Tokushima University / Educator and Researcher Directory --- Masuda, Masashi

Personal Web Page

https://researchmap.jp/masuda.masashi (researchmap)

Field of Study

○	Life sciences [Nutrition and health science]

Subject of Study

Book / Paper

Book:

1.	Masashi Masuda : 第4章ミネラル(マンガン，モリブデン，クロム), Medicus SHUPPAN, Osaka, Dec. 2023.
2.	Masashi Masuda, Yuji Shiozaki and Makoto Miyazaki : Chapter 10 - Lipotoxicity in the pathogenesis of chronic kidney disease complications, Academic Press, Aug. 2023. (Link to Publication Site) ● Publication site (DOI): 10.1016/C2021-0-02221-5 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/C2021-0-02221-5 (DOI: 10.1016/C2021-0-02221-5)
3.	Yutaka Taketani, Masashi Masuda and Hirokazu Ohminami : フィトケミカルの機能と作用メカニズム, Jun. 2023.
4.	Masashi Masuda, Hironori Yamamoto, 竹井悠一郎, 中橋乙起, 足立雄一郎, Kohta Ohnishi, Hirokazu Ohminami, Hisami Okumura, Hiroshi Sakaue, 宮崎淳, Eiji Takeda and Yutaka Taketani : All-trans retinoic acid reduces the transcriptional regulation of intestinal sodium-dependent phosphate co-transporter gene (Npt2b), The Vitamin Society of Japan, Nov. 2020. (Summary) ビタミン欠乏(VAD)ラットにall-transレチノイン酸(ATRA)を投与後，腸管のNpt2b発現を中心としたリン吸収への影響と，ラットNpt2b遺伝子プロモーターを用いたATRAによるNpt2b生化学転写調節機構について検討した．VADラットにATRAを腹腔内投与した18時間後，血漿リン濃度はビタミンAによる影響を認めなかったが，腸管リン酸取り込み活性，Npt2b蛋白発現量およびmRNA発現量はATRA投与により抑制された．マウス胎児線維芽細胞株NIH3T3細胞を用いたルシフェラーゼアッセイの結果，レチノイン酸受容体(RAR)/レチノイドX受容体存在下においてATRAおよびRARアゴニスト濃度依存的にNpt2b遺伝子プロモーター活性は低下した．デリーションアッセイの結果，ATRAによるNpt2b遺伝子プロモーター活性の低下は，転写因子CCAAT/enhancer-binding protein(C/EBP)依存的であることが示唆された． (Keyword) all-trans retinoic acid (ATRA) / retinoic acid receptor (RAR) / CCAAT/enhancer-binding protein (C/EBP) / small intestine / type II sodium-dependent phosphate co-transporter (Npt2b) (Link to Publication Site) ● Publication site (DOI): 10.20632/vso.94.11_545 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390571704642711680 ● Search Scopus @ Elsevier (DOI): 10.20632/vso.94.11_545 (DOI: 10.20632/vso.94.11_545, CiNii: 1390571704642711680)
5.	坂井麻衣子, Kohta Ohnishi, Masashi Masuda, Hirokazu Ohminami, Hisami Okumura, 原太一 and Yutaka Taketani : イソラムネチンはJ774.1マウスマクロファージ様細胞株においてTFEB非依存的にリソソームのタンパク質分解を促進, Oct. 2020.
6.	多々納(福田) 詩織, Hironori Yamamoto, 中橋乙起, 吉川亮平, 林眞由, 岸本麻希, 伊美友紀子, Hisami Okumura, Kohta Ohnishi, Masashi Masuda and Yutaka Taketani : 成長期における食餌性リンによるα-klotho発現制御, Jun. 2020.
7.	Shigeru Sugiyama, Toshihiro Moriga, Masahiro Katoh, Kei-ichiro Murai, Toshihide Horikawa, Naohiro Shimoda, Akihiro Furube, Shin-ichiro Yanagiya, Masamichi Ogasawara, Takashi Yamamoto, Yoshitoshi Nakamura, Chikako Asada, Chizuru Sasaki, Hideji TANAKA, Masaki Takeuchi, Yutaka Taketani, Hisami Okumura, Masashi Masuda and Toshihiro Okamoto : 枯渇資源と技術開発, 徳島大学産業院出版部, Tokushima, Mar. 2020. (Summary) 2017年度から徳島大学重点クラスター``人類の恒久的繁栄に向けた対枯渇資源対応技術の開発''として活動した成果を，一般の読者にもわかりやすいように公表した徳島大学産業院出版部から始めて出版した書籍である．
8.	Masashi Masuda, 新井田裕樹, Yutaka Taketani and Takeshi Nikawa : ビタミンD欠乏とサルコペニアについて, Kodansha, Tokyo, Apr. 2018.
9.	Masashi Masuda : ビタミンの栄養, Kodansha, Tokyo, Nov. 2016.
10.	Masashi Masuda : 脂質異常症, Kodansha, Tokyo, Jan. 2016.
11.	Yutaka Taketani and Masashi Masuda : リン摂取と循環器疾患, May 2014.

Academic Paper (Judged Full Paper):

