Eiji Takeda : Caveolin-1 in extracellular matrix vesicles secreted from osteoblasts., Bone, Vol.41, No.1, 52-58, 2007. (要約) Caveolin-1 is an essential and signature protein of caveolae, which are small invaginations of the plasma membrane enriched in cholesterol and sphingolipids. Although high levels of expression of caveolin-1 have been demonstrated in osteoblasts as well as endothelial cells, fibroblasts, and muscular cells, the role of caveolin-1 in osteoblasts has not been clarified. Here, we show that caveolin-1 is secreted from osteoblasts in the form of matrix vesicles; extracellular vesicles released from the plasma membrane of osteoblasts. In this study, caveolae and matrix vesicles were similarly enriched in cholesterol and sphingomyelin in fractions isolated from mineralizing MC3T3-E1 cells. Interestingly, in the MC3T3-E1 cells caveolin-1 was enriched in the matrix vesicle fraction as well as the caveolar membrane fraction, and the amount of caveolin-1 in the matrix vesicle fraction increased as differentiation progressed. Localization of caveolin-1 in matrix vesicles was also confirmed in murine tibia. Furthermore, overexpression of caveolin-1 enhanced matrix calcification in MC3T3-E1 cells, whereas knockdown of caveolin-1 diminished it. These results suggest that secreted caveolin-1 as a component of matrix vesicles may play an important role in osteoblast calcification. (キーワード) 3T3 Cells / Alkaline Phosphatase / Animals / Base Sequence / Calcification, Physiologic / Caveolin 1 / Cell Differentiation / Cholesterol / DNA Primers / Extracellular Matrix / Gene Expression / Mice / Microscopy, Immunoelectron / Osteoblasts / Phosphates / RNA Interference / Secretory Vesicles / Sphingomyelins / Tibia (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bone.2007.02.030 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17448744 ● Search Scopus @ Elsevier (PMID): 17448744 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bone.2007.02.030 (DOI: 10.1016/j.bone.2007.02.030, PubMed: 17448744)
27.	Masashi Kuwahata, Y Tomoe, Nagakatsu Harada, S Amano, Hiroko Segawa, S Tatsumi, Mikiko Ito, T Oka and Ken-ichi Miyamoto : Characterization of the molecular mechanisms involved in the increased insulin secretion in rats with acute liver failure., Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Vol.1772, No.1, 60-65, 2007. (要約) To investigate the mechanism of hyperinsulinaemia in rats with acute liver failure induced by the administration of d-galactosamine (GalN), we focused on the role of polyprimidine tract-binding protein (PTB) in islet insulin synthesis. Recent reports indicate that PTB binds and stabilizes mRNA encoding insulin and insulin secretory granule proteins, including islet cell autoantigen 512 (ICA512), prohormone convertase 1/3 (PC1/3), and PC2. In the present study, glucose-stimulated insulin secretion was significantly increased in GalN-treated rats compared to controls. Levels of mRNA encoding insulin 1, ICA512, and PC1/3 were increased in the pancreatic islets of GalN-treated rats. This mRNA level elevation was not prevented by pretreatment with actinomycin D. When the PTB-binding site in insulin 1 mRNA was incubated with the islet cytosolic fraction, the RNA-protein complex level was increased in the cytosolic fraction obtained from GalN-treated rats compared to the level in control rats. The cytosolic fraction obtained from pancreatic islets obtained from GalN-treated rats had an increased PTB level compared to the levels obtained from the pancreatic islets of control rats. These findings suggest that, in rats with acute liver failure, cytosolic PTB binds and stabilizes mRNA encoding insulin and its secretory granule proteins. (キーワード) Alanine Transaminase / Animals / Blood Glucose / Disease Models, Animal / Galactosamine / Hyperinsulinism / Insulin / Islets of Langerhans / Liver Failure, Acute / Male / Organ Size / Polypyrimidine Tract-Binding Protein / RNA, Messenger / Rats / Rats, Sprague-Dawley / Up-Regulation (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bbadis.2006.10.001 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17097861 ● Search Scopus @ Elsevier (PMID): 17097861 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbadis.2006.10.001 (DOI: 10.1016/j.bbadis.2006.10.001, PubMed: 17097861)
28.	Hiroko Segawa, Setsuko Yamanaka, Akemi Onitsuka, Yuka Tomoe, Masashi Kuwahata, Mikiko Ito, Yutaka Taketani and Ken-ichi Miyamoto : Parathyroid hormone-dependent endocytosis of renal type IIc Na-Pi cotransporter., American Journal of Physiology, Renal Physiology, Vol.292, No.1, F395-F403, 2007. (要約) Hereditary hypophosphatemic rickets with hypercalciuria results from mutations of the renal type IIc Na-P(i) cotransporter gene, suggesting that the type IIc transporter plays a prominent role in renal phosphate handling. The goal of the present study was to investigate the regulation of the type IIc Na-P(i) cotransporter by parathyroid hormone (PTH). Type IIc Na-P(i) cotransporter levels were markedly increased in thyroparathyroidectomized (TPTX) rats. Four hours after administration of PTH, type IIc transporter protein levels were markedly decreased in the apical membrane fraction but recovered to baseline levels at 24 h. Immunohistochemical analyses demonstrated the presence of the type IIc transporter in the apical membrane and subapical compartments in the proximal tubular cells in TPTX animals. After administration of PTH, the intensity of immunoreactive signals in apical and subapical type IIc transporter decreased in the renal proximal tubular cells in TPTX rats. Colchicine completely blocked the internalization of the type IIc transporter. In addition, leupeptin prevented the PTH-mediated degradation of the type IIa transporter in lysosomes but had no effect on PTH-mediated degradation of the lysosomal type IIc transporter. In PTH-treated TPTX rats, the internalization of the type IIc transporter occurred after administration of PTH(1-34) (PKA and PKC activator) or PTH(3-34) (PKC activator). Thus the present study demonstrated that PTH is a major hormonal regulator of the type IIc Na-P(i) cotransporter in renal proximal tubules. (キーワード) Animals / Blotting, Northern / Cell Membrane / Endocytosis / Immunohistochemistry / Kidney / Lysosomes / Male / Microscopy, Fluorescence / Microtubules / Microvilli / Parathyroid Hormone / Parathyroidectomy / Peptide Fragments / Phosphates / RNA / Rats / Rats, Wistar / Sodium-Phosphate Cotransporter Proteins, Type IIa / Thyroidectomy (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajprenal.00100.2006 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16985216 ● Search Scopus @ Elsevier (PMID): 16985216 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00100.2006 (DOI: 10.1152/ajprenal.00100.2006, PubMed: 16985216)
29.	宮本賢一, 瀬川博子, 伊藤美紀子, 辰巳佐和子, 竹谷豊 : リンとビタミンDの相互作用, 整形・災害外科, Vol.49, No.12, 1365-1370, 2006年. (キーワード) Transporter / Kidney / FGF23 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1520291855700655232 (CiNii: 1520291855700655232)
30.	Ken-ichi Miyamoto, Mikiko Ito, Hiroko Segawa and Masashi Kuwahata : Molecular mechanism in biological transport in the kidney: Sodium-dependent glucose, phosphate, amino acid transporters., Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.64, 145-149, 2006. (キーワード) Amino Acid Transport Systems, Neutral / Amino Acids, Neutral / Animals / Biological Transport / GABA Plasma Membrane Transport Proteins / Glucose / Humans / Kidney Tubules / Phosphates / Sodium-Glucose Transporter 1 / Sodium-Glucose Transporter 2 / Sodium-Phosphate Cotransporter Proteins, Type IIa / Sodium-Phosphate Cotransporter Proteins, Type IIc (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16523877 ● Search Scopus @ Elsevier (PMID): 16523877 (PubMed: 16523877)
31.	宮本賢一, 瀬川博子 : FGF23, 医学のあゆみ, Vol.216, No.2, 185-186, 2006年.
32.	宮本賢一, 瀬川博子, 伊藤美紀子, 辰巳佐和子, 竹谷豊 : 栄養素の代謝と生理機能, 病態栄養専門師のための病態栄養ガイドブック, 14-19, 2006年. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1020000781987488265 (CiNii: 1020000781987488265)
33.	瀬川博子, 塩澤和代, 鬼塚朱美, 荒波史, 古谷順也, 伊藤美紀子, 桑波田雅士, 宮本賢一 : リン酸トランスポーターをめぐる最近の話題, 腎と透析, Vol.61, No.1, 125-130, 2006年. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1010282256960838282 (CiNii: 1010282256960838282)
34.	宮本賢一, 伊藤美紀子, 瀬川博子, 桑波田雅士 : ナトリウム・グルコース，ナトリウム・リン，ナトリウム・アミノ酸共役トランスポーター, 日本臨牀, Vol.64, No.2, 145-149, 2006年.
35.	宮本賢一, 竹谷豊, 伊藤美紀子, 瀬川博子 : ナトリウム依存症リントランスポータ-の調節機構, Annual Review 腎臓, 216-220, 2006年. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1020000781987488258 (CiNii: 1020000781987488258)
36.	瀬川博子, 宮本賢一 : 生体内におけるリンの役割, --- 光と影 ---, 腎と透析, Vol.60, No.1, 36-41, 2006年. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1020000781987488257 (CiNii: 1020000781987488257)
37.	Yoshio Inoue, Hiroko Segawa, Ichiro Kaneko, Setsuko Yamanaka, Kenichiro Kusano, Eri Kawakami, Junya Furutani, Mikiko Ito, Masashi Kuwahata, Hitoshi Saito, Naoshi Fukushima, Shigeaki Kato, Hiro-omi Kanayama and Ken-ichi Miyamoto : Role of the vitamin D receptor in FGF23 action on phosphate metabolism, The Biochemical Journal, Vol.390, No.1, 325-331, 2005. (要約) FGF23 (fibroblast growth factor 23) is a novel phosphaturic factor that influences vitamin D metabolism and renal re-absorption of Pi. The goal of the present study was to characterize the role of the VDR (vitamin D receptor) in FGF23 action using VDR(-/-) (VDR null) mice. Injection of FGF23M (naked DNA encoding the R179Q mutant of human FGF23) into VDR(-/-) and wildtype VDR(+/+) mice resulted in an elevation in serum FGF23 levels, but had no effect on serum calcium or parathyroid hormone levels. In contrast, injection of FGF23M resulted in significant decreases in serum Pi levels, renal Na/Pi co-transport activity and type II transporter protein levels in both groups when compared with controls injected with mock vector or with FGFWT (naked DNA encoding wild-type human FGF23). Injection of FGF23M resulted in a decrease in 25-hydroxyvitamin D 1a-hydroxylase mRNA levels in VDR(-/-) and VDR(+/+) mice, while 25-hydroxyvitamin D 24-hydroxylase mRNA levels were significantly increased in FGF23M-treated animals compared with mock vector control- or FGF23WT-treated animals. The degree of 24-hydroxylase induction by FGF23M was dependent on the VDR, since FGF23M significantly reduced the levels of serum 1,25(OH)2D3 [1,25-hydroxyvitamin D3] in VDR(+/+) mice, but not in VDR(-/-) mice. We conclude that FGF23 reduces renal Pi transport and 25-hydroxyvitamin D 1a-hydroxylase levels by a mechanism that is independent of the VDR. In contrast, the induction of 25-hydroxyvitamin D 24-hydroxylase and the reduction of serum 1,25(OH)2D3 levels induced by FGF23 are dependent on the VDR. (キーワード) fibroblast growth factor 23 / kidney / phosphate transport / vitamin D receptor (出版サイトへのリンク) ● Publication site (DOI): 10.1042/BJ20041799 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15885032 ● Search Scopus @ Elsevier (PMID): 15885032 ● Search Scopus @ Elsevier (DOI): 10.1042/BJ20041799 (DOI: 10.1042/BJ20041799, PubMed: 15885032)
38.	Ken-ichi Miyamoto, Mikiko Ito, Masashi Kuwahata, Shigeaki Kato and Hiroko Segawa : Inhibition of Intestinal Sodium-dependent Inorganic phosphate Transport by Fibroblast Growth Factor 23, Therapeutic Apheresis and Dialysis, Vol.9, No.4, 331-335, 2005. (要約) The mechanisms by which fibroblast growth factor 23 (FGF23) alters inorganic phosphate (Pi) homeostasis is not entirely clear. In the present study, we examined the effect of FGF23 on intestinal sodium-dependent Pi transport in mice. Injection of FGF23(R179Q) markedly reduced serum Pi and 1,25(OH)2D3 levels in normal mice. Those animals show the reduction of intestinal sodium-dependent Pi transport activity and the amount of type IIb sodium-dependent Pi cotransporter (type IIb NaPi) protein in the brush border membrane vesicles. In vitamin D receptor null mice (VDR-/-), FGF23(R179Q) had no effect on intestinal sodium-dependent Pi transport activity and type IIb NaPi protein levels. The present study suggests that FGF23(R179Q) reduces intestinal sodium-dependent Pi transport activity and type IIb NaPi protein levels by a mechanism that is dependent on VDR. (キーワード) Fibroblast growth factor 23 / Inorganic phosphate / Small intestine / Vitamin D receptor (出版サイトへのリンク) ● Publication site (DOI): 10.1111/j.1744-9987.2005.00292.x (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16076377 ● Search Scopus @ Elsevier (PMID): 16076377 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1744-9987.2005.00292.x (DOI: 10.1111/j.1744-9987.2005.00292.x, PubMed: 16076377)
39.	Akira Matsuo, Tamotsu Negoro, Tomohisa Seo, Yuki Kitao, Masanori Shindo, Hiroko Segawa and Ken-ichi Miyamoto : Inhibitory effect of JTP-59557, a new triazole derivative, on intestinal phosphate transport in vitro and in vivo, European Journal of Pharmacology, Vol.517, No.1-2, 111-119, 2005. (要約) JTP-59557 [(-)-4-(2-tert-Butyl-4,5-dichlorophenyl)-5-(5-trifluoromethylpyridin-2-ylsulfanyl)-4H-[1,2,4]triazol-3-ol] showed an inhibitory effect on Na(+)-dependent inorganic phosphate (Pi) transport in intestinal brush border membrane vesicles with an IC(50) value of 0.40 microM in rabbit and with an IC(50) of 0.19 microM in rat, without affecting Na(+)-independent Pi and Na(+)-dependent d-glucose transport activities. In Chinese hamster ovary (CHO) cells expressing human type IIb Na/Pi cotransporter (type IIb), JTP-59557 decreased human type IIb-mediated Pi uptake with an IC(50) of 0.12 microM. In rabbit intestinal brush border membrane vesicles, JTP-59557 behaved as a noncompetitive inhibitor with respect to Pi. In an in vivo study, single administration of JTP-59557 significantly decreased the intestinal Pi absorption rate, when either Pi solution or laboratory chow was given to rats. In this report, we show that JTP-59557 is a potent, selective, stereospecific, noncompetitive inhibitor of intestinal Na/Pi cotransporters including type IIb, and it may represent a new class of intestinal Pi absorption inhibitor. (キーワード) JTP-59557 / Type 2b Na/Pi cotransporter / Intestinal Na+-dependent Pi transport / Pi absorption (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.ejphar.2005.05.003 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15961073 ● Search Scopus @ Elsevier (PMID): 15961073 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2005.05.003 (DOI: 10.1016/j.ejphar.2005.05.003, PubMed: 15961073)
40.	Mikiko Ito, Yuko Sakai, Mari Furumoto, Hiroko Segawa, Sakiko Haito, Setsuko Yamanaka, Rie Nakamura, Masashi Kuwahata and Ken-ichi Miyamoto : Vitamin D and phosphate regulate fibroblast growth factor-23 in K-562 cells, American Journal of Physiology, Endocrinology and Metabolism, Vol.288, No.6, E1101-E1109, 2005. (要約) Fibroblast growth factor-23 (FGF-23) has been recently identified as playing an important pathophysiological role in phosphate homeostasis and vitamin D metabolism. To elucidate the precise physiological regulation of FGF-23, we characterized the mouse FGF-23 5'-flanking region and analyzed its promoter activity. The 5'-flanking region of the mouse FGF-23 gene contained a TFIID site (TATA box) and several putative transcription factor binding sites, including MZF1, GATA-1 and c-Ets-1 motifs, but it did not contain the typical sequences of the vitamin D response element. Plasmids encoding 554-bp (pGL/-0.6), 364-bp (pGL/-0.4) and 200-bp (pGL/-0.13) promoter regions containing the TFIID element and +1-bp fragments drove the downstream expression of a luciferase reporter gene in transfection assays. We also found that FGF-23 mRNA was expressed in K-562 erythroleukemia cell lines but not in MC3T3-E1, Raji, or Hep G2 human carcinoma cells. Treatment with 1,25-dihydroxyvitamin D3 in the presence of high phosphate markedly stimulated pGL/-0.6 activity, but calcium had no effect. In addition, the plasma FGF-23 levels were affected by the dietary and plasma inorganic phosphate concentrations. Finally, the levels of plasma FGF-23 in vitamin D receptor-null mice were significantly lower than in wild-type mice. The presents study demonstrated that vitamin D and the plasma phosphate level are important regulators of the transcription of the mouse FGF-23 gene. (キーワード) Animals / Base Sequence / Calcitriol / Cloning, Molecular / DNA / Fibroblast Growth Factors / Humans / K562 Cells / Male / Mice / Mice, Inbred C57BL / Mice, Knockout / Molecular Sequence Data / Phosphates / Polymerase Chain Reaction / Promoter Regions, Genetic / RNA, Messenger / Receptors, Calcitriol / Vitamin D Response Element (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajpendo.00502.2004 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15671080 ● Search Scopus @ Elsevier (PMID): 15671080 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.00502.2004 (DOI: 10.1152/ajpendo.00502.2004, PubMed: 15671080)
41.	Mikiko Ito, Naoko Matsuka, Michiyo Izuka, Sakiko Haito, Yuko Sakai, Rie Nakamura, Hiroko Segawa, Masashi Kuwahata, Hironori Yamamoto, Wesley J Pike and Ken-ichi Miyamoto : Characterization of inorganic phosphate transport in osteoclast-like cells, American Journal of Physiology, Cell Physiology, Vol.288, No.4, 921-931, 2005. (要約) Osteoclasts possess inorganic phosphate (Pi) transport systems to take up external Pi during bone resorption. In the present study, we characterized Pi transport in mouse osteoclast-like cells that were obtained by differentiation of macrophage RAW264.7 cells with receptor activator of NF-kappaB ligand (RANKL). In undifferentiated RAW264.7 cells, Pi transport into the cells was Na+ dependent, but after treatment with RANKL, Na+-independent Pi transport was significantly increased. In addition, compared with neutral pH, the activity of the Na+-independent Pi transport system in the osteoclast-like cells was markedly enhanced at pH 5.5. The Na+-independent system consisted of two components with Km of 0.35 mM and 7.5 mM. The inhibitors of Pi transport, phosphonoformic acid, and arsenate substantially decreased Pi transport. The proton ionophores nigericin and carbonyl cyanide p-trifluoromethoxyphenylhydrazone as well as a K+ ionophore, valinomycin, significantly suppressed Pi transport activity. Analysis of BCECF fluorescence indicated that Pi transport in osteoclast-like cells is coupled to a proton transport system. In addition, elevation of extracellular K+ ion stimulated Pi transport, suggesting that membrane voltage is involved in the regulation of Pi transport activity. Finally, bone particles significantly increased Na+-independent Pi transport activity in osteoclast-like cells. Thus, osteoclast-like cells have a Pi transport system with characteristics that are different from those of other Na+-dependent Pi transporters. We conclude that stimulation of Pi transport at acidic pH is necessary for bone resorption or for production of the large amounts of energy necessary for acidification of the extracellular environment. (キーワード) Na+-dependent phosphate cotransporter / RAW264.7 / phosphate uptake (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajpcell.00412.2004 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15601753 ● Search Scopus @ Elsevier (PMID): 15601753 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpcell.00412.2004 (DOI: 10.1152/ajpcell.00412.2004, PubMed: 15601753)
42.	Masashi Kuwahata, Yasuko Kuramoto, Yuka Tomoe, Emi Sugata, Hiroko Segawa, Mikiko Ito, Tatsuzo Oka and Ken-ichi Miyamoto : Posttranscriptional regulation of albumin gene expression by branched-chain amino acids in rats with acute liver injury, Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Vol.1739, No.1, 62-69, 2004. (要約) We previously demonstrated that the integration of albumin mRNA into functional polysomes was regulated by the supply of branched-chain amino acids (BCAA) in the liver of galactosamine-treated rats. To study the mechanism of this regulation, we investigated interaction between rat liver proteins and albumin transcripts. When albumin transcript was incubated with ribosome salt wash (RSW) extracts prepared from liver, a specific RNA-protein complex (p65) formed. Competition experiments showed that a pyrimidine-rich sequence in the coding region of albumin mRNA was required for the formation of p65. The level of p65 was increased in the RSW extracts prepared from liver of galactosamine-treated rats infused with a standard amino acid formula, compared with a BCAA-enriched amino acid formula. The protein in p65 appears to be polypyrimidine tract-binding protein (PTB), because the formation of p65 was reduced in the RSW extracts pre-incubated with anti-PTB antibody. In cell-free translation analysis, immunodepletion of PTB from rabbit reticulocyte lysate caused an increase in albumin translation. These results suggest that binding of PTB to albumin mRNA suppresses its translation. A supply of BCAA may interfere with this binding and improve the translation efficiency of albumin mRNA in injured liver. (キーワード) Albumin mRNA / Polypyrimidine tract-binding protein / Translation efficiency / Branched-chain amino acid / Acute liver injury (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bbadis.2004.08.011 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15607118 ● Search Scopus @ Elsevier (PMID): 15607118 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbadis.2004.08.011 (DOI: 10.1016/j.bbadis.2004.08.011, PubMed: 15607118)
43.	Hiroko Segawa, Setsuko Yamanaka, Mikiko Ito, Masashi Kuwahata, Masayuki Shono, Tadashi Yamamoto and Ken-ichi Miyamoto : Internalization of renal type IIc Na/Pi cotransporter in response to a high phosphate diet, American Journal of Physiology, Renal Physiology, Vol.288, No.3, 587-596, 2004. (要約) Dietary phosphate levels regulate the renal brush-border type IIa Na-Pi cotransporter. Another Na-Pi cotransporter, type IIc, colocalizes with type IIa Na-Pi cotransporter in the apical membrane of renal proximal tubular cells. The goal of the present study was to determine whether dietary phosphate levels also rapidly regulate the type IIc Na-Pi cotransporter. Type IIa and type IIc transporter protein levels were increased in rats chronically fed a low-Pi diet compared with those fed a normal-Pi diet. Two hours after beginning a high-Pi diet, type IIa transporter levels were decreased, whereas type IIc protein levels remained unchanged. Western blot analysis of brush-border membrane prepared 4 h after beginning a high-Pi diet showed a significant reduction in type IIc transporter protein levels, and immunohistochemistry showed translocation of the type IIc-immunoreactive signal from the entire brush border to subapical membrane. Membrane fractionation studies revealed a decrease in apical membrane type IIc protein without changes in total cortical type IIc protein, which is compatible with redistribution of type IIc protein from the apical membrane to the dense membrane fraction. The microtubule-disrupting reagent colchicine prevented this reduction in apical type IIc transporter at the apical membrane but had no effect on type IIa transporter levels. These data suggest that the type IIc Na-Pi cotransporter level is rapidly regulated by rapid adaptation to dietary Pi in a microtubule-dependent manner. Furthermore, the mechanisms of the internalization of the type IIc transporter are distinct from those of the type IIa transporter. (キーワード) Animals / Diet / Down-Regulation / Immunoblotting / Immunohistochemistry / Kidney / Kidney Cortex / Kidney Tubules, Proximal / Male / Membranes / Microscopy, Fluorescence / Microtubules / Microvilli / Peptides / Phosphates / Phosphorus, Dietary / Rats / Rats, Wistar / Sodium-Phosphate Cotransporter Proteins / Sodium-Phosphate Cotransporter Proteins, Type IIa / Symporters (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajprenal.00097.2004 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15561978 ● Search Scopus @ Elsevier (PMID): 15561978 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00097.2004 (DOI: 10.1152/ajprenal.00097.2004, PubMed: 15561978)
44.	Ken-ichi Miyamoto, Hiroko Segawa, Mikiko Ito and Masashi Kuwahata : Physiological Regulation of Renal Sodium-Dependent Phosphate Cotransporters, The Japanese Journal of Physiology, Vol.54, No.2, 93-102, 2004. (要約) The physiological regulation of renal Pi reabsorption is mediated by renal type II Na/Pi cotransporters (type IIa and type IIc). The type IIa transporter is regulated, among other factors, by dietary Pi intake and parathyroid hormone (PTH). The PTH-induced inhibition of Pi reabsorption is mediated by endocytosis of the type IIa transporter from the brush-border membrane and subsequent lysosomal degradation. Type IIa is part of the heteromeric protein complexes organized by PDZ proteins. Furthermore, during Pi depletion the type IIc Na/Pi cotransporter is induced in the apical membrane of proximal tubular cells. The type IIc transporter is also regulated by PTH via internalization, but by a vesicular transport pathway distinct from that used by the type IIc transporter. Studying the mechanisms of type IIa and type IIc transporters has increased the understanding of the control of proximal tubular Pi handling and thus of overall Pi homeostasis. (キーワード) kidney / phosphate / transporter / parathyroid hormone (出版サイトへのリンク) ● Publication site (DOI): 10.2170/jjphysiol.54.93 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15182416 ● CiNii @ 国立情報学研究所 (CRID): 1390001205043873664 ● Search Scopus @ Elsevier (PMID): 15182416 ● Search Scopus @ Elsevier (DOI): 10.2170/jjphysiol.54.93 (DOI: 10.2170/jjphysiol.54.93, PubMed: 15182416, CiNii: 1390001205043873664)
45.	Hiroko Segawa, Ichiro Kaneko, Setsuko Yamanaka, Mikiko Ito, Masashi Kuwahata, Yoshio Inoue, Shigeaki Kato and Ken-ichi Miyamoto : Intestinal Na-Pi cotransporter adaptation to dietary Pi content in vitamin D receptor null mice., American Journal of Physiology, Renal Physiology, Vol.287, No.1, F39-F47, 2004. (要約) Recent studies suggest that vitamin D may play a role in intestinal Na(+)-dependent phosphate transport adaptation to variable levels of dietary P(i). Therefore, the goal of the current study was to assess Na(+)-dependent P(i) cotransport activity in transgenic mice to determine whether vitamin D is an essential mediator of this process. Intestinal brush-border membrane (BBM), Na(+)-dependent P(i) cotransport activity was significantly decreased in vitamin D receptor (VDR) null [VDR (-/-)] mice compared with wild-type (VDR+/+) mice. While intestinal Na-P(i) cotransporter (type IIb) mRNA levels were similar in VDR (-/-) and VDR (+/+) mice, type IIb Na-P(i) cotransporter protein expression was markedly suppressed in VDR (-/-) mice compared with VDR (+/+) mice. Furthermore, Na-P(i) cotransport activity in renal BBM was similar in VDR (-/-) and VDR (+/+) mice, but type IIa Na-P(i) cotransporter protein expression was decreased in VDR (-/-) mice. After administration of a low-P(i) diet, type IIb protein expression was significantly increased in VDR (+/+) and VDR (-/-) mice, and type IIb protein expression was present in the intestinal BBM of VDR (-/-) mice. These data demonstrate that intestinal Na-P(i) cotransport adaptation to a low-P(i) diet occurs independently of vitamin D. (キーワード) Animals / Diet / Gene Expression Regulation / Genotype / 免疫組織化学 (immunohistochemistry) / Mice / ノックアウトマウス (knockout mice) / Microvilli / Phosphates / Phosphorus, Dietary / Polymerase Chain Reaction / Receptors, Calcitriol / Sodium-Phosphate Cotransporter Proteins / Sodium-Phosphate Cotransporter Proteins, Type IIa / Sodium-Phosphate Cotransporter Proteins, Type IIb / Symporters / ビタミンD (vitamin D) (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajprenal.00375.2003 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14996670 ● Search Scopus @ Elsevier (PMID): 14996670 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00375.2003 (DOI: 10.1152/ajprenal.00375.2003, PubMed: 14996670)
46.	Mikiko Ito, Sachi Iidawa, Michiyo Izuka, Sakiko Haito, Hiroko Segawa, Masashi Kuwahata, Ichiro Ohkido, Hiroshi Ohno and Ken-ichi Miyamoto : Interaction of a farnesylated protein with rwnal type a Na/Pi co-transporter in response to parathyroid hormone and dietary phosphate., The Biochemical Journal, Vol.377, No.3, 607-616, 2004. (要約) Treatment with PTH (parathyroid hormone) or a high-P(i) diet causes internalization of the type IIa sodium-dependent phosphate (Na/P(i) IIa) co-transporter from the apical membrane and its degradation in the lysosome. A dibasic amino acid motif (KR) in the third intracellular loop of the co-transporter is essential for protein's PTH-induced retrieval. To elucidate the mechanism of internalization of Na/P(i) IIa, we identified the interacting protein for the endocytic motif by yeast two-hybrid screening. We found a strong interaction of the Na/P(i) IIa co-transporter with a small protein known as the PEX19 (human peroxisomal farnesylated protein; PxF, Pex19p). PEX19 can bind to the KR motif, but not to a mutant with this motif replaced with NI residues. PEX19 is highly expressed in mouse and rat kidney. Western blot analysis indicates that PEX19 is located in the cytosolic and brush-border membrane fractions (microvilli and the subapical component). Overexpression of PEX19 stimulated the endocytosis of the Na/P(i) IIa co-transporter in opossum kidney cells in the absence of PTH. In conclusion, the present study indicates that PEX19 may be actively involved in controlling the internalization and trafficking of the Na/P(i) IIa co-transporter. (キーワード) Amino Acid Sequence / Animals / Cell Line / Down-Regulation / Gene Library / Humans / Kidney / Kidney Tubules, Proximal / Male / Membrane Proteins / Mice / Microvilli / Molecular Sequence Data / Opossums / Parathyroid Hormone / Peptides / Phosphates / Rats / Rats, Wistar / シグナル伝達 (signal transduction) / Sodium-Phosphate Cotransporter Proteins / Sodium-Phosphate Cotransporter Proteins, Type IIa / Symporters / Transfection / Two-Hybrid System Techniques (出版サイトへのリンク) ● Publication site (DOI): 10.1042/BJ20031223 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14558883 ● Search Scopus @ Elsevier (PMID): 14558883 ● Search Scopus @ Elsevier (DOI): 10.1042/BJ20031223 (DOI: 10.1042/BJ20031223, PubMed: 14558883)
47.	Mikiko Ito, Iidawa Sachi, Izuka Michiyo, Haito Sakiko, Hiroko Segawa, Masashi Kuwahata, Ohkido Ichiro, Ohno Hiroshi and Ken-ichi Miyamoto : Cloning and characterization of three PHEX homologues in Drosophila., Journal of Bone and Mineral Metabolism, Vol.22, No.1, 3-11, 2004. (要約) Inactivating mutations and/or deletions of PHEX ( Phosphate-regulating gene with Homologies to Endopeptidase on the X chromosome) are responsible for X-linked hypophosphatemic rickets in humans. In the present study, three Drosophila PHEX homologues (dPHEX-1, -2, -3) were isolated by the screening of a Drosophila cDNA library and expressed sequence tag (EST) database. The structural region involving motif II: (456)WMXXXTKXXAXXK(468) (numbered according to human PHEX), motif VI: (602)WW(603), and motif VIII: (746)CXLW(749) was conserved in the dPHEX family. Zinc-coordinating motifs (HEFTH and GENIADNGG) were also conserved in the dPHEX family. All three dPHEX genes were expressed during all stages of Drosophila development. The expression of dPHEX-1 was suppressed by dietary phosphate deprivation, but the expression of dPHEX-2 and that of dPHEX-3 were not affected. In-situ hybridization showed a ubiquitous distribution of dPHEX-1 and dPHEX-2, while dPHEX-3 was highly expressed in the larval brain. In an analysis of subcellular localization, dPHEX-1 was localized to intracellular organelles and dPHEX-3 was localized predominately in the plasma membrane of Drosophila embryonic S2 cells. Homozygosity of a dPHEX-1 mutation, a transposon insertion in the dPHEX-1 promoter region, was completely lethal at an early stage of embryonic development. The present study indicates that three homologues are likely involved in the phosphate homeostasis of Drosophila. (キーワード) Alternative Splicing / Amino Acid Sequence / Animals / Base Sequence / Cell Line / Cell Membrane / Cloning, Molecular / Crosses, Genetic / Databases, Nucleic Acid / Drosophila / Drosophila Proteins / Embryo, Nonmammalian / Endoplasmic Reticulum / Exons / Gene Components / Gene Expression / Gene Expression Regulation, Developmental / Genotype / Golgi Apparatus / Homozygote / Humans / Immunohistochemistry / In Situ Hybridization / Microscopy, Fluorescence / Molecular Sequence Data / Mutagenesis, Insertional / PHEX Phosphate Regulating Neutral Endopeptidase / Phosphates / Proteins / Reverse Transcriptase Polymerase Chain Reaction / Sequence Homology, Amino Acid / Transfection (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s00774-003-0440-8 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14691680 ● CiNii @ 国立情報学研究所 (CRID): 1573950399836536704 ● Search Scopus @ Elsevier (PMID): 14691680 ● Search Scopus @ Elsevier (DOI): 10.1007/s00774-003-0440-8 (DOI: 10.1007/s00774-003-0440-8, PubMed: 14691680, CiNii: 1573950399836536704)
48.	Hiroko Segawa, Eri Kawakami, Ichiro Kaneko, Masashi Kuwahata, Mikiko Ito, Kenichiro Kusano, Hitoshi Saito, Naoshi Fukushima and Ken-ichi Miyamoto : Effect of hydrolysis-resistant FGF23-R179Q on dietary phosphate regulation of the renal type-II Na/Pi transporter., Pflügers Archiv : European Journal of Physiology, Vol.446, No.5, 585-592, 2003. (要約) Fibroblast growth factor 23 (FGF23), a phosphaturic factor, is involved in the regulation of renal inorganic phosphate (Pi) reabsorption. Proteolysis-resistant FGF23 mutants expressed in rodents reduce Pi uptake in both intestine and kidney, independent of parathyroid hormone action. In the present study, we investigated whether FGF23 affects dietary regulation of Na(+)-dependent Pi (Na/Pi) cotransport in the rat kidney using wild-type FGF23 and an R179Q mutant, which disrupts a consensus proteolytic cleavage motif. Rats injected with naked human FGF23 DNA (wild-type or R179Q mutant) expressed the human FGF23 transcript in the liver. In those animals, plasma calcium and parathyroid hormone levels were not affected by FGF23 (either wild-type or R179Q mutant). FGF23-R179Q did, however, significantly decrease plasma Pi and renal Na/Pi cotransport activity and also the level of type-IIc Na/Pi cotransporter protein in brush-border membrane vesicles (BBMVs) from normal rat kidney. Western blot and immunohistochemical analyses in rats fed a low-Pi diet showed the levels of types-IIa and -IIc Na/Pi cotransporters to be markedly increased. After injection of FGF23-R179Q DNA into the rats fed a low-Pi diet, the levels of the types-IIa and -IIc transporter proteins were decreased. The FGF23 mutant thus blunts the signalling of Pi deprivation to the renal type-II Na/Pi cotransporter, suggesting that the FGF23 pathway could be involved in the signalling of dietary Pi. (キーワード) Animals / カルシウム (calcium) / Fibroblast Growth Factors / 遺伝子発現 (gene expression) / Humans / Hydrolysis / 免疫組織化学 (immunohistochemistry) / Kidney Tubules, Proximal / Male / Mutagenesis, Site-Directed / Parathyroid Hormone / Phosphates / Phosphorus, Dietary / RNA, Messenger / Rats / Rats, Wistar / シグナル伝達 (signal transduction) / Sodium / Sodium-Phosphate Cotransporter Proteins / Sodium-Phosphate Cotransporter Proteins, Type II / Symporters / Vitamin D (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s00424-003-1084-1 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12851820 ● Search Scopus @ Elsevier (PMID): 12851820 ● Search Scopus @ Elsevier (DOI): 10.1007/s00424-003-1084-1 (DOI: 10.1007/s00424-003-1084-1, PubMed: 12851820)
49.	桑波田雅士, 瀬川博子, 伊藤美紀子, 宮本賢一 : 肝障害モデルラットへのBCAA高含有製剤投与による低アルブミン血症改善機構の検討, 日本病態栄養学会誌, Vol.5, No.1, 21-25, 2002年.
50.	Hiroko Segawa, Ichiro Kaneko, Akira Takahashi, Masashi Kuwahata, Mikiko Ito, Ohkido Ichiro, Sawako Tatsumi and Ken-ichi Miyamoto : Growth-related renal Type II Na/Pi cotransporter., The Journal of Biological Chemistry, Vol.277, No.22, 19665-19672, 2002. (キーワード) DEPENDENT PHOSPHATE COTRANSPORTER / BORDER MEMBRANE-VESICLES / AMINO-ACID TRANSPORTER / RAT-KIDNEY / IDENTIFICATION / EXPRESSION / NAPI-2 / REABSORPTION / ONTOGENY / OOCYTES (出版サイトへのリンク) ● Publication site (DOI): 10.1074/jbc.M200943200 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11880379 ● CiNii @ 国立情報学研究所 (CRID): 1572824501584477568 ● Search Scopus @ Elsevier (PMID): 11880379 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M200943200 (DOI: 10.1074/jbc.M200943200, PubMed: 11880379, CiNii: 1572824501584477568)
51.	桑波田雅士, 瀬川博子, 伊藤美紀子, 宮本賢一 : 肝障害モデルラットへのBCAA高含有製剤投与による低アルブミン血症改善機構の検討, 日本病態栄養学会誌, Vol.5, No.1, 21-25, 2002年.
52.	Osamu Yanagida, Yoshikatsu Kanai, Arthit Chairoungdua, Do Kyung Kim, Hiroko Segawa, Tomoko Nii, Seok Ho Cha, Hirotaka Matsuo, Jun-ichi Fukushima, Yoshiki Fukasawa, Yoshiko Tani, Yutaka Taketani, Hiroshi Uchino, Ju Young Kim, Jun Inatomi, Isao Okayasu, Ken-ichi Miyamoto, Eiji Takeda, Tomoyuki Goya and Hitoshi Endou : Human L-type amino acid transporter 1(LAT1):/characterization of function and expression in tumor cell lines, Biochimica et Biophysica Acta (BBA) - Biomembranes, Vol.1514, No.2, 291-302, 2001. (要約) System L is a major nutrient transport system responsible for the transport of large neutral amino acids including several essential amino acids. We previously identified a transporter (L-type amino acid transporter 1: LAT1) subserving system L in C6 rat glioma cells and demonstrated that LAT1 requires 4F2 heavy chain (4F2hc) for its functional expression. Since its oncofetal expression was suggested in the rat liver, it has been proposed that LAT1 plays a critical role in cell growth and proliferation. In the present study, we have examined the function of human LAT1 (hLAT1) and its expression in human tissues and tumor cell lines. When expressed in Xenopus oocytes with human 4F2hc (h4F2hc), hLAT1 transports large neutral amino acids with high affinity (K(m)= approximately 15- approximately 50 microM) and L-glutamine and L-asparagine with low affinity (K(m)= approximately 1.5- approximately 2 mM). hLAT1 also transports D-amino acids such as D-leucine and D-phenylalanine. In addition, we show that hLAT1 accepts an amino acid-related anti-cancer agent melphalan. When loaded intracellularly, L-leucine and L-glutamine but not L-alanine are effluxed by extracellular substrates, confirming that hLAT1 mediates an amino acid exchange. hLAT1 mRNA is highly expressed in the human fetal liver, bone marrow, placenta, testis and brain. We have found that, while all the tumor cell lines examined express hLAT1 messages, the expression of h4F2hc is varied particularly in leukemia cell lines. In Western blot analysis, hLAT1 and h4F2hc have been confirmed to be linked to each other via a disulfide bond in T24 human bladder carcinoma cells. Finally, in in vitro translation, we show that hLAT1 is not a glycosylated protein even though an N-glycosylation site has been predicted in its extracellular loop, consistent with the property of the classical 4F2 light chain. The properties of the hLAT1/h4F2hc complex would support the roles of this transporter in providing cells with essential amino acids for cell growth and cellular responses, and in distributing amino acid-related compounds. (キーワード) Amino Acid Transport Systems / Amino Acids, Essential / Animals / Antigens, CD / Antigens, CD98 / Carrier Proteins / DNA Probes / DNA, Complementary / Fetus / Humans / Molecular Sequence Data / Oocytes / Protein Biosynthesis / RNA, Complementary / RNA, Messenger / Substrate Specificity / Tumor Cells, Cultured / Xenopus (出版サイトへのリンク) ● Publication site (DOI): 10.1016/S0005-2736(01)00384-4 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11557028 ● Search Scopus @ Elsevier (PMID): 11557028 ● Search Scopus @ Elsevier (DOI): 10.1016/S0005-2736(01)00384-4 (DOI: 10.1016/S0005-2736(01)00384-4, PubMed: 11557028)
53.	Tomoko Nii, Hiroko Segawa, Yutaka Taketani, Yoshiko Tani, Makiko Ohkido, Sachie Kishida, Mikiko Ito, Hitoshi Endou, Yoshikatsu Kanai, Eiji Takeda and Ken-ichi Miyamoto : ) Molecular events involved in up-regulating human Na+-independent neutral amino acid transporter LAT1 during T-cell activation, The Biochemical Journal, Vol.358, No.3, 693-704, 2001. (キーワード) elongation / promoter / run-on assay
54.	Tomoko Nii, Yutaka Taketani, Yoshiko Tani, Ichiro Ohkido, Hiroko Segawa, Hitonori Yamamoto, Kyoko Morita, Kanshi Minamitani, Masanori Minagawa, Toshiyuki Yasuda, Hiroo Niimi, Akimitsu Miyauchi, Ken-ichi Miyamoto and Eiji Takeda : Direct demonstration of humorally mediated inhibition of the transcription of phosphate transporter in XLH patients, Clinical and Experimental Nephrology, Vol.5, No.3, 144-152, 2001. (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s101570170002 (文献検索サイトへのリンク) ● Summary page in Scopus @ Elsevier: 2-s2.0-17944363928 (DOI: 10.1007/s101570170002, Elsevier: Scopus)
55.	Kanako Katai, Ken-ichi Miyamoto, Sachie Kishida, Hiroko Segawa, Tomoko Nii, Hiroko Tanaka, Yoshiko Tani, Hidekazu Arai, Sawako Tatsumi, Kyoko Morita, Yutaka Taketani and Eiji Takeda : Regulation of intestinal Na+-dependent phosphate co-transporters by a low-phosphate diet and 1,25-dihydroxyvitamin D3., The Journal of Biochemistry, Vol.343, No.3, 705-712, 1999.
56.	Kanako Katai, Hiroko Segawa, Hiromi Sakata-Haga, Kyoko Morita, Hidekazu Arai, Sawako Tatsumi, Yutaka Taketani, Ken-ichi Miyamoto, Setsuji Hisano, Yoshihiro Fukui and Eiji Takeda : Acute regulation by dietary phosphate of the sodium-dependent phosphate transporter (NaP(i)-2) in rat kidney., The Journal of Biochemistry, Vol.121, No.1, 50-55, 1997.