1.	Shinobu Miyazaki-Anzai, Masashi Masuda, Audrey L Keenan, Yuji Shiozaki, Jose G Miranda and Makoto Miyazaki : Activation of the IKK2/NF-κB pathway in VSMCs inhibits calcified vascular stiffness in CKD, JCI Insight, Vol.9, No.7, 12:e174977, 2024. (Summary) IKK2/NF-κB pathway-mediated inflammation in vascular smooth muscle cells (VSMCs) has been proposed to be an etiologic factor in medial calcification and stiffness. However, the role of the IKK2/NF-κB pathway in medial calcification remains to be elucidated. In this study, we found that chronic kidney disease (CKD) induces inflammatory pathways through the local activation of the IKK2/NF-κB pathway in VMSCs associated with calcified vascular stiffness. Despite reducing the expression of inflammatory mediators, complete inhibition of the IKK2/NF-κB pathway in vitro and in vivo unexpectedly exacerbated vascular mineralization and stiffness. In contrast, activation of NF-κB by SMC-specific IκBα deficiency attenuated calcified vascular stiffness in CKD. Inhibition of the IKK2/NF-κB pathway induced cell death of VSMCs by reducing anti-cell death gene expression, whereas activation of NF-κB reduced CKD-dependent vascular cell death. In addition, increased calcification of extracellular vesicles through the inhibition of the IKK2/NF-κB pathway induced mineralization of VSMCs, which was significantly reduced by blocking cell death in vitro and in vivo. This study reveals that activation of the IKK2/NF-κB pathway in VSMCs plays a protective role in CKD-dependent calcified vascular stiffness by reducing the release of apoptotic calcifying extracellular vesicles. (Keyword) Humans / NF-kappa B / Signal Transduction / Vascular Stiffness / Muscle, Smooth, Vascular / Renal Insufficiency, Chronic (Tokushima University Institutional Repository) ● Metadata: 119162 (Link to Publication Site) ● Publication site (DOI): 10.1172/jci.insight.174977 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38470493 ● Search Scopus @ Elsevier (PMID): 38470493 ● Search Scopus @ Elsevier (DOI): 10.1172/jci.insight.174977 (Tokushima University Institutional Repository: 119162, DOI: 10.1172/jci.insight.174977, PubMed: 38470493)
2.	Yuki Mori, Masashi Masuda, Risa Yoshida-Shimizu, Saki Aoyagi, Yuichiro Adachi, The Anh Nguyen, Yusuke Maruyama, Yosuke Okumura, Yuki Kamei, Maiko Sakai, Kohta Ohnishi, Hirokazu Ohminami and Yutaka Taketani : All-trans retinoic acid induces lipophagy through the activation of the AMPK-Beclin1 signaling pathway and reduces Rubicon expression in adipocytes., The Journal of Nutritional Biochemistry, Vol.126, 2024. (Summary) Lipophagy is defined as a lipolysis pathway that degrades lipid droplet (LD) via autophagy. All-trans retinoic acid (atRA), a metabolite of vitamin A, stimulates lipolysis through hormone-sensitive lipase and β-oxidation. However, the regulation of lipolysis by atRA-induced autophagy in adipocytes remains unclear. In this study, we investigated the effect of atRA on autophagy in epididymal fat of mice and the molecular mechanisms of autophagy in 3T3-L1 adipocytes. Western blotting showed that atRA decreased the expression of p62, a cargo receptor for autophagic degradation, and increased the expression of the lipidated LC3B (LC3B-II), an autophagy marker, in epididymal fat. Next, we confirmed that atRA increased autophagic flux in differentiated 3T3-L1 cells using the GFP-LC3-RFP-LC3ΔG probe. Immunofluorescent staining revealed that the colocalization of LC3B with perilipin increased in differentiated 3T3-L1 cells treated with atRA. The knockdown of Atg5, an essential gene in autophagy induction, partly suppressed the atRA-induced release of non-esterified fatty acid (NEFA) from LDs in differentiated 3T3-L1 cells. atRA time-dependently elicited the phosphorylation of AMPK and Beclin1, autophagy-inducing factors, in mature 3T3-L1 adipocytes. Inversely, atRA decreased the protein expression of Rubicon, an autophagy repressor, in differentiated 3T3-L1 cells and epididymal fat. Interestingly, the expression of ALDH1A1, atRA-synthesizing enzymes, increased in epididymal fat with decreased protein expression of Rubicon in aged mice. These results suggest that atRA may partially induce lipolysis through lipophagy by activating the AMPK-Beclin1 signaling pathway in the adipocytes and increased atRA levels may contribute to decreased Rubicon expression in the epididymal fat of aged mice. (248/250 words). (Keyword) Mice / Animals / AMP-Activated Protein Kinases / Beclin-1 / Signal Transduction / Lipolysis / Tretinoin / Autophagy / Adipocytes / 3T3-L1 Cells (Tokushima University Institutional Repository) ● Metadata: 119349 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jnutbio.2024.109589 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38295886 ● Search Scopus @ Elsevier (PMID): 38295886 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jnutbio.2024.109589 (Tokushima University Institutional Repository: 119349, DOI: 10.1016/j.jnutbio.2024.109589, PubMed: 38295886)
3.	Yosuke Okumura, Kotaro Abe, Shoko Sakai, Yuki Kamei, Yuki Mori, Yuichiro Adachi, Masaki Takikawa, Ayano Kitamura, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda, Taiho Kambe, Hironori Yamamoto and Yutaka Taketani : Elevated luminal inorganic phosphate suppresses intestinal Zn absorption in 5/6 nephrectomized rats., American Journal of Physiology, Renal Physiology, Vol.326, No.3, F411-F419, 2024. (Summary) binder might be useful for the treatment of hypozincemia and hyperphosphatemia. (Keyword) Humans / Rats / Animals / Phosphates / Hyperphosphatemia / Zinc / Renal Insufficiency, Chronic / Nephrectomy / Intestinal Absorption (Tokushima University Institutional Repository) ● Metadata: 119347 (Link to Publication Site) ● Publication site (DOI): 10.1152/ajprenal.00310.2023 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38234299 ● Search Scopus @ Elsevier (PMID): 38234299 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00310.2023 (Tokushima University Institutional Repository: 119347, DOI: 10.1152/ajprenal.00310.2023, PubMed: 38234299)
4.	Ayari Tsumura, Hisami Yamanaka-Okumura, Hana Kawakami, Shiori Yamamoto, Mayu Oura, Hiroshi Tatano, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : Investigation of Amino Acid and Fatty Acid Profiles of Japanese Diets Using the Food Exchange Lists for Diabetes Diet., Journal of Nutritional Science and Vitaminology, Vol.70, No.1, 25-35, 2024. (Summary) Dietary Reference Intakes for Japanese provide target values for proteins, fats, and carbohydrates. However, they do not provide information on reference values for amino acids (AAs) and fatty acids (FAs), which determine the quality of foods in detail. Therefore, we evaluated AAs and FAs using the Food Exchange Lists-Dietary Guidance for Persons with Diabetes (in Japanese) Utilization, Second Edition Sample Menus and Practice (FELD) as an ideal Japanese diet. Based on FELD, 15 different daily meal patterns were employed with combinations of three levels of carbohydrates %energy (high carbohydrate [HC], 60%; middle carbohydrate [MC], 55%; and low carbohydrate [LC], 50%) and five levels of energy (1,200-2,000 kcal). Using the Japanese Food Composition Table 2020 adjusted for 1,000 kcal, 18 AAs, 49 FAs, and calorie densities (CDs, kcal/g) were calculated and compared among the three groups. Dietary AA was rich in glutamic acid, aspartic acid, and leucine; in order, no significant differences were observed among HC, MC, and LC for 18 AAs. Dietary FA was higher for 18:1 total, 16:0, and 18:2 n-6. Moreover, 16:0, 20:0, and 18:1 total in LC and 22:0 and 18:3 n-3 in MC were significantly higher than those in HC. The HC, MC, and LC CD was low at 0.82, 0.84, and 0.93 kcal/g, respectively. No significant differences in 18 AAs and CD were noted among HC, MC, and LC in FELD; however, significant differences were observed in the FA profiles. This study suggests the importance of evaluating diet using AA and FA units. (Keyword) Fatty Acids / Amino Acids / Dietary Carbohydrates / Diet / Dietary Fats / diabetes mellitus (Link to Publication Site) ● Publication site (DOI): 10.3177/jnsv.70.25 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38417849 ● CiNii @ National Institute of Informatics (CRID): 1390017843874880896 ● Summary page in Scopus @ Elsevier: 2-s2.0-85186634749 (DOI: 10.3177/jnsv.70.25, PubMed: 38417849, CiNii: 1390017843874880896, Elsevier: Scopus)
5.	Ayari Tsumura, Hisami Yamanaka-Okumura, Hana Kawakami, Shiori Yamamoto, Mayu Oura, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : Amino acid and fatty acid profiles of the average Japanese diet: Fusion of the National Health and Nutrition Examination Survey and the Food Composition Database, Human Nutrition and Metabolism, Vol.33, 200200, 2023. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.hnm.2023.200200 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1360863416724271488 ● Summary page in Scopus @ Elsevier: 2-s2.0-85162872341 (DOI: 10.1016/j.hnm.2023.200200, CiNii: 1360863416724271488, Elsevier: Scopus)
6.	Naoko Oda, Kohei Sugihara, Takashi Uebanso, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda, Hisami Yamanaka-Okumura and Yutaka Taketani : Dietary phosphate disturbs of gut microbiome in mice., Journal of Clinical Biochemistry and Nutrition, Vol.73, No.3, 221-227, 2023. (Summary) were observed in high phosphate diet group. Furthermore, high phosphate diet induced reduction of microbial diversity and decreased mRNA levels of colonic tight junction markers. These results suggest that the excessive intake of dietary phosphate disturbs gut microbiota and affects intestinal barrier function. (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.23-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37970557 ● Search Scopus @ Elsevier (PMID): 37970557 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.23-9 (DOI: 10.3164/jcbn.23-9, PubMed: 37970557)
7.	Yuki Kamei, Yosuke Okumura, Yuichiro Adachi, Yuki Mori, Maiko Sakai, Kohta Ohnishi, Hirokazu Ohminami, Masashi Masuda, Hisami Yamanaka-Okumura and Yutaka Taketani : Humoral and cellular factors inhibit phosphate-induced vascular calcification during the growth period., Journal of Clinical Biochemistry and Nutrition, Vol.73, No.3, 198-204, 2023. (Summary) , obvious calcification was observed in the adult aorta but not in the young aorta. Furthermore, culture in high Pi medium increased the mRNA level of tissue-nonspecific alkaline phosphatase (TNAP), which degrades pyrophosphate, only in the adult aorta. Collectively, our findings indicate that the aorta in growing mouse may be resistant to Pi-induced vascular calcification via a mechanism in which high serum fetuin-A levels and suppressed TNAP expression. (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.23-11 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37970550 ● Search Scopus @ Elsevier (PMID): 37970550 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.23-11 (DOI: 10.3164/jcbn.23-11, PubMed: 37970550)
8.	Masashi Masuda : Studies on the pathophysiological roles of fat-soluble vitamin and bioactive lipids in mineral and bone disorder., Vitamins, Vol.96, No.12, 501-511, 2022. (Tokushima University Institutional Repository) ● Metadata: 118521 (Tokushima University Institutional Repository: 118521)
9.	Yilimulati Yimamu, Ayako Ohtani, Yuichiro Takei, Airi Furuichi, Yuki Kamei, Hisami Okumura, Hirokazu Ohminami, Masashi Masuda, Makoto Miyazaki, Hironori Yamamoto and Yutaka Taketani : 25-hydroxyvitamin D-1α-hydroxylase (CYP27B1) induces ectopic calcification., Journal of Clinical Biochemistry and Nutrition, Vol.71, No.2, 103-111, 2022. (Summary) Vascular calcification is an important pathogenesis related to cardiovascular disease and high mortality rate in chronic kidney disease (CKD) patients. It has been well-known that hyper-phosphatemia induces osteochondrogenic transition of vascular smooth muscle cells (VSMCs) resulting ectopic calcification in aortic media, cardiac valve, and kidney. However, the detailed mechanism of the ectopic calcification has been not clarified yet. Here, we found that the co-localization of CYP27B1 with the calcified lesions of aorta and arteries in kidney of klotho mutant () mice, and then investigated the role of CYP27B1 in the mineralization of the VSMCs. Under high phosphate condition, overexpression of CYP27B1 induced calcification and osteocalcin mRNA expression in the VSMCs. Inversely, siRNA- inhibited high phosphate-induced calcification of the VSMCs. We also found that the accumulated CYP27B1 protein was glycosylated in the kidney of mice. Therefore, overexpression of CYP27B1-N310A and CYP27B1-T439A, which are a mutation for -linked glycosylation site (N310A) and a mutation for -linked glycosylation site (T439A) in CYP27B1, decreased calcium deposition and expression of RUNX2 induced by high phosphate medium in VSMCs compared with wild-type CYP27B1. These results suggest that extra-renal expression of glycosylated CYP27B1 would be required for ectopic calcification of VSMCs under hyperphosphatemia. (Tokushima University Institutional Repository) ● Metadata: 117147 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.22-16 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36213783 ● Search Scopus @ Elsevier (PMID): 36213783 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.22-16 (Tokushima University Institutional Repository: 117147, DOI: 10.3164/jcbn.22-16, PubMed: 36213783)
10.	Masashi Masuda, Risa Yoshida-Shimizu, Yuki Mori, Kohta Ohnishi, Yuichiro Adachi, Maiko Sakai, Serina Kabutoya, Hirokazu Ohminami, Hirokazu Ohminami, Hironori Yamamoto, Makoto Miyazaki and Yutaka Taketani : Sulforaphane induces lipophagy through the activation of AMPK-mTOR-ULK1 pathway signaling in adipocytes., The Journal of Nutritional Biochemistry, Vol.106, 109017, 2022. (Summary) Lipophagy, a form of selective autophagy, degrades lipid droplet (LD) in adipose tissue and the liver. The chemotherapeutic isothiocyanate sulforaphane (SFN) contributes to lipolysis through the activation of hormone-sensitive lipase and the browning of white adipocytes. However, the details concerning the regulation of lipolysis in adipocytes by SFN-mediated autophagy remain unclear. In this study, we investigated the effects of SFN on autophagy in the epididymal fat of mice fed a high-fat diet (HFD) or control-fat diet and on the molecular mechanisms of autophagy in differentiated 3T3-L1 cells. Western blotting revealed that the protein expression of lipidated LC3 (LC3-II), an autophagic substrate, was induced after 3T3-L1 adipocytes treatment with SFN. In addition, SFN increased the LC3-II protein expression in the epididymal fat of mice fed an HFD. Immunofluorescence showed that the SFN-induced LC3 expression was co-localized with LDs in 3T3-L1 adipocytes and with perilipin, the most abundant adipocyte-specific protein, in adipocytes of mice fed an HFD. Next, we confirmed that SFN activates autophagy flux in differentiated 3T3-L1 cells using the mCherry-EGFP-LC3 and GFP-LC3-RFP-LC3 probe. Furthermore, we examined the induction mechanisms of autophagy by SFN in 3T3-L1 adipocytes using western blotting. ATG5 knockdown partially blocked the SFN-induced release of fatty acids from LDs in mature 3T3-L1 adipocytes. SFN time-dependently elicited the phosphorylation of AMPK, the dephosphorylation of mTOR, and the phosphorylation of ULK1 in differentiated 3T3-L1 cells. Taken together, these results suggest that SFN may provoke lipophagy through AMPK-mTOR-ULK1 pathway signaling, resulting in partial lipolysis of adipocytes. (Keyword) 3T3-L1 Cells / AMP-Activated Protein Kinases / Adipocytes, White / Animals / autophagy / Autophagy-Related Protein-1 Homolog / Isothiocyanates / Lipolysis / Mice / signal transduction / Sulfoxides / TOR Serine-Threonine Kinases (Tokushima University Institutional Repository) ● Metadata: 117431 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jnutbio.2022.109017 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35461903 ● Search Scopus @ Elsevier (PMID): 35461903 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jnutbio.2022.109017 (Tokushima University Institutional Repository: 117431, DOI: 10.1016/j.jnutbio.2022.109017, PubMed: 35461903)