学術論文(紀要・その他):

1.	瀬川博子 : リン代謝調節機構―多臓器連関―, 日本小児体液研究会誌, Vol.14, 3-8, 2022年. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1520011108762033920 (CiNii: 1520011108762033920)
2.	金子一郎, 宇賀穂, 塩﨑雄治, 宮本賢一, 瀬川博子 : 生体内リン恒常性を維持するビタミンD作用, ビタミン, Vol.95, No.56, 280-285, 2021年. (要約) 無機リン酸(リン)は生体内で多くの生化学反応に必要であるため，血中リン濃度は一定範囲内に維持されている．低リン血症はくる病/骨軟化症の原因となり，高リン血症は慢性腎臓病(CKD)や透析患者において心血管疾患発症のリスクファクターとなる．副甲状腺ホルモン(PTH)や線維芽細胞増殖因子23(FGF23)は，腎臓でのリン再吸収を抑制することでリン利尿ホルモンとして機能している．活性型ビタミンD[1,25(OH) <sub>2</sub>D]は小腸でのリン吸収を促進することに加え，PTHやFGF23の産生調節も行い，生体内リン恒常性を保っている．<br> FGF23シグナル活性化は，尿中リン排泄を亢進させ，低リン血症性くる病を引き起こす(FGF23関連低リン血症性くる病)．また，ビタミンD依存性くる病では，小腸でのリン吸収抑制に加えて，成長期における尿中リン排泄の亢進が低リン血症の原因となる．近年，FGF23中和抗体(Burosumab)が開発され，腎臓リン再吸収と1,25(OH) <sub>2</sub>D産生を改善することでくる病患者に有益な効果を示し，欧米及び日本でFGF23関連低リン血症性くる病・骨軟化症の治療薬として承認されている．一方，X連鎖性低リン血症性くる病モデル動物を用いた実験では，ビタミンD製剤単独投与でも低リン血症性くる病の症状を改善できることが示された．この作用の特徴は，FGF23が高値を示すにも関わらずリン再吸収の改善がみとめられることである．<br> CKD患者では，しばしば副甲状腺機能亢進や心血管疾患，骨異栄養症など骨ミネラル代謝異常(CKD-MBD: 慢性腎臓病に伴う骨ミネラル代謝異常)が出現する．CKDにおける高リン血症および1,25(OH) <sub>2</sub>D低下を予防・治療することで患者のQOLや予後を改善することが報告されている．<br> このように腎臓でのリン再吸収調節は骨ミネラル代謝に極めて重要である．我々は，リンとビタミンD代謝に注目し，疾患の発症および予防を分子レベルで理解することに努めている． (キーワード) Phosphate / Vitamin D / VDR / Rickets / CKD (出版サイトへのリンク) ● Publication site (DOI): 10.20632/vso.95.5-6_280 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390574047045835904 ● Search Scopus @ Elsevier (DOI): 10.20632/vso.95.5-6_280 (DOI: 10.20632/vso.95.5-6_280, CiNii: 1390574047045835904)
3.	小池萌, 佐々木すみれ, 瀬川博子 : 唾液腺のリン代謝における役割, バイオサイエンスとインダストリー, Vol.38, No.4, 66-73, 2021年.
4.	Yasuhiro Ichida, Shuichi Ohtomo, Tessai Yamamoto, Naoaki Murao, Yoshinori Tsuboi, Yoshiki Kawabe, Hiroko Segawa, Naoshi Horiba, Ken-Ichi Miyamoto and rgen J Floege : Evidence of an intestinal phosphate transporter alternative to type IIb sodium-dependent phosphate transporter in rats with chronic kidney disease., Nephrology, Dialysis, Transplantation, Vol.36, No.1, 68-75, 2021. (要約) Phosphate is absorbed in the small intestine via passive flow and active transport.NaPi-IIb, a type II sodium-dependent phosphate transporter, is considered to mediate active phosphate transport in rodents. To study the regulation of intestinal phosphate transport in chronic kidney disease (CKD), we analyzed the expression levels of NaPi-IIb, pituitary-specific transcription factor 1 (PiT-1) and PiT-2 and the kinetics of intestinal phosphate transport using two CKD models. CKD was induced in rats via adenine orThy1 antibody injection. Phosphate uptake by intestinal brush border membrane vesicles (BBMV) and the messenger RNA (mRNA) expression of NaPi-IIb, PiT-1 and PiT-2 were analyzed. The protein expression level of NaPi-IIb was measured by mass spectrometry (e.g. liquid chromatography tandem mass spectrometry). In normal rats, phosphate uptake into BBMV consisted of a single saturable component and its Michaelis constant (Km) was comparable to that of NaPi-IIb. The maximum velocity (Vmax) correlated with mRNA and protein levels of NaPi-IIb. In the CKD models, intestinal phosphate uptake consisted of two saturable components. The Vmax of the higher-affinity transport, which is thought to be responsible for NaPi-IIb, significantly decreased and the decrease correlated with reduced NaPi-IIb expression. The Km of the lower-affinity transport was comparable to that of PiT-1 and -2. PiT-1 mRNA expression was much higher than that of PiT-2, suggesting that PiT-1 was mostly responsible for phosphate transport. This study suggests that the contribution of NaPi-IIb to intestinal phosphate absorption dramatically decreases in rats with CKD and that a low-affinity alternative to NaPi-IIb, in particular PiT-1, is upregulated in a compensatory manner in CKD. (キーワード) Adenine / Animals / Intestines / Male / Phosphate Transport Proteins / Phosphates / Rats / Rats, Inbred F344 / Rats, Wistar / Renal Insufficiency, Chronic / Sodium / Sodium-Phosphate Cotransporter Proteins, Type III / Sodium-Phosphate Cotransporter Proteins, Type IIb / Transcription Factor Pit-1 (徳島大学機関リポジトリ) ● Metadata: 118944 (出版サイトへのリンク) ● Publication site (DOI): 10.1093/ndt/gfaa156 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32879980 ● Search Scopus @ Elsevier (PMID): 32879980 ● Search Scopus @ Elsevier (DOI): 10.1093/ndt/gfaa156 (徳島大学機関リポジトリ: 118944, DOI: 10.1093/ndt/gfaa156, PubMed: 32879980)
5.	辰巳佐和子, 野村憲吾, 宮川淳美, 木戸慎介, 瀬川博子 : リンセンシングと腸管, Clinical Calcium, Vol.22, No.10, 81-85, 2012年. (要約) Small intestine plays an important role in the sensing of various nutrients. There is information that would imply the existence of a dietary phosphate sensing mechanism within the intestine. Recent studies suggest that intestinal factors may involve in the alteration of renal phosphate transport. The elucidation of the phosphate sensing mechanism is expected to provide molecular basis for the prevention of the hyperphosphatemia in chronic kidney disease patients. (キーワード) Animals / Homeostasis / Humans / Hyperphosphatemia / Intestine, Small / Phosphates / Renal Insufficiency, Chronic / Signal Transduction (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23023634 ● Search Scopus @ Elsevier (PMID): 23023634 (PubMed: 23023634)
6.	桑原煩治, 大井彰子, 野村憲吾, 辰巳佐和子, 木戸慎介, 瀬川博子, 宮本賢一 : リン酸トランスポーターをめぐる最近の話題., 消化と吸収, Vol.34, No.3, 181-190, 2012年. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1572824500599676928 (CiNii: 1572824500599676928)
7.	瀬川博子, 大井彰子, 宮本賢一 : リン酸トランスポーターと疾患, Bio Clinica 腎臓トランスポーター異常による疾患, Vol.Vol26, No.No11, 23-27, 2011年.
8.	宮本賢一, 古谷順也, 桑原頌冶, 大井彰子, 瀬川博子 : ペプチドトランスポーターの機能と生理作用, 栄養・食品機能とトランスポーター, 63-80, 2011年.
9.	Zun Liu, Hiroko Segawa, Cumhur Aydin, Monica Reyes, G Reinhold Erben, S Lee Weinstein, Min Chen, Vladimir Marshansky, F Leopold Fröhlich and Murat Bastepe : Transgenic overexpression of the extra-large Gs variant XLs enhances Gs-mediated responses in the mouse renal proximal tubule in vivo., Endocrinology, Vol.152, No.4, 1222-1233, 2011. (要約) XLs, a variant of the stimulatory G protein -subunit (Gs), can mediate receptor-activated cAMP generation and, thus, mimic the actions of Gs in transfected cells. However, it remains unknown whether XLs can act in a similar manner in vivo. We have now generated mice with ectopic transgenic expression of rat XLs in the renal proximal tubule (rptXLs mice), where Gs mediates most actions of PTH. Western blots and quantitative RT-PCR showed that, while Gs and type-1 PTH receptor levels were unaltered, protein kinase A activity and 25-hydroxyvitamin D 1--hydroxylase (Cyp27b1) mRNA levels were significantly higher in renal proximal tubules of rptXLs mice than wild-type littermates. Immunohistochemical analysis of kidney sections showed that the sodium-phosphate cotransporter type 2a was modestly reduced in brush border membranes of male rptXLs mice compared to gender-matched controls. Serum calcium, phosphorus, and 1,25 dihydroxyvitamin D were within the normal range, but serum PTH was 30% lower in rptXLs mice than in controls (152 ± 16 vs. 222 ± 41 pg/ml; P < 0.05). After crossing the rptXLs mice to mice with ablation of maternal Gnas exon 1 (E1(m-/+)), male offspring carrying both the XLs transgene and maternal Gnas exon 1 ablation (rptXLs/E1(m-/+)) were significantly less hypocalcemic than gender-matched E1(m-/+) littermates. Both E1(m-/+) and rptXLs/E1(m-/+) offspring had higher serum PTH than wild-type littermates, but the degree of secondary hyperparathyroidism tended to be lower in rptXLs/E1(m-/+) mice. Hence, transgenic XLs expression in the proximal tubule enhanced Gs-mediated responses, indicating that XLs can mimic Gs in vivo. (キーワード) Animals / Blotting, Northern / Blotting, Western / Cell Line / Female / GTP-Binding Protein alpha Subunits, Gs / Humans / 免疫組織化学 (immunohistochemistry) / Kidney Tubules, Proximal / ノックアウトマウス (knockout mice) / Polymerase Chain Reaction / Rats / Reverse Transcriptase Polymerase Chain Reaction (出版サイトへのリンク) ● Publication site (DOI): 10.1210/en.2010-1034 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21303955 ● Search Scopus @ Elsevier (PMID): 21303955 ● Search Scopus @ Elsevier (DOI): 10.1210/en.2010-1034 (DOI: 10.1210/en.2010-1034, PubMed: 21303955)
10.	金子一郎, 杉野紗貴子, 瀬川博子, 宮本賢一 : 腎臓と骨代謝関連ホルモン, THE BONE, Vol.24, No.4, 55-58, 2010年. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1010000782037286160 (CiNii: 1010000782037286160)
11.	宮本賢一, 山口誠一, 辰巳佐和子, 木戸慎介, 瀬川博子 : フォスファトニンとリン, 腎と透析, Vol.69, No.2, 200-202, 2010年.
12.	桑波田雅士, 瀬川博子, 伊藤美紀子, 宮本賢一 : 肝障害モデルラットのアルブミン遺伝子転写後調節機構と分岐鎖アミノ酸製剤, 必須アミノ酸研究, No.172, 45-50, 2005年. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1520010380897734784 (CiNii: 1520010380897734784)

総説・解説:

1.	小池萌, 東彩生, 小宮蒼, 塩﨑雄治, 瀬川博子 : リン管理―CKD-MBDと栄養, 腎と透析, Vol.96, No.1, 112-116, 2024年1月. (出版サイトへのリンク) ● Publication site (DOI): 10.24479/kd.0000001175 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390580793827920896 ● Search Scopus @ Elsevier (DOI): 10.24479/kd.0000001175 (DOI: 10.24479/kd.0000001175, CiNii: 1390580793827920896)
2.	小池萌, 塩﨑雄治, 瀬川博子 : 無機リン酸の恒常性維持, 腎と透析, Vol.95, No.3, 267-271, 2023年9月. (出版サイトへのリンク) ● Publication site (DOI): 10.24479/kd.0000000864 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390860620061733888 ● Search Scopus @ Elsevier (DOI): 10.24479/kd.0000000864 (DOI: 10.24479/kd.0000000864, CiNii: 1390860620061733888)
3.	Megumi Koike, Minori Uga, Yuji Shiozaki, Ken-ichi Miyamoto and Hiroko Segawa : Regulation of Phosphate Transporters and Novel Regulator of Phosphate Metabolism, Endocrines, Vol.4, No.3, 607-615, Aug. 2023. (出版サイトへのリンク) ● Publication site (DOI): 10.3390/endocrines4030043 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.3390/endocrines4030043 (DOI: 10.3390/endocrines4030043)
4.	瀬川博子 : 私とGordon Research Conference, 腎と透析, Vol.95, No.1, 5, 2023年7月. (出版サイトへのリンク) ● Publication site (DOI): 10.24479/kd.0000000802 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390016195131585024 ● Search Scopus @ Elsevier (DOI): 10.24479/kd.0000000802 (DOI: 10.24479/kd.0000000802, CiNii: 1390016195131585024)
5.	瀬川博子 : リン代謝調節機構の理解―リン代謝の基本から最近の話題までー, 日本栄養・食糧学会誌, Vol.76, No.4, 217-222, 2023年. (要約) リンは, 人体の必須元素の一つであり, ATP合成, シグナル伝達, 骨のミネラル化など, 多様なプロセスに必要とされる．リンは, 肉や魚など動物性タンパク質を含む食品に多く含まれる他, 乳製品, 種子類に含まれる．リンは多くの食品に含まれており, 通常の食事では不足や欠乏しない．血中リン酸 (Pi) 濃度は, 腸管からの吸収, 骨形成, 骨吸収および, 腎からの排泄と再吸収が様々な因子に応答し, そのバランスが保たれている．腸管や腎臓のPi吸収, 再吸収は, Piを輸送するトランスポーターが担っており, それらをリン調節ホルモンである副甲状腺ホルモン, 活性型ビタミンDやfibroblast growth factor 23が厳密に制御している．リンバランスの破綻は, 成長のみならず生命予後にまで影響する．本総説では, 生体内リン恒常性調節機構について基本事項から最近我々が同定した新規リン代謝調節因子について概説する． (キーワード) 小腸 / 腎臓 (kidney) / 骨 / トランスポーター / FGF23 (徳島大学機関リポジトリ) ● Metadata: 119319 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1050300533201873408 (徳島大学機関リポジトリ: 119319, CiNii: 1050300533201873408)
6.	谷藤和也, 小池萌, 宇賀稔, 塩﨑雄治, 瀬川博子 : Ca，Pホメオスタシス, 腎と透析, Vol.93, No.5, 736-741, 2022年11月. (キーワード) 活性型ビタミンD / FGF23 / CaSR (出版サイトへのリンク) ● Publication site (DOI): 10.24479/kd.0000000375 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390577133295330048 ● Search Scopus @ Elsevier (DOI): 10.24479/kd.0000000375 (DOI: 10.24479/kd.0000000375, CiNii: 1390577133295330048)
7.	瀬川博子 : 泌尿器系の構造と機能, 管理栄養士養成のための栄養学教育モデル・カリキュラム準拠栄養学の基本-人体の理解と栄養学の基礎-, 69-77, 2022年9月.
8.	瀬川博子 : 循環器系の構造と機能, 管理栄養士養成のための栄養学教育モデル・カリキュラム準拠栄養学の基本-人体の理解と栄養学の基礎-, 44-51, 2022年9月.
9.	瀬川博子, 小池萌, 塩﨑雄治, 宮本賢一 : 抗老化因子を制御するミネラル栄養学-リン代謝恒常制御の重要性, 実験医学増刊∼栄養・代謝物シグナルと食品機能∼, Vol.40, No.7, 45-50, 2022年3月.
10.	谷藤和也, 塩﨑雄治, 瀬川博子 : 骨を維持する栄養素, 体育の科学, Vol.71, No.11, 801-806, 2021年11月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1520572360407947392 (CiNii: 1520572360407947392)
11.	小池萌, 佐々木すみれ, 瀬川博子 : 第9章唾液腺のリン代謝における役割, 唾液による健康効果の最前線∼技術と市場∼, 81-87, 2021年9月.
12.	小池萌, 瀬川博子, 宮本賢一 : リントランスポーターと疾患., 別冊・医学のあゆみ-トランスポーターのすべて―, Vol.271, No.1, 97-102, 2020年8月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1522825129999441536 (CiNii: 1522825129999441536)
13.	Sawako Tatsumi, Kanako Katai, Ichiro Kaneko, Hiroko Segawa and Ken-ichi Miyamoto : NAD metabolism and the SLC34 family: evidence for a liver-kidney axis regulating inorganic phosphate., Pflügers Archiv : European Journal of Physiology, Vol.471, No.1, 109-122, Sep. 2018. (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s00424-018-2204-2 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30218374 ● Search Scopus @ Elsevier (PMID): 30218374 ● Search Scopus @ Elsevier (DOI): 10.1007/s00424-018-2204-2 (DOI: 10.1007/s00424-018-2204-2, PubMed: 30218374)
14.	Ichiro Kaneko, Sawako Tatsumi, Hiroko Segawa and Ken-ichi Miyamoto : Control of phosphate balance by the kidney and intestine., Clinical and Experimental Nephrology, Vol.21, No.Suppl 1, 21-26, Nov. 2016. (要約) The prevention and correction of hyperphosphatemia are major goals of the treatment of chronic kidney disease (CKD)-bone mineral disorders, and thus, Pi balance requires special attention. Pi balance is maintained by intestinal absorption, renal excretion, and bone accretion. The kidney is mainly responsible for the plasma Pi concentration. In CKD, reduced glomerular filtration rate leads to various Pi metabolism abnormalities, and Pi absorption in the small intestine also has an important role in Pi metabolism. Disturbances in Pi metabolism are mediated by a series of complex changes in regulatory hormones originating from the skeleton, intestine, parathyroid gland, and kidney. In this review, we describe the regulation of type II sodium-dependent Pi co-transporters by the kidney and intestine, including the regulation of Pi transport, circadian rhythm, and the vicious circle between salivary Pi secretion and intestinal Pi absorption in animals with and without CKD. (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s10157-016-1359-4 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27900568 ● Search Scopus @ Elsevier (PMID): 27900568 ● Search Scopus @ Elsevier (DOI): 10.1007/s10157-016-1359-4 (DOI: 10.1007/s10157-016-1359-4, PubMed: 27900568)
15.	Ichiro Kaneko, Hironori Yamamoto, Kayo Ikuta, Sawako Tatsumi, Hiroko Segawa and Ken-ichi Miyamoto : Transcriptional regulation of sodium-phosphate cotransporter gene expression., Molecular, Genetic, and Nutritional Aspects of Major and Trace Minerals, 437-445, Sep. 2016. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/B978-0-12-802168-2.00036-1 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.1016/B978-0-12-802168-2.00036-1 (DOI: 10.1016/B978-0-12-802168-2.00036-1)
16.	Hiroko Segawa, Yuji Shiozaki, Ichiro Kaneko and Ken-ichi Miyamoto : The Role of Sodium-Dependent Phosphate Transporter in Phosphate Homeostasis., Journal of Nutritional Science and Vitaminology, Vol.61 Suppl, S119-121, 2015. (要約) Inorganic phosphate (Pi) is an essential compound for several biologic functions. Pi levels outside the normal range, however, contribute to several pathological processes. Hypophosphatemia leads to bone abnormalities, such as rickets/osteomalacia. Hyperphosphatemia contributes to vascular calcification in patients with chronic kidney disease and hemodialysis patients and is independently associated with cardiac mortality.Pi homeostasis is regulated by the coordinated function of renal and intestinal sodium-dependent phosphate (NaPi) transporters with dietary Pi, parathyroid hormone, 1,25-dihydroxyvitamin D3, and fibroblast growth factor 23. The type II NaPi transporter/SLC34 family, with three members identified to date, is mainly responsible for Pi homeostasis in the body. SLC34A1 and SCL34A3 are predominantly expressed in the kidney, whereas SLC34A2 is expressed in the small intestine. The role of each SLC34 in the body was recently established by studies of gene-targeted mice. Mutation of SLC34A1 causes Fanconi syndrome and mutation of SLC34A3 causes autosomal recessive hereditary hypophosphatemic rickets with hypercalciuria. SLC34A2 is thought to be a major intestinal NaPi transporter and mutation of SLC34A2 causes pulmonary alveolar microlithiasis. A detailed understanding of Pi regulation in the body is important toward maintaining health. (出版サイトへのリンク) ● Publication site (DOI): 10.3177/jnsv.61.S119 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26598821 ● Summary page in Scopus @ Elsevier: 2-s2.0-84950320878 (DOI: 10.3177/jnsv.61.S119, PubMed: 26598821, Elsevier: Scopus)
17.	金子一郎, 瀬川博子, 辰巳佐和子, 宮本賢一 : 遺伝性リン代謝異常症, 日本腎臓学会誌, Vol.57, No.4, 758-765, 2015年. (徳島大学機関リポジトリ) ● Metadata: 114834 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1010000781855761042 ● Summary page in Scopus @ Elsevier: 2-s2.0-84938153583 (徳島大学機関リポジトリ: 114834, CiNii: 1010000781855761042, Elsevier: Scopus)
18.	Shinsuke Kido, Ichiro Kaneko, Sawako Tatsumi, Hiroko Segawa and Ken-ichi Miyamoto : Vitamin D and type II sodium-dependent phosphate cotransporters., Contributions to Nephrology, Vol.180, 86-97, May 2013. (要約) The type II sodium-dependent Pi (NaPi) cotransporters (NaPi-IIa, NaPi-IIb and NaPi-IIc) contribute to renal and intestinal Pi absorption. 1,25-Dihydroxyvitamin D [1,25(OH)2D3] is an important factor for NaPi-II transporters in the small intestine and kidney. In a previous study, low levels of 1,25(OH)2D3 appeared to suppress the expression of renal NaPi cotransporters. We identified a functional vitamin D receptor-responsive element in the human NaPi-IIa and NaPi-IIc genes in renal epithelial cells. In an analysis of vitamin D receptor (VDR)-null mice, we observed early onset of hypophosphatemia. The cause of the hypophosphatemia in VDR-null mice before weaning appeared to be increased plasma parathyroid hormone (PTH) levels during the suckling periods. A rescue diet (high calcium diet) decreased plasma PTH levels in VDR-null mice. The reduced plasma PTH levels normalized the renal Npt2a and Npt2c protein levels in weanling animals. Thus, the dietary intervention completely normalized the expression of the renal Pi transporters (Npt2a/Npt2c) in VDR-null mice, suggesting that the lack of VDR activity was not the cause of the impaired renal Pi reabsorption. In suckling animals, 1,25(OH)2D3 may be essential for the prevention of the phosphaturic action of PTH. In adult animals, 1,25(OH)2D3 is thought to be an important factor for posttranscriptional regulation of the Npt2b gene in the small intestine. Fibroblast growth factor 23 (FGF23) is a novel phosphaturic factor that influences vitamin D metabolism and renal reabsorption of Pi. We characterized the role of the VDR in the action of FGF23 using VDR-null mice. FGF23 reduced renal Pi transport and 25-hydroxyvitamin D 1a-hydroxylase levels by a mechanism that was independent of the VDR. By contrast, the induction of 25-hydroxyvitamin D 24-hydroxylase and the reduction in serum 1,25(OH)2D3 levels induced by FGF23 were dependent on the VDR. Thus, the VDR is not essential for the phosphaturic action of FGF23, but is essential for control of the plasma 1,25(OH)2D3 level. Moreover, FGF23 reduces intestinal NaPi transport activity and Npt2b protein levels by a mechanism that is dependent on the VDR. Klotho functions as a co-receptor for FGF23 and is increased by 1,25(OH)2D3. Klotho induces phosphaturia by inhibiting the renal NaPi-IIa transporter. In this review, we discuss the roles of 1,25(OH)2D3/VDR in the regulation of renal type II NaPi cotransporters in the kidney and small intestine. (キーワード) Absorption / Animals / Calcitriol / Calcium, Dietary / Familial Hypophosphatemic Rickets / Fibroblast Growth Factors / Gene Expression Regulation / Glucuronidase / Humans / Hypophosphatemia / Intestinal Absorption / Kidney Tubules / Mice / Mice, Knockout / Parathyroid Hormone / Phosphates / Phosphorus, Dietary / Receptors, Calcitriol / Renal Osteodystrophy / Sodium / Sodium-Phosphate Cotransporter Proteins, Type II / Vitamin D (出版サイトへのリンク) ● Publication site (DOI): 10.1159/000346786 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23652552 ● Search Scopus @ Elsevier (PMID): 23652552 ● Search Scopus @ Elsevier (DOI): 10.1159/000346786 (DOI: 10.1159/000346786, PubMed: 23652552)
19.	瀬川博子, 佐々木祥平, 向井朋, 真鍋舞, 木戸慎介, 辰巳佐和子, 宮本賢一 : リンの体内動態(腸管,腎臓における吸収と排泄機序/リン輸送体の機能作用), Clinical Calcium, Vol.22, No.10, 13-20, 2012年9月.
20.	Ken-ichi Miyamoto, Sakiko Haito-Sugino, Shoji Kuwahara, Akiko Ohi, Kengo Nomura, Mikiko Ito, Masashi Kuwahata, Shinsuke Kido, Sawako Tatsumi, Ichiro Kaneko and Hiroko Segawa : Sodium-dependent phosphate cotransporters: lessons from gene knockout and mutation studies., Journal of Pharmaceutical Sciences, Vol.100, No.9, 3719-3730, May 2011. (要約) Inorganic phosphate (Pi) is an essential physiological compound, highlighted by the syndromes caused by hypo or hyperphosphatemic states. Hyperphosphatemia is associated with ectopic calcification, cardiovascular disease, and increased mortality in patients with chronic kidney disease (CKD). As phosphate control is not efficient with diet or dialysis, oral Pi binders are used in over 90% of patients with renal failure. However, achieving tight control of serum Pi is difficult, and lower levels of serum Pi (severe hypophosphatemia) do not lead to better outcomes. The inhibition of sodium-dependent Pi (NaPi) transporter would be a preferable method to control serum Pi levels in patients with CKD or patients undergoing dialysis. Three types of NaPi transporters (types I-III) have been identified: solute carrier series SLC17A1 (NPT1/NaPi-I/OATv1), SLC34 (NaPi-IIa, NaPi-IIb, NaPi-IIc), and SLC20 (PiT1, PiT2), respectively. Knockout mice have been created for types I-III NaPi transporters. In this review, we discuss the roles of the NaPi transporters in Pi homeostasis. (キーワード) Animals / Gene Knockdown Techniques / ノックアウトマウス (knockout mice) / ノックアウトマウス (knockout mice) / Mutation / Phosphate Transport Proteins / Sodium (出版サイトへのリンク) ● Publication site (DOI): 10.1002/jps.22614 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21567407 ● Search Scopus @ Elsevier (PMID): 21567407 ● Search Scopus @ Elsevier (DOI): 10.1002/jps.22614 (DOI: 10.1002/jps.22614, PubMed: 21567407)
21.	宮本賢一, 瀬川博子, 伊藤美紀子 : リン代謝関連分子の新展開, 判断と治療, Vol.93, No.6, 972-976, 2005年6月. (キーワード) FGF23 / リン利尿 / PHEX / リントランスポーター
22.	宮本賢一, 伊藤美紀子, 瀬川博子 : 生体のリン調節機構とFGF23, 腎と骨代謝, Vol.18, No.2, 99-104, 2005年.
23.	宮本賢一, 伊藤美紀子, 瀬川博子 : カルシトニンの腎への作用, Clinical Calcium, Vol.15, No.3, 478-482, 2005年.
24.	宮本賢一, 伊藤美紀子, 瀬川博子 : リン酸代謝関連遺伝子群と骨粗鬆症, CLINICAL CALCIUM, Vol.15, No.5, 783-788, 2005年.
25.	宮本賢一, 瀬川博子, 伊藤美紀子 : 薬理作用と生理作用ー腸管への作用ー, 日本臨牀, Vol.63, No.10, 202-204, 2005年. (キーワード) 小腸 / カルシウム / マグネシウム / リン / 輸送
26.	宮本賢一, 伊藤美紀子, 瀬川博子, 桑波田雅士 : 副甲状腺ホルモン(PTH)による腎カルシウム，リン，ビタミンD代謝調節について, THE BONE, Vol.18, No.1, 33-38, 2004年. (キーワード) 副甲状腺ホルモン / 無機リン酸輸送担体 / 腎近位尿細管 / エンドサイトーシス / ビタミンD / カルシウム (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1010282256868935447 (CiNii: 1010282256868935447)
27.	宮本賢一, 瀬川博子, 伊藤美紀子, 桑波田雅士 : 腸管のリントランスポーター, 腎と透析, Vol.55, No.6, 12-16, 2004年. (キーワード) リン / トランスポーター / 小腸
28.	宮本賢一, 瀬川博子, 伊藤美紀子, 桑波田雅士 : 新しいリン調節薬の開発と実用化の可能性, 腎と骨代謝, Vol.17, No.4, 371-377, 2004年. (キーワード) 高リン血症 / 小腸 / リントランスポーター / 阻害薬
29.	宮本賢一, 瀬川博子, 伊藤美紀子, 桑波田雅士 : PHEXの真の基質`phosphatonin' とは何か?, THE BONE, Vol.17, No.5, 77-80, 2003年9月. (キーワード) フォスファトニン / 低リン血症 / 骨石灰化 / リン再吸収 / 腎臓 / クル病
30.	宮本賢一, 瀬川博子, 伊藤美紀子, 桑波田雅士 : 遺伝性くる病, 臨床雑誌内科, Vol.92, No.1, 89-92, 2003年7月.
31.	Ken-ichi Miyamoto, Mikiko Ito, Hiroko Segawa and Masashi Kuwahata : Molecular targets of hyper-phosphatamia in chronic renal failure, Nephrology, Dialysis, Transplantation, Vol.18, No.Suppl 3, iii79-iii80, Jun. 2003. (要約) Dietary phosphate restriction can prevent or retard the progress of chronic renal failure (CRF) and secondary hyperparathyroidism. The klotho gene is involved in the development of a syndrome resembling human ageing, and klotho mutant mice show abnormal calcium/vitamin D metabolism, developing hyperphosphataemia and vascular calcification. Phosphate retention rescues the phenotype of klotho mice. The level of expression of klotho RNA was greatly reduced in the kidneys of all CRF patients. Dietary P(i) restriction induced klotho expression, which enhances the beneficial effect of P(i) restriction in patients with CRF and/or on haemodialysis. (キーワード) Chronic Renal Failure / Dietary Phosphate / Hyperphosphatacmia / Klotho / Secondary Hyperpara-Thyroidism (出版サイトへのリンク) ● Publication site (DOI): 10.1093/ndt/gfg1020 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12771308 ● Search Scopus @ Elsevier (PMID): 12771308 ● Search Scopus @ Elsevier (DOI): 10.1093/ndt/gfg1020 (DOI: 10.1093/ndt/gfg1020, PubMed: 12771308)
32.	宮本賢一, 伊藤美紀子, 桑波田雅士, 瀬川博子 : リンの消化吸収機構とリン低下薬, 臨床透析, Vol.19, No.1, 29-35, 2003年. (キーワード) 高リン血症 / とらんすぽーたー / リン吸着薬 / 食事性リン / 小腸
33.	伊藤美紀子, 瀬川博子, 宮本賢一 : リン輸送とその異常, 医学のあゆみ, 109-111, 2003年.
34.	Ken-ichi Miyamoto, Mikiko Ito, Masashi Kuwahata and Hiroko Segawa : Sensing mechanisms of inorganic phosphate in mammalian cells, Current Topics in Medical Chemistry, Vol.3, 65-75, 2003.
35.	伊藤美紀子, 瀬川博子, 宮本賢一 : リン代謝における上皮小体ホルモン(PTH)の役割, CLINICAL CALCIUM, Vol.12, No.12, 1650-1653, 2002年12月.
36.	宮本賢一, 瀬川博子, 河野智子, 伊藤美紀子, 桑波田雅士, 金井好克 : アミノ酸トランスポーターの構造機能と栄養学的重要性, 必須アミノ酸研究, Vol.165, 13-19, 2002年11月.
37.	宮本賢一, 桑波田雅士, 瀬川博子, 伊藤美紀子 : 魚油(n-3系脂肪酸)の摂取と疾患予防, 四国医学雑誌, Vol.58, No.4-5, 201-204, 2002年10月. (キーワード) Fish Oil / Oxidation / Fatty acid / EPA / DHA (徳島大学機関リポジトリ) ● Metadata: 110552 (徳島大学機関リポジトリ: 110552)
38.	桑波田雅士, 瀬川博子, 伊藤美紀子, 宮本賢一 : 生体内の無機リン酸感受機構, 腎と骨代謝, Vol.15, No.1, 27-32, 2002年. (キーワード) リンセンサー / 腎臓 / 脳 / リントランスポーター / 食餌性リン
39.	瀬川博子, 伊藤美紀子, 桑波田雅士 : 成長に必要なリントランスポーター, 腎と骨代謝, Vol.15, No.4, 365-370, 2002年. (キーワード) 成長 / リン / 腎臓 / 骨
40.	桑波田雅士, 伊藤美紀子, 瀬川博子, 宮本賢一 : リン代謝の最近の理解とリン調節薬の将来, 透析療法ネクストII 透析骨症は防げる, 43-48, 2002年. (キーワード) 高リン血症 / リントランスポーター / リン調節薬 / 腎性骨症 / リンセンサー
41.	伊藤美紀子, 瀬川博子, 桑波田雅士, 宮本賢一 : リンの代謝調節, --- リントランスポーターの役割 ---, CLINICAL CALCIUM, Vol.11, No.10, 1297-1301, 2001年10月.