11.	Yuichiro Adachi, Masashi Masuda, Iori Sakakibara, Takayuki Uchida, Yuki Niida, Yuki Mori, Yuki Kamei, Yosuke Okumura, Hirokazu Ohminami, Kohta Ohnishi, Hisami Okumura, Takeshi Nikawa and Yutaka Taketani : All-trans retinoic acid changes muscle fiber type via increasing GADD34 dependent on MAPK signal., Life Science Alliance, Vol.5, No.7, 2022. (Summary) All-trans retinoic acid (ATRA) increases the sensitivity to unfolded protein response in differentiating leukemic blasts. The downstream transcriptional factor of PERK, a major arm of unfolded protein response, regulates muscle differentiation. However, the role of growth arrest and DNA damage-inducible protein 34 (GADD34), one of the downstream factors of PERK, and the effects of ATRA on GADD34 expression in muscle remain unclear. In this study, we identified ATRA increased the GADD34 expression independent of the PERK signal in the gastrocnemius muscle of mice. ATRA up-regulated GADD34 expression through the transcriptional activation of gene via inhibiting the interaction of homeobox Six1 and transcription co-repressor TLE3 with the MEF3-binding site on the gene promoter in skeletal muscle. ATRA also inhibited the interaction of TTP, which induces mRNA degradation, with AU-rich element on mRNA via p-38 MAPK, resulting in the instability of mRNA. Overexpressed GADD34 in C2C12 cells changes the type of myosin heavy chain in myotubes. These results suggest ATRA increases GADD34 expression via transcriptional and post-transcriptional regulation, which changes muscle fiber type. (Keyword) Animals / Gene Expression Regulation / MAP Kinase Signaling System / Mice / Muscle Fibers, Skeletal / Protein Phosphatase 1 / RNA, Messenger / Transcription Factors / Tretinoin (Tokushima University Institutional Repository) ● Metadata: 117429 (Link to Publication Site) ● Publication site (DOI): 10.26508/lsa.202101345 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35318262 ● Search Scopus @ Elsevier (PMID): 35318262 ● Search Scopus @ Elsevier (DOI): 10.26508/lsa.202101345 (Tokushima University Institutional Repository: 117429, DOI: 10.26508/lsa.202101345, PubMed: 35318262)
12.	Kohta Ohnishi, Yano Satoshi, Fujimoto Moe, Sakai Maiko, Harumoto Erika, Furuichi Airi, Masashi Masuda, Hirokazu Ohminami, Hisami Okumura, Hara Taichi and Yutaka Taketani : Identification of Dietary Phytochemicals Capable of Enhancing the Autophagy Flux in HeLa and Caco-2 Human Cell Lines, Antioxidants, Vol.9, No.12, E1193, 2020. (Keyword) autophagy / Dietary phytochemicals / structureactivity relationship (Tokushima University Institutional Repository) ● Metadata: 115876 (Link to Publication Site) ● Publication site (DOI): 10.3390/antiox9121193 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85096821054 (Tokushima University Institutional Repository: 115876, DOI: 10.3390/antiox9121193, Elsevier: Scopus)
13.	Yoko Narasaki, Michiyo Yamasaki, Sayaka Matsuura, Mayumi Morinishi, Tomomi Nakagawa, Mami Matsuno, Misaki Katsumoto, Sachi Nii, Yuka Fushitani, Kohei Sugihara, Tsuneyuki Noda, Takeshi Yoneda, Masashi Masuda, Hisami Okumura, Eiji Takeda, Hiroshi Sakaue, Hironori Yamamoto and Yutaka Taketani : Phosphatemic Index Is a Novel Evaluation Tool for Dietary Phosphorus Load: A Whole-Foods Approach., Journal of Renal Nutrition, Vol.30, No.6, 493-502, 2020. (Tokushima University Institutional Repository) ● Metadata: 114726 (Link to Publication Site) ● Publication site (DOI): 10.1053/j.jrn.2020.02.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32778471 ● Search Scopus @ Elsevier (PMID): 32778471 ● Search Scopus @ Elsevier (DOI): 10.1053/j.jrn.2020.02.005 (Tokushima University Institutional Repository: 114726, DOI: 10.1053/j.jrn.2020.02.005, PubMed: 32778471)
14.	Masashi Masuda, Hironori Yamamoto, Yuichiro Takei, Otoki Nakahashi, Yuichiroh Adachi, Kohta Ohnishi, Hirokazu Ohminami, Hisami Yamanaka-Okumura, Hiroshi Sakaue, Makoto Miyazaki, Eiji Takeda and Yutaka Taketani : All-trans retinoic acid reduces the transcriptional regulation of intestinal sodium-dependent phosphate co-transporter gene (Npt2b)., The Biochemical Journal, Vol.477, No.4, 817-831, 2020. (Summary) Inorganic phosphate (Pi) homeostasis is regulated by intestinal absorption via type II sodium-dependent co-transporter (Npt2b) and by renal reabsorption via Npt2a and Npt2c. Although we previously reported that vitamin A-deficient (VAD) rats had increased urine Pi excretion through the decreased renal expression of Npt2a and Npt2c, the effect of vitamin A on the intestinal Npt2b expression remains unclear. In this study, we investigated the effects of treatment with all-trans retinoic acid (ATRA), a metabolite of vitamin A, on the Pi absorption and the Npt2b expression in the intestine of VAD rats, as well as and the underlying molecular mechanisms. In VAD rats, the intestinal Pi uptake activity and the expression of Npt2b were increased, but were reduced by the administration of ATRA. The transcriptional activity of reporter plasmid containing the promoter region of the rat Npt2b gene was reduced by ATRA in NIH3T3 cells overexpressing retinoic acid receptor (RAR) and retinoid X receptor (RXR). On the other hand, CCAAT/enhancer-binding proteins (C/EBP) induced transcriptional activity of the Npt2b gene. Knockdown of the C/EBP gene and a mutation analysis of the C/EBP responsible element in the Npt2b gene promoter indicated that C/EBP plays a pivotal role in the regulation of Npt2b gene transcriptional activity by ATRA. EMSA revealed that the RAR/RXR complex inhibits binding of C/EBP to Npt2b gene promoter. Together, these results suggest that ATRA may reduce the intestinal Pi uptake by preventing C/EBP activation of the intestinal Npt2b gene. (Tokushima University Institutional Repository) ● Metadata: 114417 (Link to Publication Site) ● Publication site (DOI): 10.1042/BCJ20190716 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32016357 ● Search Scopus @ Elsevier (PMID): 32016357 ● Search Scopus @ Elsevier (DOI): 10.1042/BCJ20190716 (Tokushima University Institutional Repository: 114417, DOI: 10.1042/BCJ20190716, PubMed: 32016357)
15.	Maiko Sakai, Kohta Ohnishi, Masashi Masuda, Hirokazu Ohminami, Hisami Okumura, Taichi Hara and Yutaka Taketani : Isorhamnetin, a 3'-methoxylated flavonol, enhances the lysosomal proteolysis in J774.1 murine macrophages in a TFEB-independent manner., Bioscience, Biotechnology, and Biochemistry, 2020. (Summary) Lysosome is the principal organelle for the ultimate degradation of cellular macromolecules, which are delivered through endocytosis, phagocytosis, and autophagy. The lysosomal functions have been found to be impaired by fatty foods and aging, and more importantly, the lysosomal dysfunction in macrophages has been reported as a risk of atherosclerosis development. In this study, we searched for dietary polyphenols which possess the activity for enhancing the lysosomal degradation in J774.1, a murine macrophage-like cell line. Screening test utilizing DQ-BSA digestion identified isorhamnetin (3'--methylquercetin) as an active compound. Interestingly, structural comparison to inactive flavonols revealed that the chemical structure of the B-ring moiety in isorhamnetin is the primary determinant of its lysosome-enhancing activity. Unexpectedly isorhamnetin failed to inhibit mTORC1-TFEB signaling, a master regulator of lysosomal biogenesis and function. Our data suggested that the other molecular mechanism might be critical for the regulation of lysosomes in macrophages. ANOVA: analysis of variance; ApoE: apolipoprotein E; ATP6V0D2: ATPase H transporting V0 subunit d2; BAF: bafilomycin A1; BODIPY: boron dipyrromethene; BSA: bovine serum albumin; CTSD: cathepsin D; CTSF: cathepsin F; DMEM: Dulbecco's modified eagle medium; DMSO: dimethyl sulfoxide; EGCG: epigallocatechin-3-gallate; FBS: fetal bovine serum; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HPLC: high-performance liquid chromatography; LAMP1: lysosomal-associated membrane protein 1; LAMP2A: lysosomal-associated membrane protein 2A; LC-MS/MS: liquid chromatography tandem mass spectrometry; MITF: microphthalmia-associated transcription factor; MRM: multiple reaction monitoring; mTORC1: mechanistic target of rapamycin complex 1; PBS: phosphate-buffered saline; PPARγ: peroxisome proliferator-activated receptor γ; RT-qPCR: reverse transcription quantitative polymerase chain reaction; SDS: sodium dodecyl sulfate; SNARE: soluble N-ethylmaleimide-sensitive-factor attachment protein receptor; TBS: Tris-buffered saline; TFA: trifluoroacetic acid; TFE3: transcription factor binding to IGHM enhancer 3; TFEB: transcriptional factor EB; TFEC: transcription factor EC; V-ATPase: vacuolar-type proton ATPase. (Keyword) Isorhamnetin / TFEB / lysosome / macrophage / polyphenol (Tokushima University Institutional Repository) ● Metadata: 116062 (Link to Publication Site) ● Publication site (DOI): 10.1080/09168451.2020.1727309 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32046625 ● Summary page in Scopus @ Elsevier: 2-s2.0-85079428723 (Tokushima University Institutional Repository: 116062, DOI: 10.1080/09168451.2020.1727309, PubMed: 32046625, Elsevier: Scopus)
16.	Yuki Niida, Masashi Masuda, Yuichiro Adachi, Aika Yoshizawa, Hirokazu Ohminami, Yuki Mori, Kohta Ohnishi, Hisami Okumura, Takayuki Uchida, Takeshi Nikawa, Hironori Yamamoto, Makoto Miyazaki and Yutaka Taketani : Reduction of stearoyl-CoA desaturase (SCD) contributes muscle atrophy through the excess endoplasmic reticulum stress in chronic kidney disease, Journal of Clinical Biochemistry and Nutrition, Vol.67, No.2, 179-187, 2020. (Summary) <p>Skeletal muscle atrophy is associated with mortality and poor prognosis in patients with chronic kidney disease (CKD). However, underlying mechanism by which CKD causes muscle atrophy has not been completely understood. The quality of lipids (lipoquality), which is defined as the functional features of diverse lipid species, has recently been recognized as the pathology of various diseases. In this study, we investigated the roles of the stearoyl-CoA desaturase (SCD), which catalyzes the conversion of saturated fatty acids into monounsaturated fatty acids, in skeletal muscle on muscle atrophy in CKD model animals. In comparison to control rats, CKD rats decreased the SCD activity and its gene expression in atrophic gastrocnemius muscle. Next, oleic acid blocked the reduction of the thickness of C2C12 myotubes and the increase of the endoplasmic reticulum stress induced by SCD inhibitor. Furthermore, endoplasmic reticulum stress inhibitor ameliorated CKD-induced muscle atrophy (the weakness of grip strength and the decrease of muscle fiber size of gastrocnemius muscle) in mice and the reduction of the thickness of C2C12 myotubes by SCD inhibitor. These results suggest that the repression of SCD activity causes muscle atrophy through excessive endoplasmic reticulum stress in CKD.</p> (Keyword) skeletal muscle atrophy / endoplasmic reticulum stress / chronic kidney disease / stearoyl-CoA desaturase / saturated fatty acid (Tokushima University Institutional Repository) ● Metadata: 114720 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.20-24 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33041516 ● CiNii @ National Institute of Informatics (CRID): 1390566775163696384 ● Search Scopus @ Elsevier (PMID): 33041516 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.20-24 (Tokushima University Institutional Repository: 114720, DOI: 10.3164/jcbn.20-24, PubMed: 33041516, CiNii: 1390566775163696384)
17.	Keisuke Kawamoto, Masae Sakuma, Sarasa Tanaka, Masashi Masuda, Mari Nakao-Muraoka, Yuki Niida, Yurino Nakamatsu, Mikiko Ito, Yutaka Taketani and Hidekazu Arai : High-fat diets provoke phosphorus absorption from the small intestine in rats., Nutrition, Vol.72, 2019. (Tokushima University Institutional Repository) ● Metadata: 114416 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.nut.2019.110694 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32007805 ● Search Scopus @ Elsevier (PMID): 32007805 ● Search Scopus @ Elsevier (DOI): 10.1016/j.nut.2019.110694 (Tokushima University Institutional Repository: 114416, DOI: 10.1016/j.nut.2019.110694, PubMed: 32007805)
18.	Mari Tajiri, Otoki Nakahashi, Tomohiro Kagawa, Masashi Masuda, Hirokazu Ohminami, Masayuki Iwano, Eiji Takeda, Yutaka Taketani and Hironori Yamamoto : Association of increased renal Cyp24a1 gene expression with low plasma 1,25-dihydroxyvitamin D levels in rats with streptozotocin-induced diabetes., Journal of Clinical Biochemistry and Nutrition, Vol.66, No.1, 49-56, 2019. (Summary) Decreases in plasma vitamin D concentrations have been reported in diabetes, although the mechanism involved in this decrease is unclear. Here, we investigated the association between Cyp24a1, a vitamin D catabolic enzyme, and abnormalities in vitamin D metabolism in streptozotocin-induced diabetes rats, an animal model of type 1 diabetes. Plasma 1,25-dihydroxyvitamin D [1,25(OH)2D] levels were significantly lower in streptozotocin-induced diabetes rats and renal Cyp24a1 mRNA expression levels were increased. Western blotting analysis of streptozotocin-induced diabetes rats kidney tissues with anti-CYP24A1 antibody showed a strong signal around 40 kDa, which differs from the predicted 50-55 kDa molecular weight for full-length Cyp24a1 and could represent the Cyp24a1-splicing variant that lacks exons 1 and 2. We observed high levels of renal Cyp24a1-splicing variant mRNA expression in streptozotocin-induced diabetes rats. We also confirmed transcriptional up-regulation of endogenous Cyp24a1 mRNA expression through glucocorticoid receptors by glucocorticoid in opossum kidney proximal cells. Taken together, our results indicated that high Cyp24a1 expression levels may play a role in the decrease of plasma 1,25(OH)2D levels in streptozotocin-induced diabetes rats. High plasma corticosterone levels in diabetes may affect transcriptional regulation to promote increases in Cyp24a1 expression. (Tokushima University Institutional Repository) ● Metadata: 114242 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.19-79 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32001956 ● Search Scopus @ Elsevier (PMID): 32001956 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.19-79 (Tokushima University Institutional Repository: 114242, DOI: 10.3164/jcbn.19-79, PubMed: 32001956)
19.	Shiori Fukuda-Tatano, Hironori Yamamoto, Otoki Nakahashi, Ryouhei Yoshikawa, Mayu Hayashi, Maki Kishimoto, Yukiko Imi, Hisami Okumura, Kohta Ohnishi, Masashi Masuda and Yutaka Taketani : Regulation of α-Klotho Expression by Dietary Phosphate During Growth Periods., Calcified Tissue International, Vol.104, No.6, 667-678, 2019. (Summary) Inorganic phosphate (Pi) is an essential nutrient for maintaining various biological functions, particularly during growth periods. Excess intake of dietary Pi increases the secretion of fibroblast growth factor 23 (FGF23) and parathyroid hormone to maintain plasma Pi levels. FGF23 is a potent phosphaturic factor that binds to the α-klotho/FGFR complex in the kidney to promote excretion of Pi into the urine. In addition, excess intake of dietary Pi decreases renal α-klotho expression. Down-regulation or lack of α-klotho induces a premature aging-like phenotype, resulting from hyperphosphatemia, and leading to conditions such as ectopic calcification and osteoporosis. However, it remains unclear what effects dietary Pi has on α-klotho expression at different life stages, especially during growth periods. To investigate this, we used C57BL/6J mice in two life stages during growing period. Weaned (3 weeks old) and periadolescent (7 weeks old) were randomly divided into seven experimental groups and fed with 0.02, 0.3, 0.6, 0.9, 1.2, 1.5, or 1.8% Pi diets for 7 days. As a result, elevated plasma Pi and FGF23 levels and decreased renal α-klotho expression were observed in weaned mice fed with a high Pi diet. In addition, a high Pi diet clearly induced renal calcification in the weaned mice. However, in the periadolescent group, renal calcification was not observed, even in the 1.8% Pi diet group. The present study indicates that a high Pi diet in weaned mice has much greater adverse effects on renal α-klotho expression and pathogenesis of renal calcification compared with periadolescent mice. (Tokushima University Institutional Repository) ● Metadata: 113367 (Link to Publication Site) ● Publication site (DOI): 10.1007/s00223-019-00525-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30671592 ● Search Scopus @ Elsevier (PMID): 30671592 ● Search Scopus @ Elsevier (DOI): 10.1007/s00223-019-00525-0 (Tokushima University Institutional Repository: 113367, DOI: 10.1007/s00223-019-00525-0, PubMed: 30671592)