国際会議:

1.	Yuji Shiozaki, Minori Uga, Mizuki Miura, Aoi Komiya, Kazuya Tanifuji, Megumi Koike, Ken-ichi Miyamoto and Hiroko Segawa : Analysis of regulation of Tmem174 expression by Pi concentration and PTH signaling in opossum kidney cells., Physiology, Biology and Pathology of Phosphate Gordon Research Conference, Grand Galvez in Galveston, Texas, United States, Feb. 2023.
2.	Hiroko Segawa : Renal Phosphate Handling, Physiology, Biology and Pathology of Phosphate Gordon Research Conference, Galveston, TX, United States, Feb. 2023. (キーワード) 高リン血症 (hyperphosphatemia) / transporter / FGF23 / PTH / 腎疾患 (kidney disease)
3.	Uga Minori, Ichiro Kaneko, Sasaki Sumire, Koike Megumi, Tanifuji Kazuya, Yuji Shiozaki, Jurutka W. Peter and Hiroko Segawa : The role of intestinal Cytochrome P450 in vitamin D metabolism, 22nd International Congress of Nutrition in Tokyo, Dec. 2022.
4.	Yasuhiro Ichida, Daniel Weis, Shuichi Ohtomo, Nadine Kaesler, Christoph Kuppe, Tessai Yamamoto, Naoaki Murao, Hiroko Segawa, Yoshiki Kawabe, Naoshi Horiba, Ken-ichi Miyamoto and Jürgen Floege : PiT-2 Is the Main Transporter Responsible for Intestinal Phosphate Absorption in Human., American Society of Nephrology kidney week2019., Nov. 2019.
5.	Hiroko Segawa, Yuki Arima, Ai Hanazaki, Megumi Koike, Kazuya Tanifuji and Ken-ichi Miyamoto : Intestinal Environmental Control and Renal Protection by Intestinal Alkaline Phosphatase (IAP)., American Society of Nephrology kidney week2019., Nov. 2019.
6.	Tetsuhiko Sato, Megumi Koike, Hiroko Segawa, Ken-ichi Miyamoto and Masafumi Fukagawa : Possible Clinical Relevance of Growth Hormone-Stimulated α-Klotho Upregulation., American Society of Nephrology kidney week2019., Nov. 2019.
7.	Sawako Tatsumi, Ichiro Kaneko, Hiroko Segawa and Ken-ichi Miyamoto : Daily oscillation of the plasma inorganic phosphate concentration; Impact of Nampt deficient mice., ASN (American Society of Nephrology), Kidney Week 2018, Oct. 2018.
8.	T Fujii, Hiroko Segawa, A Hamazaki, K Ikuta, A Kushi, Ichiro Kaneko, Sawako Tatsumi and Ken-ichi Miyamoto : In Vivo Responses of Phosphorus-Based Food Additives with Different Forms, American Society of Nephrology Kidney week., Nov. 2017.
9.	Sawako Tatsumi, Miyagawa Atsumi, Fujii Osamu, Ogata Mao, Ichiro Kaneko, Hiroko Segawa and Ken-ichi Miyamoto : Hepatectomy-Induced Hypophosphatemia: Mechanisms Underlying Downregulation of Phophate Transport in the Small Intestine., American Society of Nephrology. Kidney Week2016., Nov. 2016.
10.	Ikuta Kayo, Hiroko Segawa, Yuki Shihoko, Ichiro Kaneko, Hanazaki Ai, Fujii Toru, Kushi Aoi, Sawako Tatsumi and Ken-ichi Miyamoto : Salivary Pi Handling May Be under the Control of Gastrointestinal Pi Sensing., American Society of Nephrology.Kidney Week2016., Nov. 2016.
11.	Ichiro Kaneko, Saini K. Rimpi, Witfield Kerr G., Ito Mikiko, Hiroko Segawa, Sawako Tatsumi, Ken-ichi Miyamoto, Haussler R. Mark and Jurutka W. Peter : FGF23: A Nurr1-dependent Phosphaturic Hormone Gene That is Transcriptionally Regulated by 1,25-dihydroxyvitamin D, XVIII International Congress on Nutrition and Metabolism in Renal Disease 2016, Apr. 2016.
12.	Ichiro Kaneko, Saini K Rimpi, Whitfield G.Kerr, Mikiko Ito, Hiroko Segawa, Sawako Tatsumi, Ken-ichi Miyamoto, R.Haussler Mark and W.Jurutka Peter : A Nurr1-dependent phosphaturic hormonegene that is transcriptionally regulated by 1.25-dihydroxyvitamin D., XVIII International Congress on Nutrition and Metabolism in Renal Desease(ICRNM2016), Apr. 2016.
13.	Hanazaki Ai, Hiroko Segawa, Ikuta Kayo, Fujii Toru, Ichiro Kaneko, Yuki Shihoko, Nishiguchi Shiori, Notsu Keijiro, Shiozaki Yuji, Sawako Tatsumi and Ken-ichi Miyamoto : Genetic Deletion of NaPi-2c Rescue Phenotype of klotho Knockout Mice wi thout Improving Severe Hyperphosphat emia., American Society of Nephrology Kidney week., Nov. 2015.
14.	Yuki Shihoko, Hiroko Segawa, Sasaki Shohei, Ikuta Kayo, Ichiro Kaneko, Fujii Toru, Hanazaki Ai, Nishiguchi Shiori, Keijiro Notsu, Aki Eriko, Shiozaki Yuji, Sawako Tatsumi and Ken-ichi Miyamoto : Disruption of intestinal alkaline phosphatase (Akp3) affects the phosphate homeostasis., ACN2015 Asian Congress of Nutrition., May 2015.
15.	Haruna Sakaguchi, Sawako Tatsumi, Ogata Mao, Osamu Fujii, Arakaki Tomohiro, Miyagawa Atsumi, Nagamoto Kenta, Takahama Wako, Hirobata Yukiko, Yasui Akihiro, Ichiro Kaneko, Hiroko Segawa and Ken-ichi Miyamoto : Bone-kidney axis regulating phosphate homeostasis: Study of osteocyte-ablated mice., ACN2015 Asian Congress of Nutrition., May 2015.
16.	Ichiro Kaneko, Hsieh Jui-Cheng, Whitfield Kerr G., Hiroko Segawa, Ken-ichi Miyamoto, Haussler R. Mark and Jurutka W. Peter : 1,25-Dihydroxyvitamin D enhances human tryptophan hydroxylase gene expression through vitamin D responsive elements in human brain cells., 12th Asian Congress of Nutrition 2015, May 2015.
17.	Hiroko Segawa, Ichiro Kaneko, Yuji Shiozaki, Sawako Tatsumi and Ken-ichi Miyamoto : The role of Na+-dependent Phosphate transporters in the body., ACN2015 Asian Congress of Nutrition., May 2015.
18.	生田かよ, Hiroko Segawa, 佐々木祥平, Ichiro Kaneko, 塩崎雄治, Sawako Tatsumi and Ken-ichi Miyamoto : Inorganic Phosphate Handling in Salivary Glands., American Society of Nephrology (米国腎臓学会), ペンシルバニアコンベンションセンター(フィラデルフィア), Nov. 2014.
19.	K Nomura, Sawako Tatsumi, A Miyagawa, Y Shiozaki, S Sasaki, Hiroko Segawa and Ken-ichi Miyamoto : Hepatectomy Hypophosphatemia:A Novel Phosphaturic Factor in the Liver Kidney Axis., American Society of Nephrology(46)KIDNEY WEEK2013, Nov. 2013.
20.	Shinsuke Kido, Hiroko Segawa, Sawako Tatsumi, Ken-ichi Miyamoto and 他4名 : Molecular mechanisms of cadmium (Cd) dependent fibroblast growth factor 23 secretion in bone, Americal Society Nephrology, Kidney Week, Nov. 2012.
21.	Sawako Tatsumi, Hiroko Segawa, Shinsuke Kido, Ken-ichi Miyamoto and 他6名 : Mechanisms of hyperphosphatemia in the osteocyte-abelated mice, Americal Society Nephrology, Kidney Week, San Diego, Nov. 2012.
22.	R Hatano, Hiroko Segawa, A Tamura, Ken-ichi Miyamoto, A Tsukita and S Asano : The membrane cytoskeletal crosslinker ezrin is essential for the regulation of phosphate homeostasis in the kidney, Americal Society Nephrology, Kidney Week., Nov. 2012.
23.	Ken-ichi Miyamoto, R Ohnishi, S Shiozaki, Hiroko Segawa and Sawako Tatsumi : Clinical consequences of gene mutations involved in renal phosphate transport, International Symposium on Epithelial Barrier and Transport 2012, Sep. 2012.
24.	K Miyamoto, R Ohnishi, Y Shiozaki, Hiroko Segawa and Sawako Tatsumi : Clinical consequences of gene mutations involved in renal phosphate transport., International Symposium on Epithelial Barrier and Transport 2012, Sep. 2012.
25.	Hiroko Segawa, J Furutani and Ken-ichi Miyamoto : Dietary inorganic phosphorus and intestinal peptide absorption, XVI International Congress on Nutrition and Metabolism in Renal Disease 2012, Jun. 2012.
26.	T Mukai, Hiroko Segawa, Sawako Tatsumi, Shinsuke Kido, Ken-ichi Miyamoto and 他7名 : The role of salivary glands in phosphate homeostasis, XVI International Congress on Nutrition and Metabolism in Renal Disease 2012, Jun. 2012.
27.	Shinsuke Kido, Y Hashimoto, Hiroko Segawa, Sawako Tatsumi and Ken-ichi Miyamoto : Muscle atrophy in patients with CKD results from FGF23/Klotho-mediated suppression of Insulin/IGF-I signaling, XVI International Congress on Nutrition and Metabolism in Renal Disease 2012, Jun. 2012.
28.	Sawako Tatsumi, Y Yamaguchi, T Kamatani, K Nomura, A Yoshimi, Shinsuke Kido, Hiroko Segawa and Ken-ichi Miyamoto : Inorganic phosphate ion homeostasis;osteocyte-kidney axis, The1st HDphysiology International SymposiumIntegrative Multi-l Systems Biology for in SilicoCardiology and Pharmacokinetics, Jan. 2012.
29.	Kengo Nomura, Sawako Tatsumi, Yuji Shiozaki, Seiichi Yamaguchi, Tatsuya Kamatani, Hiroko Segawa, Shinsuke Kido and Ken-ichi Miyamoto : Post-Hepatectomy Hypophosphatemia in Rats, Journal of the American Society of Nephrology, Philadelphia, Nov. 2011.
30.	Hiroko Segawa, Tomo Mukai, Saori Ohnishi, Shohei Sasaki, Akiko Ohi, Shoji Kuwahara, Shinsuke Kido, Sawako Tatsumi, Yasuko Ishikawa, Otoya Ueda, Naoshi Horiba, Kou-ichi Jishage, Naoshi Fukushima and Ken-ichi Miyamoto : Role of Sodium-Dependent Phosphate(Pi)Transporter(Npt2b)on Salivary Pi Secretion, Journal of the American Society of Nephrology, Philadelphia, Nov. 2011.
31.	Ryo Hatano, Atsushi Tamura, Hiroko Segawa, Ken-ichi Miyamoto, Sachiko Tsukita and Shinji Asano : Ezrin Is Essential for the Phosphate Reabeorption in the Renal Proximai Tubule, Journal of the American Society of Nephrology, Philadelphia, Nov. 2011.
32.	Akiko Ohi, Sakiko Haito-Sugino, Mikiko Ito, Yuji Shiozaki, Kengo Nomura, Yuri Kusaka, Shohei Sasaki, Saori Ohnishi, Seiichi Yamaguchi, Shinsuke Kido, Sawako Tatsumi, Hiroko Segawa and Ken-ichi Miyamoto : Molecular Consequences of the SLC34A3 Mutations of Hereditary Hypophosphatemic Rickets with Hypercalciuria(HHRH), Journal of the American Society of Nephrology, Philadelphia, Nov. 2011.
33.	Jun Guo, Hiroko Segawa, Minlin Liu, Lige Song, F Richard Bringhurst, Ken-ichi Miyamoto, Henry M Kronenberg and Harald Juppner : Phospholipase C signaling through the PTH/PTHrP receptor is required for serum phosphate homeostasis but not for serum 1,25(OH)2D3, American Society for Bone and Mineral Reseach, カリフォルニア, Sep. 2011.
34.	Shoko Ikeda, Hironori Yamamoto, Mina Kozai, Masashi Masuda, Sarasa Tanaka, Otoki Nakahashi, Hiroko Segawa, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : Regulation of Renal Sodium-Dependent Phosphate Co-Transporters During Lipopolysaccharide-Induced Acute Inflammation., American Bone and Mineral Research (ASBMR) annual meeting, San Diego, CA, USA, Sep. 2011.
35.	Hironori Yamamoto, Masashi Masuda, Mina Kozai, Sarasa Tanaka, Otoki Nakahashi, Shoko Ikeda, Hiroko Segawa, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : All-Trans-Retinoic Acid Inhibits Intestinal Phosphate Uptake and Type IIb Sodium-Dependent Phosphate Co-Transporter Gene Expression in Rat., American Bone and Mineral Research (ASBMR) annual meeting, San Diego, CA, USA, Sep. 2011.
36.	辰巳佐和子, Seiichi Yamaguchi, Tatsuya Kamatani, Yuji Shiozaki, Kengo Nomura, Yukiko Saito, 木戸慎介, 瀬川博子, 宮本賢一 : Phosphate Homeostasis in Osteocyte-Ablated Mice., ASN, 2010年11月.
37.	Sawako Tatumi, Seiichi Yamaguchi, Tatsuya Kamatani, Yuji Shiozaki, Kengo Nomura, Yukiko Saito, Shinsuke Kido, Hiroko Segawa and Ken-ichi Miyamoto : Phosphate Homeostasis in Osteocyte-Ablated Mice., ASN, Nov. 2010.