20.	Yukiko Imi, Norie Yabiki, Maerjianghan Abuduli, Masashi Masuda, Hisami Okumura and Yutaka Taketani : High phosphate diet suppresses lipogenesis in white adipose tissue., Journal of Clinical Biochemistry and Nutrition, Vol.63, No.3, 181-191, 2018. (Summary) Excessive phosphate intake has been positively associated with renal and vascular dysfunction, conversely negatively associated with body fat accumulation. We investigated the effect of a high-phosphate diet on the expression of lipid metabolic genes in white adipose tissue and liver. Male 8-week-old Sprague-Dawley rats were fed a control diet containing 0.6% phosphate or a high-phosphate diet containing 1.5% phosphate for 4 weeks. In comparison to the control group, the HP group showed a significantly lower body fat mass and fasting plasma insulin level alongside decreased lipogenic and increased lipolytic gene expression in visceral fat. Additionally, the expression of genes involved in hepatic lipogenesis, hepatic glycogenesis, and triglyceride accumulation decreased in the high-phosphate group. Exogenous phosphate, parathyroid hormone, and fibroblast growth factor 23 did not directly affect the expression of lipolytic or lipogenic genes in 3T3-L1 adipocytes and HepG2 hepatocytes. Thus, the high-phosphate diet suppressed the activity of white adipose tissue by increasing lipolytic gene expression and decreasing lipogenic gene expression. These effects could have been caused by the lowered fasting plasma insulin level that occurred in response to the high-phosphate diet, but were not directly caused by the increases in plasma phosphate or phosphaturic hormones. (Tokushima University Institutional Repository) ● Metadata: 111624 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.17-141 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30487667 ● Search Scopus @ Elsevier (PMID): 30487667 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.17-141 (Tokushima University Institutional Repository: 111624, DOI: 10.3164/jcbn.17-141, PubMed: 30487667)
21.	Tomohiro Kagawa, Mina Kozai, Masashi Masuda, Nagakatsu Harada, Otoki Nakahashi, Mari Tajiri, Ryouhei Yoshikawa, Mari Nakao, Yuichiro Takei, Masayuki Iwano, Eiji Takeda, Yutaka Taketani and Hironori Yamamoto : 24-hydroxylase gene expression in renal proximal tubular cells., Biochemical and Biophysical Research Communications, Vol.500, No.2, 275-282, 2018. (Summary) ) showed dose-dependent reductions in renal Srebp1c and Cyp24a1 mRNA levels. Taken together, our results suggest that SREBP1 trans-activates CYP24A1 expression through SREBP binding elements present in the promoter. (Tokushima University Institutional Repository) ● Metadata: 112883 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2018.04.058 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29653103 ● Search Scopus @ Elsevier (PMID): 29653103 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2018.04.058 (Tokushima University Institutional Repository: 112883, DOI: 10.1016/j.bbrc.2018.04.058, PubMed: 29653103)
22.	Chise Yamaguchi, Hisami Okumura, Haruka Esumi, Masashi Masuda, Takafumi Katayama and Yutaka Taketani : Investigation of dose-dependent effects of fat on blood glucose, serum insulin, and appetite sensation., The Journal of Medical Investigation : JMI, Vol.65, No.3.4, 203-207, 2018. (Summary) , respectively. We conducted a randomized, crossover trial and measured laboratory data and appetite sensation via the visual analog scale. Each participant was provided with four different test meals. They consisted of common, basic foods and contained 75 g liquid glucose and 4 slices of crackers to which 0 g butter (control), 10 g butter (B10), 20 g butter (B20), and 40 g butter (B40) were added, respectively. The results indicated that single ingestion of butter did not influence laboratory values of glucose, insulin, glucose-dependent insulinotropic polypeptide (GIP), total bile acids, or high-sensitivity CRP (hs-CRP). Regarding postprandial appetite sensation, appetite ratings for fullness were the highest after the B40 meal (p < 0.05);however, satisfaction ratings were not significantly different after the ingestion of this meal. Ratings were significantly different after the B20 meal. In conclusion, healthy adult subjects experienced fullness and satisfaction after ingesting 20-40 g of butter. J. Med. Invest. 65:203-207, August, 2018. (Keyword) Adult / Appetite / Blood Glucose / Cross-Over Studies / Dietary Fats / Dose-Response Relationship, Drug / Female / Humans / Insulin / Male / Postprandial Period (Tokushima University Institutional Repository) ● Metadata: 112238 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.65.203 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30282861 ● Search Scopus @ Elsevier (PMID): 30282861 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.65.203 (Tokushima University Institutional Repository: 112238, DOI: 10.2152/jmi.65.203, PubMed: 30282861)
23.	Ryouhei Yoshikawa, Hironori Yamamoto, Otoki Nakahashi, Tomohiro Kagawa, Mari Tajiri, Mari Nakao, Shiori Fukuda, Hidekazu Arai, Masashi Masuda, Masayuki Iwano, Eiji Takeda and Yutaka Taketani : The age-related changes of dietary phosphate responsiveness in plasma 1,25-dihydroxyvitamin D levels and renal Cyp27b1 and Cyp24a1 gene expression is associated with renal -Klotho gene expression in mice., Journal of Clinical Biochemistry and Nutrition, Vol.62, No.1, 68-74, 2017. (Summary) mRNA expression showed a significant negative correlation with plasma 1,25-dihydroxyvitamin D levels in the high phosphate group. Our results suggest that age-related alterations in renal -Klotho expression could affect the responsiveness of dietary phosphate to vitamin D metabolism. (Tokushima University Institutional Repository) ● Metadata: 111009 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.17-20 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29371756 ● Search Scopus @ Elsevier (PMID): 29371756 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.17-20 (Tokushima University Institutional Repository: 111009, DOI: 10.3164/jcbn.17-20, PubMed: 29371756)
24.	Kohei Sugihara, Masashi Masuda, Mari Nakao, Maerjianghan Abuduli, Yukiko Imi, Naoko Oda, Toshiya Okahisa, Hironori Yamamoto, Eiji Takeda and Yutaka Taketani : Dietary phosphate exacerbates intestinal inflammation in experimental colitis., Journal of Clinical Biochemistry and Nutrition, Vol.61, No.2, 91-99, 2017. (Summary) study, the effects of phosphate on proinflammatory cytokine induction and reactive oxygen species production in RAW264.7 macrophage were examined. Dietary phosphate exacerbated intestinal inflammation in experimental colitis in a dose-dependent manner, as assessed by the clinical disease activity score, colon length, and histology. Furthermore, the high phosphate diet increased myeloperoxidase activity and proinflammatory cytokine mRNA expression through the activation of nuclear factor B in the inflamed colon. In addition, high phosphate loading in RAW264.7 cells directly enhanced reactive oxygen species production and proinflammatory cytokine gene expression. Our results demonstrated that the high phosphate diet exacerbated intestinal inflammation in experimental colitis. These findings have important therapeutic implications for inflammatory bowel disease patients. (Tokushima University Institutional Repository) ● Metadata: 110124 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.16-117 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28955125 ● Search Scopus @ Elsevier (PMID): 28955125 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.16-117 (Tokushima University Institutional Repository: 110124, DOI: 10.3164/jcbn.16-117, PubMed: 28955125)
25.	Masashi Masuda, Shinobu Miyazaki-Anzai, Audrey L. Keenan, Yuji Shiozaki, Kayo Okamura, Wallace S. Chick, Kristina Williams, Xiaoyun Zhao, Shaikh Mizanoor Rahman, Yin Tintut, Christopher M. Adams and Makoto Miyazaki : Activating transcription factor-4 promotes mineralization in vascular smooth muscle cells., JCI Insight, Vol.1, No.18, e88646, 2016. (Summary) Emerging evidence indicates that upregulation of the ER stress-induced pro-osteogenic transcription factor ATF4 plays an important role in vascular calcification, a common complication in patients with aging, diabetes, and chronic kidney disease (CKD). In this study, we demonstrated the pathophysiological role of ATF4 in vascular calcification using global Atf4 KO, smooth muscle cell-specific (SMC-specific) Atf4 KO, and transgenic (TG) mouse models. Reduced expression of ATF4 in global ATF4-haplodeficient and SMC-specific Atf4 KO mice reduced medial and atherosclerotic calcification under normal kidney and CKD conditions. In contrast, increased expression of ATF4 in SMC-specific Atf4 TG mice caused severe medial and atherosclerotic calcification. We further demonstrated that ATF4 transcriptionally upregulates the expression of type III sodium-dependent phosphate cotransporters (PiT1 and PiT2) by interacting with C/EBP . These results demonstrate that the ER stress effector ATF4 plays a critical role in the pathogenesis of vascular calcification through increased phosphate uptake in vascular SMCs. (Tokushima University Institutional Repository) ● Metadata: 114293 (Link to Publication Site) ● Publication site (DOI): 10.1172/jci.insight.88646 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27812542 ● Search Scopus @ Elsevier (PMID): 27812542 ● Search Scopus @ Elsevier (DOI): 10.1172/jci.insight.88646 (Tokushima University Institutional Repository: 114293, DOI: 10.1172/jci.insight.88646, PubMed: 27812542)
26.	Maerjianghan Abuduli, Hirokazu Ohminami, Tamaki Otani, Hitoshi Kubo, Haruka Ueda, Yoshichika Kawai, Masashi Masuda, Hisami Okumura, Hiroshi Sakaue, Hironori Yamamoto, Eiji Takeda and Yutaka Taketani : Effects of dietary phosphate on glucose and lipid metabolism., American Journal of Physiology, Endocrinology and Metabolism, Vol.310, No.7, E526-E538, 2016. (Summary) Recent epidemiological and animal studies have suggested that excess intake of phosphate (Pi) is a risk factor for the progression of chronic kidney disease and its cardiovascular complications. However, little is known about the impact of dietary high Pi intake on the development of metabolic disorders such as obesity and type II diabetes. In this study, we investigated the effects of dietary Pi on glucose and lipid metabolism in healthy rats. Male, 8-wk-old Sprague-Dawley rats were divided into 3 groups and given experimental diets containing varying amounts of Pi, i.e. 0.2% (low Pi, LP), 0.6% (control Pi, CP), and 1.2% (high Pi, HP). After 4 weeks, HP group showed lower visceral fat accumulation compared with other groups, accompanied by a low respiratory exchange ratio (VCO2/VO2) without alteration of locomotive activity. HP group had lower levels of plasma insulin and non-esterified fatty acids. In addition, HP group also showed suppressed expression of hepatic lipogenic genes including sterol regulatory element binding protein-1c, fatty acid synthase, and acetyl-CoA carboxylase, whereas there was no difference in hepatic fat oxidation among the groups. On the other hand, uncoupling protein 1 (UCP1) and peroxisome proliferator-activated receptor gamma coactivator alpha (PGC1) expression were significantly increased in the brown adipose tissue (BAT) of HP group. Our data demonstrated that a high Pi diet can negatively regulate lipid synthesis in the liver, and increased mRNA expression related to lipid oxidation and UCP1 in BAT, thereby preventing visceral fat accumulation. Thus, dietary Pi is a novel metabolic regulator. (Tokushima University Institutional Repository) ● Metadata: 109976 (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpendo.00234.2015 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26786774 ● Search Scopus @ Elsevier (PMID): 26786774 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.00234.2015 (Tokushima University Institutional Repository: 109976, DOI: 10.1152/ajpendo.00234.2015, PubMed: 26786774)
27.	Masashi Masuda, Shinobu Miyazaki-Anzai, L Audrey Keenan, Kayo Okamura, Jessica Kendrick, Michel Chonchol, Stefan Offermanns, M James Ntambi, Makoto Kuro-O and Makoto Miyazaki : Saturated phosphatidic acids mediate saturated fatty acid-induced vascular calcification and lipotoxicity., The Journal of Clinical Investigation, Vol.125, No.12, 4544-4558, 2015. (Summary) Recent evidence indicates that saturated fatty acid-induced (SFA-induced) lipotoxicity contributes to the pathogenesis of cardiovascular and metabolic diseases; however, the molecular mechanisms that underlie SFA-induced lipotoxicity remain unclear. Here, we have shown that repression of stearoyl-CoA desaturase (SCD) enzymes, which regulate the intracellular balance of SFAs and unsaturated FAs, and the subsequent accumulation of SFAs in vascular smooth muscle cells (VSMCs), are characteristic events in the development of vascular calcification. We evaluated whether SMC-specific inhibition of SCD and the resulting SFA accumulation plays a causative role in the pathogenesis of vascular calcification and generated mice with SMC-specific deletion of both Scd1 and Scd2. Mice lacking both SCD1 and SCD2 in SMCs displayed severe vascular calcification with increased ER stress. Moreover, we employed shRNA library screening and radiolabeling approaches, as well as in vitro and in vivo lipidomic analysis, and determined that fully saturated phosphatidic acids such as 1,2-distearoyl-PA (18:0/18:0-PA) mediate SFA-induced lipotoxicity and vascular calcification. Together, these results identify a key lipogenic pathway in SMCs that mediates vascular calcification. (Keyword) Animals / Endoplasmic Reticulum Stress / knockout mice / knockout mice / Phosphatidylethanolamines / Stearoyl-CoA Desaturase / Vascular Calcification (Link to Publication Site) ● Publication site (DOI): 10.1172/JCI82871 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26517697 ● Search Scopus @ Elsevier (PMID): 26517697 ● Search Scopus @ Elsevier (DOI): 10.1172/JCI82871 (DOI: 10.1172/JCI82871, PubMed: 26517697)
28.	Mari Nakao, Hironori Yamamoto, Otoki Nakahashi, Shoko Ikeda, Kotaro Abe, Masashi Masuda, Mariko Ishiguro, Masayuki Iwano, Eiji Takeda and Yutaka Taketani : Dietary phosphate supplementation delays the onset of iron deficiency anemia and affects iron status in rats., Nutrition Research, Vol.35, No.11, 1016-1024, 2015. (Summary) Inorganic phosphate (Pi) plays critical roles in bone metabolism and is an essential component of 2,3-diphosphoglycerate (2,3-DPG). It has been reported that animals fed a low-iron diet modulate Pi metabolism, whereas the effect of dietary Pi on iron metabolism, particularly in iron deficiency anemia (IDA), is not fully understood. In this study, we hypothesized the presence of a link between Pi and iron metabolism and tested the hypothesis by investigating the effects of dietary Pi on iron status and IDA. Wistar rats aged 4 weeks were randomly assigned to 1 of 4 experimental dietary groups: normal iron content (Con Fe)+0.5% Pi, low-iron (Low Fe)+0.5% Pi, Con Fe+1.5% Pi, and Low Fe+1.5% Pi. Rats fed the 1.5% Pi diet for 14 days, but not for 28 days, maintained their anemia state and plasma erythropoietin concentrations within the reference range, even under conditions of low iron. In addition, plasma concentrations of 2,3-DPG were significantly increased by the 1.5% Pi diets and were positively correlated with plasma Pi concentration (r=0.779; P<.001). Dietary Pi regulated the messenger RNA expression of iron-regulated genes, including divalent metal transporter 1, duodenal cytochrome B, and hepcidin. Furthermore, iron concentration in liver tissues was increased by the 1.5% Pi in Con Fe diet. These results suggest that dietary Pi supplementation delays the onset of IDA and increases plasma 2,3-DPG concentration, followed by modulation of the expression of iron-regulated genes. (Tokushima University Institutional Repository) ● Metadata: 109711 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.nutres.2015.09.001 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26475181 ● Search Scopus @ Elsevier (PMID): 26475181 ● Search Scopus @ Elsevier (DOI): 10.1016/j.nutres.2015.09.001 (Tokushima University Institutional Repository: 109711, DOI: 10.1016/j.nutres.2015.09.001, PubMed: 26475181)
29.	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. (Summary) 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. (Link to Publication Site) ● Publication site (DOI): 10.3177/jnsv.61.S173 (Link to Search Site for Scientific Articles) ● 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)
30.	Shinobu Miyazaki-Anzai, Masashi Masuda, Moshe Levi, Audrey L. Keenan and Makoto Miyazaki : Dual activation of the bile acid nuclear receptor FXR and G-protein-coupled receptor TGR5 protects mice against atherosclerosis., PLoS ONE, Vol.9, No.9, e108270, 2014. (Summary) Bile acid signaling is a critical regulator of glucose and energy metabolism, mainly through the nuclear receptor FXR and the G protein-coupled receptor TGR. The purpose of the present study was to investigate whether dual activation of FXR and TGR5 plays a significant role in the prevention of atherosclerosis progression. To evaluate the effects of bile acid signaling in atherogenesis, ApoE-/- mice and LDLR-/- mice were treated with an FXR/TGR5 dual agonist (INT-767). INT-767 treatment drastically reduced serum cholesterol levels. INT-767 treatment significantly reduced atherosclerotic plaque formation in both ApoE-/- and LDLR-/- mice. INT-767 decreased the expression of pro-inflammatory cytokines and chemokines in the aortas of ApoE-/- mice through the inactivation of NF-B. In addition, J774 macrophages treated with INT-767 had significantly lower levels of active NF-B, resulting in cytokine production in response to LPS through a PKA dependent mechanism. This study demonstrates that concurrent activation of FXR and TGR5 attenuates atherosclerosis by reducing both circulating lipids and inflammation. (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0108270 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25237811 ● Search Scopus @ Elsevier (PMID): 25237811 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0108270 (DOI: 10.1371/journal.pone.0108270, PubMed: 25237811)
31.	Shinobu Miyazaki-Anzai, Masashi Masuda, Kimberly M. Demos-Davies, Audrey L. Keenan, Sommer J. Saunders, Rumiko Masuda, Kristen Jablonski, Maria A. Cavasin, Jessica Kendrick, Michel Chonchol, Timothy A. McKinsey, Moshe Levi and Makoto Miyazaki : Endoplasmic reticulum stress effector CCAAT/enhancer-binding protein homologous protein (CHOP) regulates chronic kidney disease-induced vascular calcification., Journal of the American Heart Association, Vol.3, No.3, e000949, 2014. (Summary) Cardiovascular diseases such as atherosclerosis and vascular calcification are a major cause of death in patients with chronic kidney disease (CKD). Recently, the long-awaited results of the Study of Heart and Renal Protection trial were reported. This large randomized clinical trial found that an extensive cholesterol-lowering therapy through the combination of simvastatin and ezetimibe significantly reduced cardiovascular diseases in a wide range of patients with CKD. However, the mechanism by which this cholesterol-lowering therapy reduces CKD-dependent vascular diseases remains elusive. The objective of the present study was to determine the contribution of the oxysterol-induced pro-apoptotic transcription factor CCAAT/enhancer-binding protein homologous protein (CHOP) on the pathogenesis of CKD-dependent cardiovascular diseases through endoplasmic reticulum stress signaling. CKD increased levels of serum oxysterols such as 7-ketocholesterol in human patients and ApoE(-/-) mice. Treatment with simvastatin plus ezetimibe strongly reduced levels of serum oxysterols and attenuated CKD-dependent atherosclerosis, vascular cell death, vascular calcification, and cardiac dysfunction. This therapy also reduced aortic endoplasmic reticulum stress induced by CKD. The short hairpin RNA-mediated knockdown of CHOP and activating transcription factor-4 in vascular smooth muscle cells attenuated oxysterol-induced mineralization, osteogenic differentiation, and endoplasmic reticulum stress. In addition, CHOP deficiency protected ApoE(-/-) mice from CKD-dependent vascular calcification, cardiac dysfunction, and vascular cell death. These data reveal that the cholesterol-lowering therapy of simvastatin plus ezetimibe attenuates CKD-dependent vascular diseases through a reduction of oxysterol-mediated endoplasmic reticulum stress. CHOP plays a crucial role in the pathogenesis of CKD-dependent vascular calcification. (Keyword) Animals / Apolipoproteins E / Atherosclerosis / Azetidines / Calcinosis / Cardiovascular Diseases / Case-Control Studies / Drug Therapy, Combination / Endoplasmic Reticulum / Humans / Ketocholesterols / Lipids / Male / Mice, Inbred C57BL / Mice, Knockout / Middle Aged / Renal Insufficiency, Chronic / Simvastatin / Transcription Factor CHOP / Vascular Diseases (Link to Publication Site) ● Publication site (DOI): 10.1161/JAHA.114.000949 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24963104 ● Search Scopus @ Elsevier (PMID): 24963104 ● Search Scopus @ Elsevier (DOI): 10.1161/JAHA.114.000949 (DOI: 10.1161/JAHA.114.000949, PubMed: 24963104)
32.	Otoki Nakahashi, Hironori Yamamoto, Sarasa Tanaka, Mina Kozai, Yuichiro Takei, Masashi Masuda, Ichiro Kaneko, Yutaka Taketani, Masayuki Iwano, Ken-ichi Miyamoto and Eiji Takeda : Short-term dietary phosphate restriction up-regulates ileal fibroblast growth factor 15 gene expression in mice., Journal of Clinical Biochemistry and Nutrition, Vol.54, No.2, 102-108, 2014. (Summary) Members of the fibroblast growth factor (FGF) 19 subfamily, including FGF23, FGF15/19, and FGF21, have a role as endocrine factors which influence the metabolism of inorganic phosphate (Pi) and vitamin D, bile acid, and energy. It has been reported that dietary Pi regulates circulating FGF23. In this study, the short-term effects of dietary Pi restriction on the expression of FGF19 subfamily members in mice were analyzed. An initial analysis confirmed plasma FGF23 levels positively correlated with the amount of dietary Pi. On the other hand, ileal Fgf15 gene expression, but not hepatic Fgf21 gene expression, was up-regulated by dietary Pi restriction. In addition, we observed the increase of plasma 1,25-dihydroxyvitamin D [1,25(OH)2D] levels by dietary Pi restriction, and the up-regulation of ileal Fgf15 mRNA expression by 1,25(OH)2D3 and vitamin D receptor (VDR). Importantly, dietary Pi restriction-induced Fgf15 gene expression was prevented in VDR-knockout mice. Furthermore, diurnal variations of plasma triglyceride concentrations and hepatic mRNA expression of the bile acid synthesis enzyme Cyp7a1 as one of Fgf15 negative target genes was influenced by dietary Pi restriction. These results suggest that dietary Pi restriction up-regulates ileal Fgf15 gene expression through 1,25(OH)2D3 and VDR, and may affect hepatic bile acid homeostasis. (Tokushima University Institutional Repository) ● Metadata: 106159 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.13-109 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24688219 ● Search Scopus @ Elsevier (PMID): 24688219 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.13-109 (Tokushima University Institutional Repository: 106159, DOI: 10.3164/jcbn.13-109, PubMed: 24688219)
33.	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. (Summary) 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. (Keyword) 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 (Tokushima University Institutional Repository) ● Metadata: 106168 (Link to Publication Site) ● Publication site (DOI): 10.1152/ajprenal.00474.2013 (Link to Search Site for Scientific Articles) ● 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 (Tokushima University Institutional Repository: 106168, DOI: 10.1152/ajprenal.00474.2013, PubMed: 24500689)
34.	Masashi Masuda, Shinobu Miyazaki-Anzai, Moshe Levi, Tabitha C. Ting and Makoto Miyazaki : PERK-eIF2-ATF4-CHOP signaling contributes to TNF-induced vascular calcification., Journal of the American Heart Association, Vol.2, No.5, e000238, 2013. (Summary) Vascular calcification is a common feature in patients with chronic kidney disease (CKD). CKD increases serum levels of tumor necrosis factor- (TNF), a critical mediator of vascular calcification. However, the molecular mechanism by which TNF promotes CKD-dependent vascular calcification remains obscure. The purpose of the present study was to investigate whether TNF-induced vascular calcification in CKD is caused by the endoplasmic reticulum response involving protein kinase RNA-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor 2 (eIF2), activating transcription factor 4 (ATF4), and C/EBP homologous protein (CHOP). We examined the effects of TNF on the endoplasmic reticulum (ER) stress response of vascular smooth muscle cells (VSMCs). TNF treatment drastically induced the PERK-eIF2-ATF4-CHOP axis of the ER stress response in VSMCs. PERK, ATF4, and CHOP shRNA-mediated knockdowns drastically inhibited mineralization and osteogenesis of VSMCs induced by TNF. CKD induced by 5/6 nephrectomies activated the PERK-eIF2-ATF4-CHOP axis of the ER stress response in the aortas of ApoE-/- mice with increased aortic TNF expression and vascular calcification. Treatment of 5/6 nephrectomized ApoE-/- mice with the TNF neutralizing antibody or chemical Chaperones reduced aortic PERK-eIF2-ATF4-CHOP signaling of the ER stress increased by CKD. This resulted in the inhibition of CKD-dependent vascular calcification. These results suggest that TNF induces the PERK-eIF2-ATF4-CHOP axis of the ER stress response, leading to CKD-dependent vascular calcification. (Keyword) Activating Transcription Factor 4 / Animals / Cells, Cultured / Endoplasmic Reticulum / Endoplasmic Reticulum Stress / Male / Mice / Signal Transduction / Transcription Factor CHOP / Tumor Necrosis Factor-alpha / Vascular Calcification / eIF-2 Kinase (Link to Publication Site) ● Publication site (DOI): 10.1161/JAHA.113.000238 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24008080 ● Search Scopus @ Elsevier (PMID): 24008080 ● Search Scopus @ Elsevier (DOI): 10.1161/JAHA.113.000238 (DOI: 10.1161/JAHA.113.000238, PubMed: 24008080)
35.	Sarasa Tanaka, Hironori Yamamoto, Otoki Nakahashi, Mariko Ishiguro, Yuichiro Takei, Masashi Masuda, Mina Kozai, Shoko Ikeda, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda : Hypercholesterolemia and effects of high cholesterol diet in type IIa sodium-dependent phosphate co-transporter (Npt2a) deficient mice., The Journal of Medical Investigation : JMI, Vol.60, No.3-4, 191-196, 2013. (Summary) The type IIa sodium-dependent phosphate co-transporter (Npt2a) is important to maintain renal inorganic phosphate (Pi) homeostasis and the plasma Pi levels. It has reported that disorder of Pi metabolism in kidney can be risk factors for cardiovascular disease as well as hypercholesterolemia. However, the relationship between Pi and cholesterol metabolism has not been clarified. The current study investigated the effects of Npt2a gene ablation that is known as hypophosphatemia model on cholesterol metabolism in mice. Npt2a deficient (Npt2a(-/-)) mice and wild type mice were fed diets with or without 2% cholesterol for 12 days. Plasma lipid and lipoprotein profile analysis revealed that plasma lipid levels (total, LDL and HDL cholesterol) were significantly higher in Npt2a(-/-) mice than wild type (WT) mice. Interestingly, high cholesterol diet markedly increased plasma levels of total, LDL and HDL cholesterol in WT mice, but not Npt2a(-/-) mice. On the other hand, there were no differences in body and liver weight, intake and hepatic lipid accumulation between WT and Npt2a(-/-) mice. These results suggest that ablation of Npt2a gene induces hypercholesterolemia and affects the ability to respond normally to dietary cholesterol. (Keyword) Animals / cholesterol / Cholesterol, Dietary / Female / Hypercholesterolemia / Lipids / Liver / Male / Mice / knockout mice / Phosphates / Sodium-Phosphate Cotransporter Proteins, Type IIa (Tokushima University Institutional Repository) ● Metadata: 106356 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.60.191 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24190035 ● Summary page in Scopus @ Elsevier: 2-s2.0-84887001043 (Tokushima University Institutional Repository: 106356, DOI: 10.2152/jmi.60.191, PubMed: 24190035, Elsevier: Scopus)
36.	Masashi Masuda, Tabitha C. Ting, Moshe Levi, Sommer J. Saunders, Shinobu Miyazaki-Anzai and Makoto Miyazaki : Activating transcription factor 4 regulates stearate-induced vascular calcification., Journal of Lipid Research, Vol.53, No.8, 1543-1552, 2012. (Summary) Previously, we reported that stearate, a saturated fatty acid, promotes osteoblastic differentiation and mineralization of vascular smooth muscle cells (VSMC). In this study, we examined the molecular mechanisms by which stearate promotes vascular calcification. ATF4 is a pivotal transcription factor in osteoblastogenesis and endoplasmic reticulum (ER) stress. Increased stearate by either supplementation of exogenous stearic acid or inhibition of stearoyl-CoA desaturase (SCD) by CAY10566 induced ATF4 mRNA, phosphorylated ATF4 protein, and total ATF4 protein. Induction occurred through activation of the PERK-eIF2 pathway, along with increased osteoblastic differentiation and mineralization of VSMCs. Either stearate or the SCD inhibitor but not oleate or other fatty acid treatments also increased ER stress as determined by the expression of p-eIF2, CHOP, and the spliced form of XBP-1, which were directly correlated with ER stearate levels. ATF4 knockdown by lentiviral ATF4 shRNA blocked osteoblastic differentiation and mineralization induced by stearate and SCD inhibition. Conversely, treatment of VSMCs with an adenovirus containing ATF4 induced vascular calcification. Our results demonstrated that activation of ATF4 mediates vascular calcification induced by stearate. (Keyword) Activating Transcription Factor 4 / Animals / Cell Differentiation / Cell Line / Gene Expression Regulation, Enzymologic / Gene Knockdown Techniques / Mice / Minerals / Muscle, Smooth, Vascular / Osteoblasts / Osteogenesis / Phosphorylation / Protein-Serine-Threonine Kinases / Signal Transduction / Stearic Acids / Transcription Factor CHOP / Vascular Calcification / eIF-2 Kinase (Link to Publication Site) ● Publication site (DOI): 10.1194/jlr.M025981 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22628618 ● Search Scopus @ Elsevier (PMID): 22628618 ● Search Scopus @ Elsevier (DOI): 10.1194/jlr.M025981 (DOI: 10.1194/jlr.M025981, PubMed: 22628618)
37.	Tabitha C. Ting, Shinobu Miyazaki-Anzai, Masashi Masuda, Moshe Levi, Linda L. Demer, Yin Tintut and Makoto Miyazaki : Increased lipogenesis and stearate accelerate vascular calcification in calcifying vascular cells., The Journal of Biological Chemistry, Vol.286, No.27, 23938-23949, 2011. (Summary) Vascular calcification is recognized as an independent predictor of cardiovascular mortality, particularly in subjects with chronic kidney disease. However, the pathways by which dysregulation of lipid and mineral metabolism simultaneously occur in this particular population remain unclear. We have shown that activation of the farnesoid X receptor (FXR) blocks mineralization of bovine calcifying vascular cells (CVCs) and in ApoE knock-out mice with 5/6 nephrectomy. In contrast to FXR, this study showed that liver X receptor (LXR) activation by LXR agonists and adenovirus-mediated LXR overexpression by VP16-LXR and VP16-LXR accelerated mineralization of CVCs. Conversely, LXR inhibition by dominant negative (DN) forms of LXR and LXR reduced calcium content in CVCs. The regulation of mineralization by FXR and LXR agonists was highly correlated with changes in lipid accumulation, fatty acid synthesis, and the expression of sterol regulatory element binding protein-1 (SREBP-1). The rate of lipogenesis in CVCs through the SREBP-1c dependent pathway was reduced by FXR activation, but increased by LXR activation. SREBP-1c overexpression augmented mineralization in CVCs, whereas SREBP-1c DN inhibited alkaline phosphatase activity and mineralization induced by LXR agonists. LXR and SREBP-1c activations increased, whereas FXR activation decreased, saturated and monounsaturated fatty acids derived from lipogenesis. In addition, we found that stearate markedly promoted mineralization of CVCs as compared with other fatty acids. Furthermore, inhibition of either acetyl-CoA carboxylase or acyl-CoA synthetase reduced mineralization of CVCs, whereas inhibition of stearoyl-CoA desaturase induced mineralization. Therefore, a stearate metabolite derived from lipogenesis might be a risk factor for the development of vascular calcification. (Keyword) Acetyl-CoA Carboxylase / Alkaline Phosphatase / Animals / Blood Vessels / Calcinosis / Cattle / Cells, Cultured / Etoposide / Lipogenesis / Mice / Mice, Knockout / Orphan Nuclear Receptors / Protein Structure, Tertiary / Receptors, Cytoplasmic and Nuclear / Stearic Acids / Stearoyl-CoA Desaturase / Sterol Regulatory Element Binding Protein 1 (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M111.237065 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21596756 ● Search Scopus @ Elsevier (PMID): 21596756 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M111.237065 (DOI: 10.1074/jbc.M111.237065, PubMed: 21596756)