国内講演発表:

1.	小宮蒼, 小池萌, 宇賀穂, 東彩生, 石川茜, 柴原しおん, 塩﨑雄治, 宮本賢一, 瀬川博子 : NEP25 Tgマウス CKD-MBDモデルを用いた新規リン代謝調節機構の解明, 第9回日本栄養改善学会四国支部学術総会, 2024年6月.
2.	小池萌, 東彩生, 小宮蒼, 塩﨑雄治, 宇賀穂, 柴原しおん, 宮本賢一, 瀬川博子 : 成長を制御する新規システム-ミネラル代謝・抗老化因子 α-klotho-, 第78回日本栄養・食糧学会大会, 2024年5月.
3.	塩﨑雄治, 濱口ゆき, 宇賀穂, 柴原しおん, 小宮蒼, 東彩生, 石川茜, 小池萌, 宮本賢一, 瀬川博子 : 腎臓リン酸再吸収機構におけるリン酸排出トランスポーターXpr1の役割, 第78回日本栄養・食糧学会大会, 2024年5月.
4.	原田和, 宇賀穂, 小宮蒼, 三浦美月, 東彩生, 石川茜, 柴原しおん, 小池萌, 塩﨑雄治, 瀬川博子 : 新規リン代謝調節因子Tmem174の血中リン濃度調節における役割, 第7回日本Uremic Toxin研究会学術集会, 2024年4月.
5.	瀬川博子 : 腸管リン酸吸収機構UpToDate, 第8回CKD-MBD学会学術集会・総会, 2024年3月.
6.	宇賀穂, 塩﨑雄治, 小宮蒼, 三浦美月, 原田和, 東彩生, 石川茜, 小池萌, 宮本賢一, 金井好克, 瀬川博子 : リン代謝調節因子Tmem174によるNaPi2a内在化機序の解明, 第56回日本栄養・食糧学会中国・四国支部大会, 2023年10月.
7.	小宮蒼, 三浦美月, 小池萌, 宇賀穂, 濵口ゆき, 原田和, 東彩生, 石川茜, 塩﨑雄治, 宮本賢一, 瀬川博子 : リン感受センサーの探索, 第70回日本栄養改善学会学術総会, 2023年9月.
8.	宇賀穂, 佐々木すみれ, 三浦美月, 原田和, 小宮蒼, 東彩生, 石川茜, 小池萌, 塩﨑雄治, 金井好克, 宮本賢一, 瀬川博子 : 高リン血症を予防する新規リン代謝調節因子の同定, 第267回徳島医学会学術集会, 2023年8月.
9.	三浦美月, 佐々木すみれ, 塩﨑雄治, 小池萌, 宇賀穂, 東彩生, 長谷川智香, 網塚憲生, 宮本賢一, 瀬川博子 : Tmem174はリン酸トランスポーターを調節し高リン血症を予防する新規リン代謝調節分子である, 第41回日本骨代謝学会学術集会, 2023年7月.
10.	池戸葵, 山下美智子, 星野麻衣子, 宇賀穂, 瀬川博子, 福本誠二, 今井祐記 : 脂肪組織中の Aromatase による雄性骨量制御機構の解明, 第41回日本骨代謝学会学術集会, 2023年7月.
11.	三浦美月, 小池萌, 宇賀穂, 小宮蒼, 原田和, 東彩生, 小池萌, 宮本賢一, 瀬川博子 : Tmem174はリン酸トランスポーターを調節し高リン血症を予防する新規リン代謝調節分子である, 第8回日本栄養改善学会四国支部学術総会, 2023年5月.
12.	宇賀穂, 塩﨑雄治, 三浦美月, 小宮蒼, 原田和, 小池萌, 宮本賢一, 瀬川博子 : 新規高リン血症抑制因子Tmem174 の発現調節機構の解明, 第77回日本栄養・食糧学会大会, 2023年5月.
13.	橋村寧々, 十川竜太朗, 堤理恵, 瀬川博子, 小原亜希子, 大江健一, 卯川裕一, 向井理恵 : ホップ由来フラボノイドによる骨格筋でのアミノ酸取り込み促進作用, 第77回日本栄養・食糧学会大会, 2023年5月.
14.	塩﨑雄治, 濱口ゆき, 村本愛奈, 谷藤和也, 宇賀穂, 三浦美月, 小宮蒼, 小池萌, 宮本賢一, 瀬川博子 : 高リン負荷誘導性老化に対抗するXPR1 依存的細胞内リン酸排出機構の解明, 第77回日本栄養・食糧学会大会, 2023年5月.
15.	瀬川博子 : 生体内リン恒常性と疾患におけるリン酸トランスポーターの役割, 第31回日本医学会総会, 2023年4月.
16.	三浦美月, 佐々木すみれ, 塩﨑雄治, 谷藤和也, 小池萌, 宇賀穂, 宮本賢一, 瀬川博子 : Tmem174 はリン酸トランスポーターを調節し高リン血症を予防する., 第7回日本CKD-MBD学会学術集会・総会, 2023年3月.
17.	佐々木すみれ, 塩﨑雄治, 小池萌, 谷藤和也, 宇賀穂, 宮本賢一, 瀬川博子 : Tmem174はリン酸トランスポーターを調節し高リン血症を予防する, 第95回日本生化学会大会, 2022年11月.
18.	三浦美月, 佐々木すみれ, 小池萌, 谷藤和也, 宇賀穂, 小宮蒼, 濱口ゆき, 原田和, 塩﨑雄治, 宮本賢一, 瀬川博子 : ポリリン酸は，モノリン酸よりも腎障害およびFGF23分泌に大きな影響を与える, 第69回日本栄養改善学会学術総会, 2022年9月.
19.	瀬川博子, 塩﨑雄治, 金子一郎, 宮本賢一 : リンが関する生体機能ー成長，疾患，寿命ー, 第76回日本栄養・食糧学会大会シンポジウム 4 ミネラルの新機能, 2022年6月.
20.	瀬川博子 : リン酸バランスの生理学, 第65回日本腎臓学会学術総会, 2022年6月.
21.	瀬川博子 : 腎栄養のための腎臓の構造・機能とリン代謝調節機構研究, 第7回腎栄養オンライン情報交換会, 2022年4月.
22.	瀬川博子 : 健康と疾患におけるリン酸トランスポーターの調節, 第99回日本生理学会大会, 2022年3月.
23.	宇賀穂, 金子一郎, 佐々木すみれ, 小池萌, 谷藤和也, 川原滉太, 小宮蒼, 原田和, 浜口ゆき, 三浦美月, 塩﨑雄治, 瀬川博子 : 小腸Cytochrome P450(CYP3A)がビタミンD活性に及ぼす影響, 第54回日本栄養・食糧学会中国・四国支部大会・第7回日本栄養改善学会四国支部学術総会合同大会, 2021年10月.
24.	川原滉太, 小池萌, 佐々木すみれ, 谷藤和也, 塩﨑雄治, 金子一郎, 瀬川博子 : ライフステージに着目した生体内リン代謝の性差検討, 第68回日本栄養改善学会学術総会, 2021年10月.
25.	川原滉太, 小池萌, 佐々木すみれ, 谷藤和也, 塩﨑雄治, 金子一郎, 瀬川博子 : ライフステージに着目した生体内リン代謝の性差検討, 第75回日本栄養・食糧学会大会, 2021年7月.
26.	瀬川博子 : リン制御機構, 第5回日本CKD-MBD研究会学術集会・総会, 2021年5月.
27.	瀬川博子 : リン代謝調節機構-多臓器連関-, 第21回日本毒性学会生涯教育講習会, 2020年6月.
28.	有馬佑貴, 瀬川博子, 花崎愛, 佐々木すみれ, 小池萌, 谷藤和也, 野沢愛, 金子一郎, 宮本賢一 : Intestinal Alkaline Phosphatase(IAP)による腸管リン代謝制御と腎保護作用., 第52回日本栄養・食糧学会中国・四国支部大会., 2019年10月.
29.	瀬川博子 : リン酸ネットワーク調節機構と疾患.., 第61回歯科基礎医学会学術大会・学術シンポジウム, 2019年10月.
30.	瀬川博子, 有馬佑貴, 小池萌, 谷藤和也, 佐々木すみれ, 花崎愛, 金子一郎, 宮本賢一 : Intestinal Alkaline Phosphatase(IAP)による腸内環境制御と腎保護作用., 第66回日本栄養改善学会学術総会., 2019年9月.
31.	金子一郎, 瀬川博子, 加藤茂明, 宮本賢一 : ビタミンDによる小腸リン輸送調節機序の解明., 第66回日本栄養改善学会学術総会., 2019年9月.
32.	辰巳佐和子, 中辻翔也, 河田美紀, 桑原煩治, 金子一郎, 瀬川博子, 宮本賢一 : 腸管ニコチンアミドホスホリボシルトランスフェラーゼのリン吸収抑制効果の検討., 第66回日本栄養改善学会学術総会., 2019年9月.
33.	中辻翔也, 桑原煩治, 室岡響, 田口裕子, 古川菜摘, 森由貴, 古澤みなみ, 瀬川博子, 宮本賢一, 辰巳佐和子 : 高リン血症におけるリン管理:Nampt/NAD代謝の検討., 第7回日本腎栄養代謝研究回学術集会・総会., 2019年7月.
34.	金子一郎, Haussler R. Mark, Jurutka W. Peter, 瀬川博子, 宮本賢一 : ビタミンDとうつ病の関係:セロトニン代謝の関係, 第7回日本腎栄養代謝研究会学術集会・総会, 2019年7月.
35.	桐野留里, 瀬川博子, 花崎愛, 佐々木すみれ, 小池萌, 谷藤和也, 金子一郎, 宮本賢一 : Intestinal Alkaline Phosphatase(IAP)による内環境制御と腎保護作用., 第3回日本Uremic Toxin研究会学術集会., 2019年4月.
36.	金子一郎, 瀬川博子, 張哲然, 加藤茂明, 宮本賢一 : ビタミンDが制御する小腸リン吸収機序の解明, 第3回CKD-MBD研究会学術集会・総会, 2019年3月.
37.	篠原理沙, 辰巳佐和子, 金子一郎, 瀬川博子, 宮本賢一 : 骨細胞除去による無機リン代謝における影響:骨-腎臓-腸管連関の解析, 第57回日本栄養・食糧学会近畿支部会, 2018年12月.
38.	谷藤和也, 瀬川博子, 生田かよ, 花崎愛, 佐々木すみれ, 小池萌, 金子一郎, 石川康子, 宮本賢一 : 食物無機リン酸適応唾液-腸管-腎臓ネットワーク, 第51回日本栄養・食糧学会中国・四国支部大会, 2018年11月.
39.	瀬川博子 : リン代謝調節機構―多臓器連関―, 第4回CKD-MBDエキスパートセミナー, 2018年11月.
40.	辰巳佐和子, 齋満帆, 中辻翔也, 河田美紀, 篠原理沙, 金子一郎, 瀬川博子, 宮本賢一 : 血中リン濃度を上げない食事時間とは?:動物モデルでの検討, 第6回日本腎栄養代謝研究会学術集会・総会, 2018年7月.
41.	宮本賢一, 木戸慎介, 辰巳佐和子, 金子一郎, 瀬川博子 : カドミウム暴露と骨軟化症:バイオマーカーの探索, 第5回日本栄養改善学会四国支部学術総会, 2018年6月.
42.	張哲然, 金子一郎, 瀬川博子, 野津圭二郎, 生田かよ, 藤井公, 花崎愛, 加藤茂明, 宮本賢一 : ビタミンDによる小腸リン吸収促進機構の解明, 第5回日本栄養改善学会四国支部学術総会, 2018年6月.
43.	金子一郎, 瀬川博子, 野津圭二郎, 生田かよ, 藤井公, 花崎愛, 張哲然, 加藤茂明, 宮本賢一 : ビタミンDが制御する腸管リン吸収機序の解明, 日本ビタミン学会第70回大会, 2018年6月.
44.	瀬川博子 : 栄養素輸送体と疾患:病態解明から薬物・食事療法への展開, 第72回日本栄養・食糧学会大会, 2018年5月.
45.	金子一郎, 瀬川博子, 野津圭二郎, 生田かよ, 藤井公, 花崎愛, 張哲然, 加藤茂明, 宮本賢一 : ビタミンDが制御する腸管リン吸収機序の解明, 第72回日本栄養・食糧学会大会, 2018年5月.
46.	瀬川博子 : Dietary Phosphate intake Patterns in HD Patients: Understanding Determinants of Patient Behaviors., 2018年4月.
47.	瀬川博子, 古谷順也, 金子一郎, 宮本賢一 : FGF23-リンによる腸管窒素吸収調節, 第2回日本UremicToxin 研究学術集会, 2018年4月.
48.	瀬川博子, 金子一郎, 宮本賢一 : 腎臓と他の臓器相関による生体内リン代謝調節機構, 第95回日本生理学会大会, 2018年3月.
49.	辰巳佐和子, 篠原理沙, 金子一郎, 瀬川博子, 宮本賢一 : ミネラル代謝における骨細胞減少の効果:骨細胞-腎臓-腸管連関制御, 第72回日本栄養・食糧学会大会, 2017年11月.
50.	金子一郎, G K.Saini Rimpi, Whitfield Kerr, 伊藤美紀子, 瀬川博子, 辰巳佐和子, 宮本賢一, R.Haussler Mark, W.Jurutka Peter : リン利尿因子FGF23の転写調節機序の解明, 第50回日本栄養・食糧学会中国・四国支部大会, 2017年11月.
51.	木下瑛美, 辰巳佐和子, 藤井理, 張哲然, 金子一郎, 瀬川博子, 宮本賢一 : 腸管NAD+合成律速酵素(Nampt)と全身性NAD+代謝, 第50回日本栄養・食糧学会中国・四国支部大会, 2017年11月.
52.	佐々木すみれ, 瀬川博子, 桐野留里, 金子一郎, 辰巳佐和子, 宮本賢一 : 形態の異なるリン化合物接種に対する生体への影響, 第64回日本栄養改善学会学術総会, 2017年9月.
53.	桐野留里, 瀬川博子, 佐々木すみれ, 金子一郎, 辰巳佐和子, 宮本賢一 : 生体内リン恒常性における腸管アルカリフォスファターゼの役割, 第64回日本栄養改善学会学術総会, 2017年9月.
54.	金子一郎, 瀬川博子, 辰巳佐和子, 宮本賢一 : 脳機能における活性型ビタミンDの役割, 第64回日本栄養改善学会学術総会, 2017年9月.
55.	藤井理, 辰巳佐和子, 金子一郎, 瀬川博子, 宮本賢一 : 水溶性ビタミンB3と腸管上皮機能, 第64回日本栄養改善学会学術総会, 2017年9月.
56.	桐野留里, 瀬川博子, 金子一郎, 辰巳佐和子, 宮本賢一 : 生体内リン恒常性におけるアルカフォスファターゼの役割, 第4回日本栄養改善学会四国支部学術総会, 2017年6月.
57.	瀬川博子, 佐々木祥平, 結城志帆子, 金子一郎, 辰巳佐和子, 宮本賢一 : 生体内リン恒常性における Intestinal Alkaline Phosphatase (IAP) の役割., 第71回日本栄養·食糧学会大会, 2017年5月.
58.	辰巳佐和子, 緒方雅央, 新垣友啓, 藤井理, 金子一郎, 瀬川博子, 宮本賢一 : 骨ー腎臓連関を介した食餌性リン感受機Sensing of dietary phosphate loading in the bone-kidney axis., 第71回日本栄養·食糧学会大会, 2017年5月.
59.	瀬川博子, 金子一郎, 辰巳佐和子, 宮本賢一 : 栄養素輸送担体と健康・疾患「腸管リン吸収と慢性腎臓病」, 第71回日本栄養·食糧学会大会, 2017年5月.
60.	瀬川博子, 佐々木祥平, 結城志帆子, 金子一郎, 辰巳佐和子, 宮本賢一 : 生体内リン恒常性におけるIntestinal Alkaline Phosphatase(IAP)の役割, 第1回CKD‐MBD研究会学術集会・総会, 2017年3月.
61.	瀬川博子 : 栄養学基礎研究者によるリン利尿調節機構の解析, 第7回大阪副甲状腺ホルモン研究会学術集会, 2017年1月.
62.	高濱和子, 辰巳佐和子, 宮川淳美, 藤井理, 新垣友啓, 緒方雅央, 木下瑛美, 金子一郎, 瀬川博子, 宮本賢一 : リン代謝動態の概日リズム形成機序解明, 第49回日本栄養・食糧学会中国・四国支部大会, 2016年11月.
63.	金子一郎, Hsieh Jui-Cheng, Whitfield Kerr G., 辰巳佐和子, 瀬川博子, 宮本賢一 : 脳機能におけるビタミンDの役割, 第68回日本ビタミン学会, 2016年6月.
64.	川端優佳, 瀬川博子, 結城志帆子, 中山彰吾, 藤井公, 生田かよ, 花崎愛, 野津圭二郎, 西口詩織, 金子一郎, 辰巳佐和子, 宮本賢一 : 形態の異なるリン化合物接種に対する生体への影響, 第70回日本栄養・食糧学会大会, 2016年5月.
65.	瀬川博子 : 分子栄養学的研究によるリン代謝調節機構の解明, 第20回TFDセミナー., 2016年3月.
66.	瀬川博子, 佐々木祥平, 結城志帆子, 金子一郎, 辰巳佐和子, 宮本賢一 : 生体内リン恒常性におけるIntestinal Alkaline Phosphatase(IAP)の役割, 第1回CKD‐MBD研究会学術集会・総会, 2016年3月.
67.	金子一郎, Jui-Cheng Hsieh, G.Kerr Whitfield, 辰巳佐和子, 瀬川博子, 宮本賢一, R Mark Haussler, W Peter Jurutka : 脳機能におけるビタミンDの役割について, 第19会日本病態栄養学会年次学術集会, 2016年1月.
68.	西口詩織, 瀬川博子, 蓑島さくら, 桑原煩治, 金子一郎, 前田彰, 辰巳佐和子, 宮本賢一 : リン血症是正に対するFGF23/Klothoシグナルの解明, 第19会日本病態栄養学会年次学術集会, 2016年1月.
69.	新垣友啓, 辰巳佐和子, 緒方雅央, 阪口晴菜, 安井朗洋, 藤井理, 永元健太, 金子一郎, 瀬川博子, 宮本賢一 : 骨細胞の減少による胆汁酸代謝異常についての解析., 第19会日本病態栄養学会年次学術集会., 2016年1月.
70.	生田かよ, 瀬川博子, 結城志帆子, 金子一郎, 西口詩織, 石川康子, 上田乙也, 堀場直, 寺社下浩一, 福島直, 宮本賢一 : 生体内リン代謝調節機構における唾液腺の関与., 第38回日本分子生物学会年会・第88回日本生化学会大会合同大会, 2015年12月.
71.	瀬川博子 : -., 日本薬物動態学会第30回年会., 2015年11月.