Academic Paper (Unrefereed Paper):

1.	Masashi Masuda, Yuji Shiozaki, Yutaka Taketani and 宮崎淳 : 最前線慢性腎臓病の合併症とlipotoxicity, Farumashia, Vol.58, No.4, 329-333, 2022. (Tokushima University Institutional Repository) ● Metadata: 118681 (Link to Publication Site) ● Publication site (DOI): 10.14894/faruawpsj.58.4_329 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.14894/faruawpsj.58.4_329 (Tokushima University Institutional Repository: 118681, DOI: 10.14894/faruawpsj.58.4_329)

Review, Commentary:

1.	Masashi Masuda, 山本菜摘 and Yutaka Taketani : 腎臓病に対するビタミンAの影響, Vitamins, Vol.97, No.7, 340-343, Jul. 2023. (Tokushima University Institutional Repository) ● Metadata: 119612 (Tokushima University Institutional Repository: 119612)
2.	Yutaka Taketani, Yukiko Imi, 多々納浩, 福田詩織 and Masashi Masuda : 児童生徒の食と健康(2)児童生徒の成長と骨の健康維持, 栄養教諭 : 食育読本, No.46, 18-22, 2017. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1523388080466160256 (CiNii: 1523388080466160256)
3.	Yutaka Taketani, Yukiko Imi, 楢﨑遥子, Masashi Masuda and Hisami Okumura : Disorder of phosphorus metabolism and dietary management in chronic kidney disease, Shikoku Acta Medica, Vol.72, No.5, 171-176, Dec. 2016. (Summary) Chronic kidney disease is a common disease impacting more than 13 million individuals in Japan. CKD causes various complications including cardiovascular disease, infectious disease, and metabolic bone disease. Systemic mineral disorder caused by CKD increases cardiovascular disease and mortality risks as well as metabolic bone disease. Now, it is known as CKD-mineral and bone disease(CKD-MBD)characterized by blood biochemical abnormalities, bone abnormalities and extraskeletal calcification. Management of CKD-MBD is important to decrease cardiovascular disease and mortality risks. Hyperphosphatemia is a primary cause of CKD-MBD. Not only correction of hyperphosphatemia but also decrease in dietary phosphorus load is a key strategy for management of CKD-MBD. Here we will provide an overview of disorder of phosphorus metabolism and dietary management in CKD patients. (Tokushima University Institutional Repository) ● Metadata: 110399 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050302172854099840 (Tokushima University Institutional Repository: 110399, CiNii: 1050302172854099840)
4.	Hisami Okumura, 多々納浩, 梶浦大資, 山口智勢, Masashi Masuda and Yutaka Taketani : 生活習慣病の要:栄養教育と実践, Clinical Calcium, Vol.26, No.3, 101-106, 2016.