72.	花崎愛, 瀬川博子, 福尾真理, 金子一郎, 辰巳佐和子, 宮本賢一 : Klotho and NaPi-2c,double deletionから導くNaPi-2cの重要性., 第48回日本栄養・食糧学会中国・四国支部大会, 2015年10月.
73.	瀬川博子, 森絢加, 宮本賢一, 伊藤美紀子 : リン排泄分子としてのXenotropic and polytropic retrovirus receptor(XPR)1, 第34回腎と骨代謝研究会学術集会, 2015年10月.
74.	桑原三恵子, 坂内堅二, 瀬川博子, 宮本賢一 : ラット腎不全初期の心臓リモデリングにおける尿毒素物質の影響., 第3回日本腎不全栄養研究会学術集会・総会., 2015年7月.
75.	瀬川博子, 金子一郎, 宮本賢一 : 慢性腎臓病におけるリンコントロール., 第31回日本DDS学会学術集会., 2015年7月.
76.	桑原三恵子, 坂内堅二, 瀬川博子, 宮本賢一, 大和英之 : ラット腎不全初期における心臓モデリングには尿素毒素物質が影響している, 第5回腎不全研究会, 2014年12月.
77.	瀬川博子, 生田かよ, 塩崎雄治, 金子一郎, 宮本賢一 : Gastrointestinal phosphate handling., 上皮バリア・輸送に関するシンポジウム, 2014年11月.
78.	緒方雅央, 辰巳佐和子, 藤井理, 阪口晴菜, 新垣友啓, 宮川淳美, 永元健太, 高濱和子, 廣畠佑希子, 金子一郎, 瀬川博子, 宮本賢一 : 骨細胞除去マウスのカルシウム/リン代謝異常解析について, 第47回日本栄養・食糧学会中国・四国支部大会, 2014年10月.
79.	小林謙一, 志賀孝宏, 滝拓也, 石井京子, 石田香織, 河田哲典, 瀬川博子, 宮本賢一, 竹谷豊, 田所忠弘, 松井芳光, 山本祐司 : ビタミンB12欠乏が腎臓におけるビタミンDや無機リンの再吸収に及ぼす影響, 第87回日本生化学会大会，平成26年10月15日—10月18日，国立京都国際会館, 2014年10月.
80.	辰巳佐和子, 野村憲吾, 宮川淳美, 永元健太, 藤井理, 瀬川博子, 宮本賢一 : 肝臓切除に伴う低リン血症発症機構の解明:ニコチンアミドホスホリボシルトランスフェラーゼ(Nampt)を介した全身性リン代謝制御機構についての検討., 第32回日本骨代謝学会学術集会, 2014年7月.
81.	辰巳佐和子, 野村憲吾, 宮川淳美, 永元健太, 藤井理, 瀬川博子, 宮本賢一 : ニコチンアミドホスホリボシルトランスフェラーゼ(Nampt)を介した全身性リン代謝制御機構についての検討., 第57回日本腎臓学会学術総会, 2014年7月.
82.	宮川淳美, 辰巳佐和子, 野村憲吾, 永元健太, 瀬川博子, 宮本賢一 : NAD合成律速酵素Namptを介したリン代謝制御機構., 第68回日本栄養・食糧学会大会., 2014年6月.
83.	生田かよ, 瀬川博子, 向井朋, 佐々木祥平, 森絢香, 花崎愛, 森藤久美子, 安井可奈子, 石川康子, 上田乙也, 堀場直, 寺社下浩一, 福島直, 宮本賢一 : 生体内リン代謝調節機構における唾液腺の関与, 第68回日本栄養・食糧学会大会., 2014年6月.
84.	瀬川博子, 宮本賢一 : リン代謝調節機序におけるNaPiトランスポーターの役割., 日本農芸化学会2014年度(平成26年度)大会, 2014年3月.
85.	辰巳佐和子, 藤田みゆき, 藤井理, 野村憲吾, 瀬川博子, 宮本賢一, 木戸慎介 : 骨細胞死滅マウスにおけるカルシウム/リン代謝異常機構について., 第17回日本病態栄養学会年次学術集会, 2014年1月.
86.	野村憲吾, 辰巳佐和子, 宮川淳美, 塩崎雄治, 瀬川博子, 宮本賢一 : 肝臓切除による無機リン酸恒常性破綻機構について, 第36回日本分子生物学会年会, 2013年12月.
87.	瀬川博子 : ナトリウム依存性リン酸トランスポーターがかわる生体内リン感受機構, 細胞センサーの分子機構・相互関連・ネットワーク研究会, 2013年11月.
88.	瀬川博子 : CKD-MBDに関するリン代謝の基礎研究における進展, 第28回Kobe Parathyroid and Bone Forum, 2013年11月.
89.	瀬川博子 : リン吸収・排泄機構―基礎研究からの最近の進展―, 学術講演会∼保存期慢性腎不全とリン∼, 2013年9月.
90.	生田かよ, 瀬川博子, 向井朋, 佐々木祥平, 森絢加, 石川康子, 上田乙也, 堀場直, 寺社下浩一, 福島直, 宮本賢一 : 生体内リン代謝調節機構における唾液腺の関与., 第86回日本生化学会大会, 2013年9月.
91.	塩崎雄治, 瀬川博子, 大西沙織, 大井彰子, 杉野紗貴子, 簑島さくら, 伊藤美紀子, 木戸慎介, 辰巳佐和子, 宮本賢一 : 近位尿細管上皮細胞におけるNa+依存性無機リン酸輸送担体Npt2cの発現調節とVacuole形成, 第86回日本生化学会大会, 2013年9月.
92.	辰巳佐和子, 木戸慎介, 瀬川博子, 宮本賢一 : 骨とリン利尿因子, 第58回日本透析医学会学術集会・総会, 2013年6月.
93.	木戸慎介, 越智美佐子, 藤原真理奈, 向井朋, 塩崎雄治, 瀬川博子, 辰巳佐和子, 宮本賢一 : 慢性腎臓病に併存する骨ミネラル代謝障害(CKD-MBD)の発症並びに進展におけるFGF23の関与., 第67回日本栄養・食糧学会大会, 2013年5月.
94.	宮川淳美, 辰巳佐和子, 野村憲吾, 木戸慎介, 瀬川博子, 宮本賢一 : Nampt+/-のリン代謝の解析, 第67回日本栄養・食糧学会大会, 2013年5月.
95.	野村憲吾, 辰巳佐和子, 宮川淳美, 岡奈都紀, 塩崎雄治, 木戸慎介, 瀬川博子, 佐野光枝, 福渡努, 柴田克己, 宮本賢一 : 肝臓切除患者における低リン血症発症機構の解明., 第67回日本栄養・食糧学会大会, 2013年5月.
96.	佐々木祥平, 瀬川博子, 大西沙織, 森絢加, 向井朋, 真鍋舞, 日下祐里, 木戸慎介, 辰巳佐和子, 宮本賢一 : リン利尿におけるKlothoの役割, 第56回日本腎臓学会学術総会, 2013年5月.
97.	桑原三恵子, 坂内堅二, 菊池香織, 大和英之, 瀬川博子, 宮本賢一 : 腎機能低下に伴う心肥大には血圧以外に尿毒素物質が関与している., 第56回日本腎臓学会学術総会, 2013年5月.
98.	佐々木祥平, 瀬川博子, 大西沙織, 森絢加, 向井朋, 真鍋舞, 日下祐里, 木戸慎介, 辰巳佐和子, 宮本賢一 : リン利尿におけるKlothoの役割., 第56回日本腎臓学会学術総会, 2013年5月.
99.	日下祐里, 瀬川博子, 木戸慎介, 辰巳佐和子, 宮本賢一, 他5名 : 腸管リン吸収における腸アルカリフォスファターゼの役割, 第16回日本病態栄養学会年次学術集会, 2013年1月.
100.	木戸慎介, 瀬川博子, 辰巳佐和子, 宮本賢一, 他3名 : 慢性腎臓病におけるFGF23産生亢進の分子機能解析, 第16回日本病態栄養学会年次学術集会, 2013年1月.
101.	野村憲吾, 辰巳佐和子, 木戸慎介, 瀬川博子, 宮本賢一 : 肝臓切除に起因する低リン血漿発症機構の解明, 第16回日本病態栄養学会学術集会, 2013年1月.
102.	野村憲吾, 辰巳佐和子, 木戸慎介, 瀬川博子, 宮本賢一, 他2名 : 腎臓切除後の低リン血症発症機構の解明, 第45回日本栄養食糧学会中国・四国支部大会, 2012年11月.
103.	辰巳佐和子, 釜谷達哉, 野村憲吾, 藤田みゆき, 木戸慎介, 瀬川博子, 宮本賢一 : 骨細胞死滅マウスのり代謝異常について, 第31回腎と骨代謝研究会学術集会, 2012年10月.
104.	瀬川博子 : CKDにおけるリン代謝異常:吸収と排泄における問題点, 第30回日本骨代謝学会学術集会, 2012年7月.
105.	木戸慎介, 藤原真理奈, 瀬川博子, 辰巳佐和子, 宮本賢一 : カドミウム汚染によるリン代謝異常・骨軟化症発症機序の検討, 第30回日本骨代謝学会学術集会, 2012年7月.
106.	瀬川博子 : ナトリウム依存性リントランスポーターNaPi-2cの生理学的役割解明, 第3回ビタミンD基礎研究会, 2012年7月.
107.	瀬川博子 : 栄養素トランスポーターの同定と機能調節に関する研究, 第66回日本栄養・食糧学会大会, 2012年6月.
108.	大西沙織, 大井彰子, 杉野紗貴子, 森絢加, 瀬川博子, 宮本賢一 : HHRHの原因遺伝子Na-Pi-IIcによる細胞内vacuole形成について, 第55回日本腎臓学会学術集会, 2012年6月.
109.	瀬川博子, 宮本賢一, 大西沙織 : リン代謝調節機構, 第55回日本腎臓学会学術総会, 2012年6月.
110.	木戸慎介, 瀬川博子, 辰巳佐和子, 宮本賢一, 他2名 : 慢性腎臓病患者におけるFGF23産生亢進の分子機能解析., 第66回日本栄養・食糧学会大会, 2012年5月.
111.	辰巳佐和子, 瀬川博子, 宮本賢一, 他5名 : 骨細胞と腎臓を結ぶリン代謝調節機序, 第66回日本栄養・食糧学会大会, 2012年5月.
112.	向井朋, 瀬川博子, 木戸慎介, 辰巳佐和子, 宮本賢一, 他10名 : 生体内リン代謝調節機構における唾液腺の関与., 第66回日本栄養・食糧学会大会., 2012年5月.
113.	藤原真理奈, 木戸慎介, 瀬川博子, 辰巳佐和子, 宮本賢一 : カドミウム汚染によるリン代謝異常;骨軟化症発症機序およびバイオマーカーの探索, 第244回徳島医学会学術集会, 2012年2月.
114.	宮本賢一, 向井朋, 辰巳佐和子, 木戸慎介, 瀬川博子 : リン代謝における腸管の役割, 第15回日本病態栄養学会年次学術集会, 2012年1月.
115.	木戸慎介, 橋本由衣, 藤原真理奈, 遠藤逸朗, 瀬川博子, 辰巳佐和子, 松本俊夫, 宮本賢一 : 糖尿病に併存する腎障害・骨障害の発症及び進展におけるFGF23の関与, 第15回日本病態栄養学会年次学術集会, 2012年1月.
116.	向井朋, 瀬川博子, 石川康子, 大西沙織, 佐々木祥平, 桑原頌冶, 堀場直, 木戸慎介, 福島直, 宮本賢一 : ナトリウム依存性リン酸トランスポーターNpt2bの新たな生理機能の解析, 第15回日本病態栄養学会年次学術集会, 2012年1月.
117.	藤原真理奈, 木戸慎介, 瀬川博子, 辰巳佐和子, 宮本賢一 : カドミウム汚染によるリン代謝異常:骨軟化症発症機序の検討, 第15回日本病態栄養学会年次学術集会, 2012年1月.
118.	釜谷達哉, 辰巳佐和子, 山口誠一, 吉見文子, 木戸慎介, 瀬川博子, 宮本賢一 : 骨細胞とリン代謝, 第15回日本病態栄養学会年次学術集会, 2012年1月.
119.	橋本由衣, 木戸慎介, 藤原真理奈, 近藤剛史, 瀬川博子, 遠藤逸朗, 辰巳佐和子, 松本俊夫, 宮本賢一 : 糖尿病合併症発症におけるFGF23/Klothoの関与, 第44回日本栄養食糧学会中四国支部大会, 2011年11月.
120.	向井朋, 瀬川博子, 佐々木祥平, 桑原頌冶, 宮本賢一 : ナトリウム依存性リン酸トランスポーターNpt2bの新たな生理機能の解明, 第41回日本腎臓学会西部学術大会, 2011年9月.
121.	大西沙織, 大井彰子, 杉野紗貴子, 木戸慎介, 辰巳佐和子, 瀬川博子, 宮本賢一 : Hereditary hypophosphatemic rickets with hypercalciuria(HHRH)やFanconi's syndromeにおける低リン血症の分子機構解明, 第41回日本腎臓学会西部学術大会, 2011年9月.
122.	木戸慎介, 藤原真理奈, 瀬川博子, 辰巳佐和子, 宮本賢一 : イタイイタイ病に見られる骨障害の発症・進展におけるFGF23の関与, 第29回日本骨代謝学会学術集会, 2011年7月.
123.	山本浩範, 増田真志, 香西美奈, 瀬川博子, 竹谷豊, 宮本賢一, 武田英二 : レチノイン酸はIIb型リン酸トランスポーターNpt2b発現を抑制し小腸リン吸収を低下させる, 第29回日本骨代謝学会学術集会, 2011年7月.
124.	山本浩範, 池田翔子, 増田真志, 香西美奈, 瀬川博子, 竹谷豊, 宮本賢一, 武田英二 : 敗血症時におけるリン代謝異常の分子メカニズムの解析, 第29回日本骨代謝学会学術集会, 2011年7月.
125.	瀬川博子 : リン代謝調節機構up to date, 第56回日本透析医学会学術集会・総会, 2011年6月.
126.	瀬川博子, 古谷順也, 桑原頌冶, 辰巳佐和子, 木戸慎介, 宮本賢一 : 慢性腎臓病における食事リンによる腸管ペプチドトランスポーター調節, 第65回日本栄養・食糧学会大会, 2011年5月.
127.	木戸慎介, 藤原真理奈, 中川航司, 瀬川博子, 辰巳佐和子, 宮本賢一 : イタイイタイ病に見られる骨障害の発症・進展におけるFGF23の関与, 第65回日本・栄養食糧学会大会, 2011年5月.
128.	辰巳佐和子, 菊井聡子, 野村憲吾, 斉藤友紀子, 塩﨑雄治, 山口誠一, 木戸慎介, 瀬川博子, 宮本賢一 : リン代謝におけるカルシウム受容体の役割, 第65回日本栄養・食糧学会大会, 2011年5月.
129.	山本浩範, 増田真志, 香西美奈, 中橋乙起, 池田翔子, 竹谷豊, 瀬川博子, 宮本賢一, 武田英二 : レチノイン酸受容体RAR/RXRを介したナトリウム依存性リン酸輸送担体遺伝子の発現調節機構, 第65回日本栄養・食糧学会大会, 2011年5月.
130.	瀬川博子, 古谷順也, 菅野三喜男, 坂内堅二, 大和英之, 宮本賢一 : 蛋白源に含まれるリンの有する作用:FGF23との関係, 第22回日本腎性骨症研究会, 2011年2月.
131.	大井彰子, 瀬川博子, 花房悦世, 堀場直, 上田乙也, 寺社下浩一, 福島直, 宮本賢一 : 高リン血症治療薬の分子標的Npt2bノックアウトマウスの解析, 第14回日本病態栄養学会年次学術集会, 2011年1月.
132.	大井彰子, 瀬川博子, 花房悦世, 堀場直, 上田乙也, 寺社下浩一, 福島直, 宮本賢一 : 高リン血症治療薬の分子標的Npt2bノックアウトマウスの解析, 第14回日本病態栄養学会年次学術集会, 2011年1月.
133.	坂田雅映, 木戸慎介, 橋本由衣, 辰巳佐和子, 瀬川博子, 松本俊夫, 宮本賢一 : FGF23/Klothoを介した新たな腎尿細管リン・カルシウム代謝調節機構の解明, 第14回日本病態栄養学会年次学術集会, 2011年1月.
134.	瀬川博子 : 生体内リン代謝調節機構, 「ストレスと栄養クラスター」ミニリトリート, 2011年1月.
135.	藤原真理奈, 木戸慎介, 坂田雅映, 荒波史, 瀬川博子, 辰巳佐和子, 宮本賢一 : イタイイタイ病に見られる骨障害の発症・進展におけるFGF23の関与, 第43回日本栄養・食糧学会中国四国支部大会, 2010年11月.
136.	木戸慎介, 中川航司, 橋本由衣, 坂田雅映, 辰巳佐和子, 荒波史, 瀬川博子, 宮本賢一 : イタイイタイ病に見られるCd骨症(骨軟化症)の発症・進展におけるFGF23の関与, 第28回日本骨代謝学会学術集会, 2010年7月.
137.	宮本賢一, 花房悦世, 辰巳佐和子, 木戸慎介, 瀬川博子 : 腸管とリン代謝, 第28回日本骨代謝学会学術集会, 2010年7月.
138.	花房悦世, 瀬川博子, 堀場直, 上田乙也, 寺社下浩一, 福島直, 宮本賢一 : 小腸リン酸トランスポーターNpt2bノックアウトマウスの解析, 第64回日本栄養・食糧学会大会, 2010年5月.
139.	松本なつき, 逸見明博, 瀬川博子, 大西律子, 宮本賢一, 大和英之 : 生体内凍結技法による腎尿細管リントランスポーターの免疫組織解析, 第64回日本栄養・食糧学会大会, 2010年5月.
140.	大井彰子, 富永理恵子, 伊藤美紀子, 西山俊, 杉野紗貴子, 木戸慎介, 辰巳佐和子, 瀬川博子, 宮本賢一 : 副甲状腺(PTH)によるリン代謝調節機構の解明, 第64回日本栄養・食糧学会大会, 2010年5月.
141.	瀬川博子, 花房悦世, 堀場直, 上田乙也, 寺社下浩一, 福島直, 宮本賢一 : 高リン血症治療の標的分子探索:腸管リントランスポーターノックアウトマウスの解析, 第64回日本栄養・食糧学会大会, 2010年5月.
142.	斎藤友紀子, 辰巳佐和子, 野村憲吾, 菊井聡子, 山口誠一, 塩崎雄治, 金子一郎, 瀬川博子, 木戸慎介, 宮本賢一 : リン酸輸送担体遺伝子欠損マウスの病態解析, 第64回日本栄養・食糧学会大会, 2010年5月.
143.	金子一郎, 瀬川博子, 古谷順也, 桑原頌治, 荒波史, 富永理恵子, 花房悦世, 辰巳佐和子, 木戸慎介, 加藤茂明, 宮本賢一 : ビタミンDによるリン代謝調節機序の解明．, 第64回日本栄養・食糧学会, 2010年5月.
144.	宮本賢一, 新居智子, 瀬川博子, 伊藤美紀子, 竹谷豊, 武田英二, 金井好克, 遠藤仁 : CD98を介するアミノ酸輸送と感受システムの誘導機序, 日本栄養食糧学会大会, Vol.55, 2001年5月.

その他・研究会:

1.	瀬川博子 : 腸管リン酸吸収機構UpToDate, CKD-MBD webセミナー~これからの高P血症治療, 2024年2月.
2.	瀬川博子 : リン代謝調節機構の理解ー最近の進展ー, 第22回枚方・寝屋川CKD研究会, 2023年7月.
3.	塩﨑雄治, 三浦美月, 宇賀穂, 小宮蒼, 原田和, 東彩生, 小池萌, 宮本賢一, 瀬川博子 : 高リン血症予防に関与する新規リン代謝調節因子Transmembrane protein (Tmem) 174の同定, 第6回日本Uremic Toxin研究会学術集会, 2023年5月.
4.	Hiroko Segawa : Renal Phosphate Handling Tmem174, a regulator of phosphate transporter prevents hyperphosphatemia-, CKD-MBD Special Seminar, Mar. 2023.
5.	塩﨑雄治, 瀬川博子 : 腎リン酸トランスポーターの機能制御と疾患, 第16回トランスポーター研究会年会, 2022年7月.
6.	瀬川博子 : 基礎科学としての栄養学, 腎臓病と栄養・代謝・食事フォーラム, 2022年3月.
7.	瀬川博子 : シンポジウム2:治療ターゲットとしての腸管リン吸収機構, 第6回日本CKD-MBD研究会, 2022年3月.
8.	塩﨑雄治, 佐々木すみれ, 小池萌, 谷藤和也, 川原滉太, 浜口ゆき, 金子一郎, 宮本賢一, 瀬川博子 : 近位尿細管細胞分化におけるリン酸トランスポーターNaPi-IIcの役割, 第1回トランスポーター研究会関西西部会JTRAKansai2021∼トランスポーター研究の架け橋∼, 2021年10月.
9.	瀬川博子 : リン制御機構とカルシミメティクス, Webセミナー「オルケディア錠発売3周年記念」, 2021年6月.
10.	瀬川博子 : リンバランスに関わるトランスポーターの理解, 第3回日本CKD-MBD研究会学術集会・総会, 2019年3月.
11.	金子一郎, 瀬川博子, 張哲然, 加藤茂明, 宮本賢一 : ビタミン D が制御する小腸リン吸収機序の解明, 第3回日本CKD-MBD研究会学術集会・総会, 2019年3月.
12.	辰巳佐和子, 金子一郎, 瀬川博子, 宮本賢一 : 骨細胞除去によるミネラル代謝への影響: 骨 - 腎臓 - 腸管連関の解析, 第3回日本CKD-MBD研究会学術集会・総会, 2019年3月.
13.	瀬川博子 : 栄養素吸収調節機構―管理栄養士による基礎研究―, 第3回初雁腎・透析療法セミナー, 2018年12月.
14.	瀬川博子 : リン代謝-多臓器連関制御-, 第36回日本骨代謝学会学術集会, 2018年7月.
15.	瀬川博子 : 分子腎臓栄養学―基礎研究の理解―, 第6回日本腎栄養代謝研究会学術集会・総会, 2018年7月.
16.	宮本賢一, 木戸慎介, 辰巳佐和子, 金子一郎, 瀬川博子 : カドミウム暴露と骨軟化症:バイオマーカーの探索, 第5回日本栄養改善学会四国支部学術総会, 2018年6月.
17.	張哲然, 瀬川博子, 野津圭二郎, 生田かよ, 藤井公, 花崎愛, 加藤茂明, 宮本賢一 : ビタミンDによる小腸リン吸収促進機構の解明, 第5回日本栄養改善学会四国支部学術総会, 2018年6月.
18.	辰巳佐和子, 篠原理沙, 金子一郎, 瀬川博子, 宮本賢一 : ミネラル代謝における骨細胞減少の効果:骨細胞-腎臓-腸管連関制御, 第72回日本栄養・食糧学会大会, 2018年5月.
19.	瀬川博子 : Gastrointestinal phosphate handling., ISN FRONTIERS MEETINGS, 2018年2月.
20.	瀬川博子, 宮本賢一 : 消化管リン輸送機構の役割, 日本農芸化学会2017年度大会, 2017年3月.
21.	瀬川博子 : 栄養学的研究を用いたリン代謝調節機構の解明, 慢性腎臓病，腎不全におけるリン代謝是正の新展開∼鉄代謝とのコラボレーション∼, 2016年4月.
22.	瀬川博子 : 分子栄養学的研究によるリン代謝調節機構の解明, 第20回TFDセミナー, 2016年3月.
23.	瀬川博子, 桑原三恵子, 坂内堅二, 宮本賢一 : 慢性腎臓病における蛋白性尿毒素と心肥大の関連について, 第2回腎と栄養研究会., 2015年9月.
24.	瀬川博子 : リンのトランスポートについて, 2015年骨形態フォーラム in 伊香保, 2015年6月.
25.	瀬川博子 : 唾液リン吸着療法の有用性:動物モデルを用いた唾液リン排泄の検討., 第一回腎と栄養研究会, 2014年9月.
26.	瀬川博子 : Gastrointestinal phosphate handling., 第30回ROD-21研究会, 2014年8月.
27.	瀬川博子, 佐々木祥平, 宮本賢一 : Klothoによるリン代謝制御と老化, 第43回日本腎臓学会西部学術大会, 2013年10月.
28.	瀬川博子, 向井朋, 森絢加, 佐々木祥平, 宮本賢一 : リンの吸収と排泄の生体内調節., 第56回日本腎臓学会学術総会, 2013年5月.
29.	瀬川博子, 佐々木祥平, 向井朋, 真鍋舞, 宮本賢一 : 近位尿細管におけるりんトランスポーターNaPi2cとKlothoとの関わり, 第24回日本腎性骨症研究会, 2013年2月.
30.	瀬川博子, 佐々木祥平, 向井朋, 真鍋舞, 宮本賢一 : 近位尿細管におけるリントランスポーターNaPi2cとklothoとの関わり, 第24回日本腎性骨症研究会, 2013年1月.
31.	瀬川博子 : 高カルシウム尿を伴う低リン血症性くる病(HHRH)とType II NaPiトランスポーター, The Fifteenth Lilly International Symposium, 2012年10月.
32.	瀬川博子, 木戸慎介, 宮本賢一, 辰巳佐和子, 他3名 : リンの体内動態(腸管，腎臓における吸収と排泄機序/リン輸送体の機能作用), Clinical Calcium, Vol.22, No.10, 13-20, 2012年10月.
33.	瀬川博子 : ヒトにおけるPTHおよびFGF23による血中リン濃度低下を担う標的分子の探索, 第5回慢性腎臓病(CKD)病態研究会, 2012年7月.
34.	瀬川博子 : 腸管リン吸収機構ー基礎研究からの最近の進展, 第10回CKD合併症研究会, 2012年7月.
35.	瀬川博子 : 生体内リン代謝調節機構, 第27回小児成長研究会, 2012年2月.
36.	山口誠一, 辰巳佐和子, 釜谷達哉, 吉見文子, 木戸慎介, 瀬川博子, 宮本賢一 : 骨細胞とリン代謝, 第18回徳島骨代謝研究会, 2011年11月.
37.	瀬川博子 : 生体内リン代謝調節機構, 第15回BMC研究会, 2011年10月.
38.	藤原真理奈, 木戸慎介, 荒波史, 中川航司, 瀬川博子, 辰巳佐和子, 宮本賢一 : カドミウムによるFibroblast growth factor23(FGF23)発現調節機序の検討, 第30回腎と骨代謝研究会学術集会, 2011年10月.
39.	野村憲吾, 辰巳佐和子, 山口誠一, 塩﨑雄治, 菅生陵馬, 木戸慎介, 瀬川博子, 宮本賢一 : 肝臓切除による低リン血症発症メカニズムの解明, 第30回腎と骨代謝研究会学術集会, 2011年10月.
40.	瀬川博子 : リン酸化代謝調節機構の分子基盤解明., 第2回ビタミンD基礎研究会(KATOプロジェクトミーティング), 2011年6月.

報告書:

1.	宮本賢一, 辰巳佐和子, 金子一郎, 瀬川博子 : 大豆たん白質摂取による心肥大抑制効果の検討., 大豆たん白質研究., Vol.21, 83-89, 2019年.

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

小腸由来エクソソームを介した食事性蛋白質と骨格筋の新規機能連関 (研究課題/領域番号: 23K24770 )
抗老化因子を制御するミネラル栄養学の確立 (研究課題/領域番号: 21H03375 )
新規リンネットワーク破綻がもたらす栄養障害の分子機序解明 (研究課題/領域番号: 20K08637 )
リン代謝神経ネットワーク調節機構の存在とその破綻 (研究課題/領域番号: 17K09728 )
老化制御と食事因子：糖鎖修飾ダイエット (研究課題/領域番号: 15K12340 )
CKD-MBD治療戦略における新しい腸管リン制御の展開 (研究課題/領域番号: 26461254 )
脳室内リン制御による全身性リン過剰の克服 (研究課題/領域番号: 26293204 )
ＣＫＤ－ＭＢＤを理解するネオ・ミネラル学の展開 (研究課題/領域番号: 23689045 )
リン代謝異常を惹起する臓器相関シグナル因子の解明 (研究課題/領域番号: 23390226 )
生命予後を規定する骨・血管型リンチャネルの分子制御機構 (研究課題/領域番号: 20590975 )
FGF23/klotho/リンセンサーを介したリン代謝ホルモンの同定と機能解明 (研究課題/領域番号: 20390236 )
リンセンサーの異常を呈するノックインマウスの作製 (研究課題/領域番号: 19790585 )
FGF23/klothoによるミネラル代謝と寿命制御 (研究課題/領域番号: 18659251 )
リンセットポイントを規定するセンサー分子の統御機構解明 (研究課題/領域番号: 18390250 )
生体内リンセンサー候補分子ノックアウトマウスの解析 (研究課題/領域番号: 17790555 )
リン利尿因子フォスファトニン感受ペプチドASARM受容体の同定 (研究課題/領域番号: 17659256 )
無機リン酸トランスポートソームの機能制御とその破綻 (研究課題/領域番号: 17081013 )
Klotho老化学を裏付けるリン老化説構成回路(寿命ホルモン)の同定 (研究課題/領域番号: 16659225 )
リンセンサー分子を介したカルシウム・リン積制御機構の解明 (研究課題/領域番号: 16390244 )
生体内リンの恒常性を維持するリンセンサー複合体の解明 (研究課題/領域番号: 15790430 )
リンセンサー分子の同定と機能解析 (研究課題/領域番号: 14657254 )
リンセンサー分子の同定と新規リンシグナルネットワーク分子統制機能の解明 (研究課題/領域番号: 14370320 )
腎尿細管アミノ酸尿症の責任遺伝子解明と治療法の確立 (研究課題/領域番号: 13770601 )
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教授 : 瀬川 博子

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教授 : 瀬川博子