Proceeding of International Conference:

1.	Mori Yuki, Masashi Masuda, Nguyen The Anh, Kohta Ohnishi, Hirokazu Ohminami and Yutaka Taketani : All-trans retinoic acid induces lipolysis via autophagy in mouse adipocytes, The 3rd Japan-France Space Nutrition & Medicine Symposium, Kyoto, Nov. 2023.
2.	Masashi Masuda, Adachi Yuichiro and Yutaka Taketani : All-trans retinoic acid changes muscle fiber type via increasing GADD34 dependent on MAPK signal, The 3rd Japan-France Space Nutrition & Medicine Symposium, Kyoto, Nov. 2023.
3.	Mori Yuki, Masashi Masuda, Yoshida-Shimizu Risa, Nguyen The Anh, Kohta Ohnishi, Hirokazu Ohminami, Hamada Koichiro and Yutaka Taketani : All-trans retinoic acid induces lipolysis via autophagy in mouse adipocytes, Kern Lipid Conference 2023, Colorado, Aug. 2023.
4.	Okumura Yosuke, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda and Yutaka Taketani : Effect of phosphate on intestinal zinc absorption in 5/6 nephrectomized rats, 第22回国際栄養学会議, Online, Dec. 2022.
5.	Tsumura Ayari, Hisami Okumura, Kawakami Hana, Yamamoto Shiori, Ohura Mayu, Tatano Hiroshi, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : Investigation of Amino Acids and Fatty Acids Profiles of Japanese Diets Using the Food Exchange Chart for Diabetes Diet, 第22回国際栄養学会議(IUNS-ICN 22nd), Online, Dec. 2022.
6.	Mori Yuki, Masashi Masuda, Yoshida-Shimizu Risa, Aoyagi Saki, Adachi Yuichiro, Kohta Ohnishi, Hirokazu Ohminami, Hamada Koichiro and Yutaka Taketani : All-trans retinoic acid induces lipolysis via activation of autophagy in mouse adipocytes, 第22回国際栄養学会議(IUNS-ICN 22nd), Online, Dec. 2022.
7.	Takikawa Masaki, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : Dietary combination of sucrose and linoleic acid synergistically accumulates the intramuscular lipid and decreases the muscle strength in Zucker diabetic fatty rats, 第22回国際栄養学会議(IUNS-ICN 22nd), Online, Dec. 2022.
8.	Yuki Kamei, Okumura Yosuke, Adachi Yuichiro, mori Yuki, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : Inhibitory Mechanism of Ectopic Calcification during Growth Period, The American Society for Bone and Mineral Research 2022 Annual Meeting, Online, Sep. 2022.
9.	Yuichiro Adachi, Masashi Masuda, Kohei Sasaki, Hirokazu Ohminami, Hisami Okumura, Hironori Yamamoto and Yutaka Taketani : Hypervitaminosis A Contributes to Kidney Injury Through Excessive Endoplasmic Reticulum Stress in CKD, ASN Kidney Week 2021, Nov. 2021.
10.	Kohta Ohnishi, Moe FUJIMOTO, Maiko SAKAI, Teppei FUKUDA, Aika OHNISHI, Hirokazu Ohminami, Masashi Masuda, Hisami Okumura, Yoshichika Kawai and Yutaka Taketani : Exploration of bioactive food factors for the control of autophagy flux, The 7th International Conference on Food Factors, Dec. 2019. (Keyword) autophagy / mass spectrometry
11.	Maiko SAKAI, Kohta Ohnishi, Masashi Masuda, Hirokazu Ohminami, Hisami Okumura, Taichi HARA and Yutaka Taketani : Elucidation of the molecular mechanism underlying lysosomal activation in J774.1 cells by isorhamnetin treatment, The 7th International Conference on Food Factors, Dec. 2019.
12.	Oda Naoko, Sugihara Kohei, Miho Ikeda, Yuho Higashimura, Takashi Uebanso, Kohta Ohnishi, Hirokazu Ohminami, Masashi Masuda, Hisami Okumura and Yutaka Taketani : Dietary phosphate disturbs of gut microbiome in mice., American Society of Nephrolody Kidney Week 2019, Washington, D.C., Nov. 2019.
13.	Fukuda-Tatano Shiori, Hironori Yamamoto, Nakahashi Otoki, Yoshikawa Ryouhei, Hayashi Mayu, Kishimoto Maki, Yukiko Imi, Yamanaka-Okumura Hisami, Kohta Ohnishi, Masashi Masuda and Yutaka Taketani : Regulation of α-klotho Expression by Dietary Phosphate During Growth Periods, ASBMR 2019 Annual Meeting, Sep. 2019.
14.	Masashi Masuda, Hironori Yamamoto, Yuichiro Adachi, Kohta Ohnishi, Hirokazu Ohminami, Hisami Okumura, Makoto Miyazaki, Eiji Takeda and Yutaka Taketani : All-trans-retinoic-acid reduces intestinal phosphate uptake by the transcriptional regulation of sodium-dependent phosphate co-transporter gene (Npt2b)., ASBMR 2019 Annual Meeting, Sep. 2019.
15.	Maiko SAKAI, Kohta Ohnishi, Teppei FUKUDA, Masashi Masuda, Naomi Kanoh, Hisami Okumura, Yoshichika Kawai and Yutaka Taketani : mTORC2 signaling is critical for lysosomal activation by isorhamnetin treatment in J774.1., FAOPS2019, Mar. 2019. (Keyword) lysosome / mTORC2 / isorhamnetin
16.	Serina Kabutoya, Masashi Masuda, Yuichiro Adachi, Yilimulati Timamu, Hisami Okumura, Hironori Yamamoto and Yutaka Taketani : Hypervitaminosis A contributes to abnormal iron metabolism in CKD, American Society of Nephrology Kidney Week 2018 (San Diego, CA), Oct. 2018.
17.	Mayu Hayashi, Shiori Fukuda, Maki Kishimoto, Hironori Yamamoto, Masashi Masuda and Yutaka Taketani : High phosphate diet before pregnancy dysregulates phosphate metabolism in neonatal offspring mice, American Society of Nephrology Kidney Week 2018 (San Diego, CA), Oct. 2018.
18.	Kohno Shohei, Miyazaki-Anzai Shinobu, Masashi Masuda, Shiozaki Yuji, Keenan L. Audrey and Miyazaki Makoto : Simultaneous inhibition of FXR and TGR5 accelerates atherosclerotic formation, Kern Lipid Conference, Vail, Colorado, Aug. 2018.
19.	Yoshida Risa, Masashi Masuda, Mori Yuki, Niida Yuki, Adachi Yuichiro, Kohta Ohnishi, Hisami Okumura, Yoshichika Kawai and Yutaka Taketani : Sulforaphane induces lipolysis via lipophagy in mouse adipocyte, Kern Lipid Conference, Vail, Colorado, Aug. 2018.
20.	Niida Yuki, Masashi Masuda, Yoshizawa Aika, Adachi Yuichiro, Yimamu Yilimulati, Kabutoya Serina, Yoshida Risa, Hisami Okumura, Yoshichika Kawai, Miyazaki Makoto, Hironori Yamamoto and Yutaka Taketani : Abnormal lipid metabolism in skeletal muscle mediates chronic kidney disease-induced sarcopenia, ASN Kidney Week 2017, New Orleans, Nov. 2017.
21.	Hi Tatano, Hisami Okumura, D Kajiura, Masashi Masuda, A Hirayama, T Soga, M Tomita and Yutaka Taketani : Meat and fish consumption lead to differences in plasma N-acetylaspartate and trimethylamine N-oxide concentrations in healthy men, 12th Metabolomics Society Conference, Brisbane, Australia, Jun. 2017.
22.	Yuji Shiozaki, Masashi Masuda, Keenan Audrey, Kayo Okamura, Shinobu Miyazaki-Anzai and Makoto Miyazaki : Activating transcription factor-4 in vascular smooth muscle cells regulates vascular calcification, Kern Lipid Conference, Vail, Colorado, USA, Aug. 2016.
23.	Yukiko Imi, Masashi Masuda, Maerjianghan Abuduli, Norie Yabiki, Hisami Okumura, Makoto Miyazaki and Yutaka Taketani : High phosphorus induces the lipolysis through endoplasmic reticulum stress, Kern Lipid Conference, Vail, Colorado, USA, Aug. 2016.
24.	Hiroshi Tatano, Hisami Okumura, Daisuke Kajiura, C Kondo, A Hirayama, Kazuaki Mawatari, Yoshichika Kawai, Masashi Masuda and Yutaka Taketani : Exploring the impact of consuming different types of meat on metabolome profiles using a GC-MS metabolomics approach, 11th Metabolomics Society Conference, Dublin, Jul. 2016.
25.	福田詩織, Hironori Yamamoto, Masashi Masuda, 中尾真理 and Yutaka Taketani : Regulation of a-klotho expression by dietary phosphate during growth periods., ASN 2015 Renal week, San Diego, Nov. 2015.
26.	Yutaka Taketani, Masashi Masuda, Hisami Okumura, Sawako Tatsumi, Ken-ichi Miyamoto, Eiji Takeda and Hironori Yamamoto : Niacin and Chronic Kidney Disease., ACN2015 Asian Congress of Nutrition., May 2015.
27.	Hisami Okumura, Akiyoshi Hirayama, Syoko Wada, Daisuke Kajiura, Masashi Masuda, Eiji Takeda, Yutaka Taketani, Satoru Imura, Toru Utsunomiya, Mitsuo Shimada, Masaru Tomita and Tomoyoshi Soga : Perioperative serum and urine metabolome analysis in patients with hepatocellular carcinoma, 37th European Congress for Nutrition and Metabolism, Lisbon, Portugal, 2015, September 5-8, Sep. 2014.

Proceeding of Domestic Conference:

1.	Nana Hayashishita, Wakako Takehara, Masaki Takikawa, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : 妊娠中の食餌性リン負荷が仔に及ぼす影響について, 第8回日本CKD-MBD学会学術集会・総会, Mar. 2024.
2.	Hirokazu Ohminami, KITAMURA Ayano, Masashi Masuda, Takayuki Ise, Shusuke Yagi, Masataka Sata and Yutaka Taketani : 心不全マウスに対する高脂肪食と運動の併用効果，優秀演題アワードセッショ, 日本心臓リハビリテーション学会第7回四国支部地方会, Mar. 2024.
3.	Nguyen The Anh, Masashi Masuda, Mori Yuki, Adachi Yuichiro, Hirokazu Ohminami and Yutaka Taketani : All-trans retinoic acid induces lipolysis via autophagy in mouse hepatocytes, 第46回日本分子生物学会年会, Dec. 2023.
4.	丸山祐昌, Masashi Masuda, 木村玲奈, 山本菜摘, Hirokazu Ohminami and Yutaka Taketani : 小脳顆粒細胞のATP量に対する細胞外リン濃度の影響, 第56回日本栄養・食糧学会中国・四国支部大会, Oct. 2023.
5.	Yutaka Taketani, Yuichiro Adachi, Natsumi Yamamoto, Hirokazu Ohminami and Masashi Masuda : 慢性腎臓病とビタミンA, フォーラム2023:衛生薬学・環境トキシコロジー, Sep. 2023.
6.	Hironori Yamamoto, 中橋乙起, 石黒真理子, Masashi Masuda, Eiji Takeda, 岩野正之, 岸愼治 and Yutaka Taketani : 炎症時におけるリン・ビタミンDの役割と腎臓での代謝調節機構の解明, 第70回日本栄養改善学会学術総会, Sep. 2023.
7.	Hirokazu Ohminami, Ayano KITAMURA, MINA Matsubara, Masashi Masuda, Takayuki Ise, Shusuke Yagi, Masataka Sata and Yutaka Taketani : 動物モデルから探る心リハ栄養としての糖・脂質組成の意義, 第29回日本心臓リハビリテーション学会学術集会, Jul. 2023.
8.	森優樹, Masashi Masuda, Anh The Nguyen, Kohta Ohnishi, Hirokazu Ohminami, 濱田広一郎 and Yutaka Taketani : レチノイン酸によるリポファジーへの影響, 日本ビタミン学会第75回大会, Jun. 2023.
9.	山本菜摘, Masashi Masuda, 足立雄一郎, 春本恵里花, 野邊悠太郎, Hirokazu Ohminami, Hironori Yamamoto and Yutaka Taketani : 慢性腎臓病モデルマウスの腎臓内ビタミンA代謝調節機構, 日本ビタミン学会第75回大会, Jun. 2023.
10.	Hirokazu Ohminami, 北村彩乃, 松原未奈, Masashi Masuda, Takayuki Ise, Shusuke Yagi, Masataka Sata and Yutaka Taketani : 動物モデルから探る病期別心リハ栄養の可能性, 第12回日本リハビリテーション栄養学会学術集会, Jan. 2023.
11.	北村彩乃, Hirokazu Ohminami, 松原未奈, Masashi Masuda, Takayuki Ise, Shusuke Yagi, Masataka Sata and Yutaka Taketani : 高脂肪食が心不全マウスの骨格筋エネルギー代謝に及ぼす影響, 第26回日本病態栄養学会年次学術集会, Jan. 2023.
12.	山本菜摘, Masashi Masuda, 春本恵里花, 野邊悠太郎, Hirokazu Ohminami and Yutaka Taketani : 慢性腎臓病モデルマウスの腎臓内ビタミンA代謝変化, 第26回日本病態栄養学会年次学術集会, Jan. 2023.
13.	野邊悠太郎, Masashi Masuda, 佐々木晧平, 足立雄一郎, Hirokazu Ohminami and Yutaka Taketani : 慢性腎臓病の腎臓における all-trans retinoic acid 水酸化酵素 Cyp26b1 制御機構の解明, 第55回日本栄養・食糧学会中国・四国支部大会, Oct. 2022.
14.	Yuki Kamei, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : 成長期には血中リン濃度が高くても血管石灰化が生じないのはなぜか?, 第69回日本栄養改善学会学術総会, Sep. 2022.
15.	滝川真輝, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : スクロースとリノール酸は相乗的に筋内脂肪蓄積と筋力低下を引き起こす, 第69回日本栄養改善学会学術総会, Sep. 2022.
16.	奥村陽介, 酒井晶子, 阿部船太郎, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : 慢性腎臓病に伴う低亜鉛血症の発症機序解明, 第10回日本腎栄養代謝研究会学術集会・総会, Jul. 2022.
17.	春本恵里花, Masashi Masuda, 佐々木晧平, 足立雄一郎, 森優樹, Hirokazu Ohminami, Hironori Yamamoto and Yutaka Taketani : 高齢マウスの腎臓におけるビタミンA代謝関連遺伝子発現変化, 日本ビタミン学会第74回大会, Jun. 2022.
18.	Masashi Masuda, 足立雄一郎 and Yutaka Taketani : 骨格筋の筋繊維タイプ変化に対するビタミンAの影響, 第372回脂溶性ビタミン総合研究委員会プログラム, Jun. 2022.
19.	北村彩乃, Hirokazu Ohminami, Masashi Masuda, Hisami Okumura, Takayuki Ise, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Masataka Sata and Yutaka Taketani : 運動介入中の脂質摂取の違いが心不全マウスの病態に及ぼす影響, 第28回日本心臓リハビリテーション学会学術集会, Jun. 2022.
20.	滝川真輝, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : スクロースとリノール酸の豊富な食餌は筋繊維内脂肪を増加させる, 第63回日本生化学会中国・四国支部例会, May 2022.
21.	森優樹, Masashi Masuda, 吉田里沙, 青柳咲紀, Kohta Ohnishi, Hirokazu Ohminami, 濱田広一郎 and Yutaka Taketani : レチノイン酸によるオートファジーを介した脂肪分解への影響, 第63回日本生化学会中国・四国支部例会, May 2022.
22.	佐々木晧平, Masashi Masuda, Yuichiroh Adachi, Erika Harumoto, Hirokazu Ohminami, Hisami Okumura, Hironori Yamamoto and Yutaka Taketani : 慢性腎臓病における腎臓の小胞体ストレスを介した all-trans retinoic acid 水酸化酵素Cyp26b1制御機構の解明, 第 6 回日本CKD-MBD研究会学術集会・総会, Mar. 2022.
23.	Ayano Kitamura, Hirokazu Ohminami, Masashi Masuda, Hisami Okumura, Takayuki Ise, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Masataka Sata and Yutaka Taketani : 運動および栄養介入が心不全マウスの病態に及ぼす影響, 日本心臓リハビリテーション学会第 5 回四国支部地方会, Jan. 2022.
24.	Rena Kimura, Masashi Masuda, Natsumi Yamamoto, Yutaro Nobe, Hirokazu Ohminami, Hisami Okumura and Yutaka Taketani : 食餌性リン負荷が高齢期の脳に及ぼす影響の検討, 第 24 回・第 25 回日本病態栄養学会年次学術集会, Jan. 2022.
25.	Masashi Masuda : 慢性腎臓病におけるエピジェネティクス制御によるビタミンA代謝変動, 日本ビタミン学会第73回大会 Part2, Nov. 2021.
26.	Shiori Yamamoto, Hisami Okumura, Mayu Ohhra, Ayari Tsumura, Hana Kawakami, 多々納浩, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : 日本食品成分表を用いた魚介類・肉類・豆類・卵類のアミノ酸と脂肪酸についての特徴の比較, 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, Oct. 2021.
27.	Yutaro Nobe, Masashi Masuda, Yuichiroh Adachi, Natsumi Yamamoto, Hirokazu Ohminami, Hisami Okumura and Yutaka Taketani : 小胞体ストレスによる腸管リン酸輸送担体 Npt2b 発現調節機構の解明, 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, Oct. 2021.
28.	Ayari Tsumura, Hisami Okumura, Hana Kawakami, Mayu Ohhra, Shiori Yamamoto, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : 糖尿病食事療法のための食品交換表(第 2 版)を活用したアミノ酸・脂肪酸の調査, 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, Oct. 2021.
29.	Masaki Takikawa, Hirokazu Ohminami, Ayano Kitamura, Minami Kunihiro, Mutsumi Kondoh, Mina Matsubara, Masashi Masuda, Hisami Okumura and Yutaka Taketani : スクロースとリノール酸の組み合せは筋肉脂肪を増加させる, 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, Oct. 2021.
30.	Yuichiroh Adachi, Masashi Masuda, Iori Sakakibara, Takayuki Uchida, Hirokazu Ohminami, Hisami Okumura, Takeshi Nikawa and Yutaka Taketani : all trans レチノイン酸は小胞体ストレス応答関連因子 GADD34 の転写・転写後制御を介して筋繊維タイプ変化を引き起こす, 第 62 回日本生化学会中国・四国支部例会, Sep. 2021.
31.	Mayu Ohhra, Hisami Okumura, 平山明由, Hana Kawakami, 多々納浩, Yuji Morine, Hirokazu Ohminami, Masashi Masuda, Mitsuo Shimada, 曽我朋義, 冨田勝 and Yutaka Taketani : メタボローム解析を用いた肝切除術による肝臓のアミノ酸代謝物の変化, 第 13 回日本臨床栄養代謝学会中国四国支部学術集会, Aug. 2021.
32.	Ayari Tsumura, Hisami Okumura, Hana Kawakami, Shiori Yamamoto, Mayu Ohhra, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : 糖尿病食事療法のための食品交換表活用編(第 2 版)におけるアミノ酸，脂肪酸の調査, 第 13 回日本臨床栄養代謝学会中国四国支部学術集会, Aug. 2021.
33.	Hisami Okumura, Hina Fukagi, Hana Kawakami, Ayari Tsumura, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : シームレスな食事指導のための献立のカロリー密度調査, 第 13 回日本臨床栄養代謝学会中国四国支部学術集会, Aug. 2021.
34.	Yuki Kamei, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda, Hisami Okumura and Yutaka Taketani : 成長期における血管石灰化抑制機構の解明, 第 75 回日本栄養・食糧学会大会, Jul. 2021.
35.	Yuichiroh Adachi, Masashi Masuda, Iori Sakakibara, Takayuki Uchida, Kohei Sasaki, Yutaro Nobe, Hirokazu Ohminami, Kohta Ohnishi, Hisami Okumura, Hironori Yamamoto, Takeshi Nikawa and Yutaka Taketani : all trans レチノイン酸は小胞体ストレス応答関連因子 GADD34 の発現制御を介して筋繊維タイプ変化を誘導する, 第 75 回日本栄養・食糧学会大会, Jul. 2021.
36.	Shiori Yamamoto, Hisami Okumura, Mayu Ohhra, Ayari Tsumura, Hana Kawakami, 多々納浩, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : 日本食品成分表2020年版(八訂)を用いた魚介類・肉類・豆類・卵類のアミノ酸と脂肪酸の比較, 第75回日本栄養・食糧学会大会, Jul. 2021.
37.	Mayu Ohhra, Hisami Okumura, 平山明由, Hana Kawakami, 多々納浩, Yuji Morine, Hirokazu Ohminami, Masashi Masuda, Mitsuo Shimada, 曽我朋義, 冨田勝 and Yutaka Taketani : メタボローム解析を用いた肝切除術による肝臓の代謝物変化の検討, 第75回日本栄養・食糧学会大会, Jul. 2021.
38.	Hisami Okumura, Hina Fukagi, Hana Kawakami, Ayari Tsumura, Haruna Yoshinari, 多々納浩, Hirokazu Ohminami, Masashi Masuda and Yutaka Taketani : 食べかたのコツ(Densiet)を数値化するための主食・主菜・副菜・間食献立に関するカロリー密度解析, 第75回日本栄養・食糧学会大会, Jul. 2021.
39.	Hirokazu Ohminami, Ayano Kitamura, Miku Yamaguchi, Masaki Takikawa, Kohta Ohnishi, Masashi Masuda, Hisami Okumura, Takayuki Ise, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Masataka Sata and Yutaka Taketani : 心不全マウスを用いた心リハ評価系の確立, 第27回日本心臓リハビテーション学会, Jun. 2021.
40.	Kohei Sasaki, Masashi Masuda, Yuichiroh Adachi, Yuki Mori, Yutaro Nobe, Hirokazu Ohminami, Kohta Ohnishi, Hisami Okumura, Hironori Yamamoto and Yutaka Taketani : 慢性腎臓病における all trans retinoic acid 水酸化酵素 Cyp26b1 制御機構の解明, 日本ビタミン学会第 73 回大会 Part1, Jun. 2021.
41.	Masashi Masuda, Hironori Yamamoto, Eiji Takeda and Yutaka Taketani : All-transレチノイン酸による小腸ナトリウム依存性リン酸トランスポーター遺伝子発現抑制機構, 第366回脂溶性ビタミン総合研究委員会プログラム, Dec. 2020.
42.	坂井麻衣子, Kohta Ohnishi, 春本恵里花, Masashi Masuda, Hirokazu Ohminami, Hisami Okumura, 板倉英祐, 原太一 and Yutaka Taketani : イソラムネチンによるエンドソーム成熟過程の亢進を介した異常分子除去作用, 2020年度日本フードファクター学会・日本農芸化学会西日本支部合同大会第332回講演会, Nov. 2020.
43.	佐々木晧平, Masashi Masuda, 足立雄一郎, Kohta Ohnishi, Hirokazu Ohminami, Hisami Okumura and Yutaka Taketani : 慢性腎臓病におけるAll-trans retinoic acid (ATRA) 水酸化酵素Cyp26b1制御機構の解明, 第53回日本栄養・食糧学会中国・四国支部大会, Oct. 2020.
44.	木村玲奈, Masashi Masuda, 野邊悠太郎, Kohta Ohnishi, Hirokazu Ohminami, Hisami Okumura and Yutaka Taketani : 食餌性リン負荷は高齢マウスの脳内ATP量を減少させる, 第53回日本栄養・食糧学会中国・四国支部大会, Oct. 2020.
45.	佐守美穂, 亀井優輝, Kohta Ohnishi, 足立雄一郎, Masashi Masuda, Hirokazu Ohminami, Hisami Okumura, Yutaka Taketani, 羽田尚彦 and 井上淳詞 : NSAIDs起因性小腸傷害に対するほうれん草由来グリセロ糖脂質の影響, 第53回日本栄養・食糧学会中国・四国支部大会, Oct. 2020.
46.	奥村陽介, 酒井晶子, 阿部航太郎, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda, Hisami Okumura and Yutaka Taketani : 慢性腎臓病に伴う亜鉛代謝異常の発症機序解明, 第53回日本栄養・食糧学会中国・四国支部大会, Oct. 2020.
47.	Masashi Masuda, Hironori Yamamoto and Yutaka Taketani : All-trans retinoic acidは腸管II型ナトリウム依存性リン酸輸送担体(Npt2b)遺伝子発現を低下させる, 第22回日本骨粗鬆症学会/ 第38回日本骨代謝学会学術集会, Oct. 2020.
48.	小松原彩乃, 岸本麻希, 多々納(福田) 詩織, 林眞由, 江原みゆ, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda, Hisami Okumura and Yutaka Taketani : 妊娠前の高リン食摂取は，仔マウスの食後血中リン濃度上昇を亢進させる, 第74回日本栄養・食糧学会大会, Sep. 2020.
49.	坂井麻衣子, Kohta Ohnishi, Masashi Masuda, Hirokazu Ohminami, Hisami Okumura, 板倉英祐, 原太一 and Yutaka Taketani : MΦにおける異常タンパク質分解を促進するイソラムネチンの作用機序解析, 日本農芸化学会2020年度中四国支部大会, Sep. 2020.
50.	小松原彩乃, 岸本麻希, 林眞由, 江原みゆ, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda, Hisami Okumura and Yutaka Taketani : 妊娠前の食餌性リン負荷が，仔マウスのリン応答性に及ぼす影響, 第93回日本生化学会大会, Sep. 2020.
51.	石谷さとの, 新居紗知, 楢﨑遥子, Hisami Okumura, Hironori Yamamoto, Masashi Masuda, Kohta Ohnishi, Hirokazu Ohminami and Yutaka Taketani : 幹細胞における組織非特異的アルカリフォスファターゼ遺伝子発現とリン代謝に対するSNPrs1697421, 第93回日本生化学会大会, Sep. 2020.
52.	福田詩織, Hironori Yamamoto, 中橋乙起, Masashi Masuda and Yutaka Taketani : 成長期における過剰な食餌性リン摂取時のカルシウム摂取量の違いがα-klotho発現に及ぼす影響, 第67回日本栄養改善学会学術集会, Sep. 2020.
53.	Hironori Yamamoto, 田尻真梨, 中橋乙起, Masashi Masuda, Hirokazu Ohminami, Kohta Ohnishi, 石黒真理子, 池田涼子, 岩野正之, Eiji Takeda and Yutaka Taketani : 糖尿病時におけるビタミンD・カルシウム代謝異常の分子機構の解明, 第67回日本栄養改善学会学術集会, Sep. 2020.
54.	小松原彩乃, 岸本麻希, 林眞由, 江原みゆ, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda, Hisami Okumura and Yutaka Taketani : 妊娠前の食餌性リン負荷は，成熟仔マウスのリン応答性を攪乱する, 第67回日本栄養改善学会学術集会, Sep. 2020.
55.	小松原彩乃, 岸本麻希, 林眞由, 江原みゆ, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda, Hisami Okumura and Yutaka Taketani : 妊娠前の食餌性リン負荷が，仔マウスのリン応答性に及ぼす影響, 第61回日本生化学会中国四国支部例会, Jul. 2020.
56.	亀井優輝, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda, Hisami Okumura and Yutaka Taketani : 小児期における血中リン濃度とFetuin-Aとの関係, 第61回日本生化学会中国四国支部例会, Jul. 2020.
57.	足立雄一郎, Masashi Masuda, Kohta Ohnishi, Hirokazu Ohminami, Hisami Okumura and Yutaka Taketani : 慢性腎臓病におけるビタミンA代謝異常が転写因子XBP1に及ぼす影響, 第61回日本生化学会中国四国支部例会, Jul. 2020.
58.	Hironori Yamamoto, 石黒真理子, 田中更沙, 竹井悠一郎, Masashi Masuda, Kohta Ohnishi and Yutaka Taketani : 生体ビタミンD作用に及ぼすファイトケミカルの影響, 日本ビタミン学会第72回大会, Jun. 2020.
59.	森優樹, Masashi Masuda, 吉田里沙, 青柳咲紀, Kohta Ohnishi, Hirokazu Ohminami, Hisami Okumura, Hironori Yamamoto, 濱田広一郎 and Yutaka Taketani : レチノイン酸によるオートファジーを介した脂肪分解への影響, 日本ビタミン学会第72回大会, Jun. 2020.
60.	Hironori Yamamoto, Mari Tajiri, Otoki Nakahashi, Masashi Masuda, Hirokazu Ohminami, Kohta Ohnishi, Eiji Takeda and Yutaka Taketani : 糖尿病時におけるビタミンD・カルシウム代謝異常の分子機構の解明, The 74th Annual Meeting of Japan Society of Nutrition and Food Science, Apr. 2020. (Keyword) vitamin D / calcium / diabetes
61.	Sakai Maiko, Kohta Ohnishi, Masashi Masuda, Hirokazu Ohminami, Hisami Okumura, Hara Taichi and Yutaka Taketani : Elucidation of the molecular mechanism of lysosomal activation through mTORC2, a nutrient-sensitive signaling, The 74th Annual Meeting of Japan Society of Nutrition and Food Science, Apr. 2020. (Keyword) lysosome / mTORC2 / macrophage
62.	Fukuda Teppei, Kohta Ohnishi, Masashi Masuda, Matsuzaki Yasunori, Konno Ayumu, Fujimoto Moe, Ohnishi Aika, sakai maiko, Hirokazu Ohminami, Hisami Okumura, Hara Taichi, Hirai Hirokazu and Yutaka Taketani : Establishment of an in vivo assay system for monitoring autophagy utilizing NIR fluorescence imaging, 日本農芸化学会2020年度大会, Mar. 2020. (Keyword) autophagy / Near-infrared fluorescence imaging / Adeno-associated virus vector
63.	Maiko Sakai, Kohta Ohnishi, Masashi Masuda, Hirokazu Ohminami, Hisami Okumura, Hara Taichi and Yutaka Taketani : mTORC2 signaling controls the lysosomal activity in J774.1 macrophage-like cell., 日本農芸化学会2020年度大会, Mar. 2020. (Keyword) lysosome / macrophage / mTORC2
64.	Miho Ikeda, Naoko Oda, Takashi Uebanso, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda, Hisami Okumura and Yutaka Taketani : 高リン食が腸内環境を介して慢性腎臓病に与える影響, 第23回日本病態栄養学会年次集会, Jan. 2020.
65.	Yuuki Niida, Masashi Masuda, Aika Yoshizawa, Yuichiroh Adachi, Kohta Ohnishi, Hirokazu Ohminami, Takayuki Uchida, Hisami Okumura, Takeshi Nikawa, Hironori Yamamoto and Yutaka Taketani : 慢性腎臓病による骨格筋の脂肪酸代謝異常を介した脂肪毒性(Liptoxicity)は筋委縮(サルコペニア) を惹起する, 第23回日本病態栄養学会年次集会, Jan. 2020.
66.	Yuki Kamei, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda, Hisami Okumura and Yutaka Taketani : 小児期において血中 Fetuin-A 濃度とリン濃度は相関する, 第52回日本栄養・食糧学会中国・四国支部会, Oct. 2019.
67.	Yuki Mori, Masashi Masuda, Risa Yoshida, Saki Aoyagi, Kohta Ohnishi, Hirokazu Ohminami, Hisami Okumura, Takeshi Nikawa, 濱田広一郎 and Yutaka Taketani : レチノイン酸によるリポファジーを介した脂肪分解への影響, 第52回日本栄養・食糧学会中国•四国支部大会, Oct. 2019.
68.	Maiko SAKAI, Kohta Ohnishi, Hirokazu Ohminami, Masashi Masuda, Hisami Okumura and Yutaka Taketani : mTORC2 signaling controls the lysosomal activity by regulating of gene expressions in macrophage-like cell line., 第92回日本生化学会大会, Sep. 2019.
69.	Hironori Yamamoto, Mariko Ishiguro, Yuuichirou Takei, Otoki Nakahashi, Masashi Masuda, Yutaka Taketani and 岩野正之 : 食餌性リンはNuclear factor-E2-related factor 2を介し酸化ストレス応答・解毒関連遺伝子の発現を調節する, 第66回日本栄養改善学会学術集会, Sep. 2019.
70.	Yuuki Niida, Masashi Masuda, Aika Yoshizawa, Yuichiroh Adachi, Kohta Ohnishi, Hirokazu Ohminami, Takayuki Uchida, Hisami Okumura, Takeshi Nikawa, Hironori Yamamoto and Yutaka Taketani : 慢性腎臓病モデルラットの骨格筋における脂肪酸代謝異常が及ぼす筋萎縮への影響, 第66回日本栄養改善学会学術集会, Sep. 2019.
71.	Keiko Satoh, Masashi Masuda, 佐々木晧平, Hirokazu Ohminami, Kohta Ohnishi, Hisami Okumura, Hironori Yamamoto and Yutaka Taketani : All-trans retinoic acidによるヒストン修飾を介したFGF23発現への影響, 第7回日本腎栄養代謝研究会, Jul. 2019.
72.	Shiori Tatano, Hironori Yamamoto, Otoki Nakahashi, Ryohei Yoshikawa, Mayu Hayashi, Maki Kishimoto, Yukiko Imi, Hisami Okumura, Masashi Masuda, Kohta Ohnishi and Yutaka Taketani : 成長期における短期的・長期的食餌性リン負荷がFGF23/α-klothoシグナルに及ぼす影響, 日本ビタミン学会第71回大会, Jun. 2019.
73.	Hironori Yamamoto, Mari Nakao, Otoki Nakahashi, Masashi Masuda and Yutaka Taketani : リン制限による鉄代謝および腎性貧血への影響, 日本ビタミン学会第71回大会, Jun. 2019.
74.	Yuichiroh Adachi, Masashi Masuda, Yuuki Niida, Kohta Ohnishi, Takayuki Uchida, Hisami Okumura, Hironori Yamamoto, Takeshi Nikawa and Yutaka Taketani : レチノイン酸による小胞体ストレス感受性の影響, 日本ビタミン学会第71回大会, Jun. 2019.
75.	Maki Kishimoto, Shiori Tatano, Mayu Hayashi, Masashi Masuda and Yutaka Taketani : 妊娠期の高リン食摂取が仔の発育やリン代謝調節系に及ぼす影響, 第73回日本栄養・食糧学会大会, May 2019.
76.	Tomohiro Kagawa, Hironori Yamamoto, Otoki Nakahashi, Nagakatsu Harada, Masashi Masuda, Eiji Takeda and Yutaka Taketani : ステロール調節エレメント結合蛋白質SREBPはビタミンD代謝酵素CYP24A1の発現を調節する, 第73回日本栄養・食糧学会大会, May 2019.
77.	Keiko Satoh, Masashi Masuda, Yuichiroh Adachi, Kohta Ohnishi, Hisami Okumura, Hironori Yamamoto and Yutaka Taketani : All-trans retinoic acidによるヒストン修飾を介したFGF23発現への影響, 第73回日本栄養・食糧学会大会, May 2019.
78.	Moe Fujimoto, Kohta Ohnishi, Maiko Sakai, Teppei Fukuda, Aika Ohnishi, Masashi Masuda, Hisami Okumura, Yoshichika Kawai and Yutaka Taketani : Exploration of bioactive food factors for the control of autophagy flux, 日本農芸化学会2019年度大会, Mar. 2019. (Keyword) autophagy / 食品成分
79.	Aika Yoshizawa, Mari Nakao, Yukiko Imi, Norie Yabiki, Yuuki Niida, Masashi Masuda, Hisami Okumura and Yutaka Taketani : 慢性腎臓病に伴う骨ミネラル代謝異常(CKD-MBD)における骨ー筋連関, 第22回日本病態栄養学会年次学術集会(パシフィコ横浜), Jan. 2019.
80.	足立雄一郎, Masashi Masuda, 新井田裕樹, Kohta Ohnishi, Takayuki Uchida, Hisami Okumura, Takeshi Nikawa and Yutaka Taketani : 小胞体ストレス誘導下におけるレチノイン酸の影響, 第51回日本栄養・食糧学会中国・四国支部大会, Nov. 2018.
81.	吉田里沙, Masashi Masuda, 森優樹, 新井田裕樹, 足立雄一郎, Kohta Ohnishi, Yoshichika Kawai, Takeshi Nikawa, 山本浩範 and Yutaka Taketani : スルフォラファンのリポファジーを介した脂肪分解効果, Food Congress 2018, Sep. 2018.
82.	Hironori Yamamoto, Shiori Tatano, Masashi Masuda, 竹井悠一郎 and Yutaka Taketani : 食餌性リンはNuclear factor-E2-related factor 2を介し酸化ストレス応答・解毒関連遺伝子の発現を調節する, 第36回日本骨代謝学会学術集会(長崎ブリックホール), Jul. 2018.
83.	Yutaka Taketani, Yukiko Imi, Masashi Masuda and Hironori Yamamoto : リン過剰摂取の病態栄養学, 第36回日本骨代謝学会学術集会(長崎ブリックホール), Jul. 2018.
84.	Serina Kabutoya, Masashi Masuda, Yilimulati Yimamu, Hisami Okumura, Hironori Yamamoto and Yutaka Taketani : 慢性腎臓病における鉄代謝異常に対するレチノイン酸の影響, 日本ビタミン学会第70回大会(高槻現代劇場), Jun. 2018.
85.	Yuuki Niida, Masashi Masuda, Aika Yoshizawa, Yuichiroh Adachi, Takayuki Uchida, Kohta Ohnishi, Yoshichika Kawai, Takeshi Nikawa, Hironori Yamamoto and Yutaka Taketani : 慢性腎臓病に伴う骨格筋の飽和脂肪酸蓄積はオートファジー不全を介して筋萎縮を誘発する, 日本ビタミン学会第70回大会(高槻現代劇場), Jun. 2018.
86.	Mayu Hayashi, Shiori Tatano, Maki Kishimoto, Masashi Masuda and Yutaka Taketani : 妊娠前におけるリン過剰摂取が新生仔マウスのリン代謝調節系を撹乱する, 第59回日本生化学会中国・四国支部例会(米子市文化ホール), May 2018.
87.	Risa Yoshida, Yuuki Niida, Yuichiroh Adachi, 酒井晶子, Hisami Okumura, Kohta Ohnishi, Takayuki Uchida, Yoshichika Kawai, Hironori Yamamoto, Takeshi Nikawa, Yutaka Taketani and Masashi Masuda : スルフォラファンのリポファジーを介した脂肪分解効果, 第72回日本栄養・食糧学会大会(岡山県立大学), May 2018.
88.	Mayu Hayashi, Shiori Tatano, Maki Kishimoto, Masashi Masuda, Hisami Okumura and Yutaka Taketani : 妊娠前における食餌性リン負荷が新生仔マウスのリン代謝調節系に及ぼす影響, 第72回日本栄養・食糧学会大会(岡山県立大学), May 2018.
89.	Yutaka Taketani, 木藤有紀, Yukiko Imi, Hisami Okumura and Masashi Masuda : 2.副甲状腺ホルモン初期分泌機構とその役割 (脂溶性ビタミン総合研究委員会・第353回会議研究発表要旨), Vitamins, Vol.91, No.3, 208, 2018. (Link to Publication Site) ● Publication site (DOI): 10.20632/vso.91.3_208 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680809733632 ● Search Scopus @ Elsevier (DOI): 10.20632/vso.91.3_208 (DOI: 10.20632/vso.91.3_208, CiNii: 1390282680809733632)
90.	酒井晶子, 阿部航太郎, 伊美友紀子, Yilimurati Yimamu, 竹内綾乃, Masashi Masuda, Hisami Okumura, 神戸大朋, Hironori Yamamoto and Yutaka Taketani : 慢性腎臓病における亜鉛代謝異常と亜鉛補充食の効果, 第50回日本栄養・食糧学会中国・四国支部大会, Nov. 2017.
91.	甲谷芹奈, Masashi Masuda, 新井田裕樹, 足立雄一郎, 山田あかり, Hisami Okumura and Yutaka Taketani : 慢性腎臓病におけるレチノイン酸の腎性貧血に対する影響, 第50回日本栄養・食糧学会中国四国支部大会, Nov. 2017.
92.	吉田里沙, Masashi Masuda, 青柳咲紀, 伊美友紀子, イリムラティイマム, Hisami Okumura and Yutaka Taketani : 肥満に対するスルフォラファンの影響, 第50回日本栄養・食糧学会中国・四国支部大会, Nov. 2017.
93.	Masashi Masuda : 慢性腎臓病におけるSCD遺伝子発現変化による血管石灰化発症機序, メタルバイオサイエンス研究会, Oct. 2017.
94.	多々納浩, Hisami Okumura, 穂満史子, Masashi Masuda and Yutaka Taketani : メタボローム解析による肉及び魚摂取バイオマーカーの探索, 第64回日本栄養改善学会学術総会, Sep. 2017.
95.	穂満史子, Hisami Okumura, 多々納浩, Masashi Masuda and Yutaka Taketani : メタボロミクスによる飲料摂取バイオマーカーの探索, 第64回日本栄養改善学会学術総会, Sep. 2017.
96.	福田詩織, Hironori Yamamoto, 中橋乙起, Masashi Masuda and Yutaka Taketani : 成長期における食餌性リンによるα-klotho発現制御, 第64回日本栄養改善学会学術総会, Sep. 2017.
97.	新井田裕樹, Masashi Masuda, 足立雄一郎, イマムイリムラティ, Hisami Okumura, Hironori Yamamoto and Yutaka Taketani : 骨格筋脂質代謝異常が慢性腎臓病に伴う尿毒症性サルコペニア(筋委縮)を誘発する, 第64回日本栄養改善学会学術総会, Sep. 2017.
98.	Yutaka Taketani, 楢﨑遙子, Hisami Okumura and Masashi Masuda : 食事性リンとリン負荷指数, 第62回日本透析医学会学術集会・総会, Jun. 2017.
99.	Hironori Yamamoto, 香川知博, 中橋乙起, 石黒真理子, Masashi Masuda, Eiji Takeda and Yutaka Taketani : 生体ビタミンD代謝の日内リズムの制御機構の解明, 日本ビタミン学会第69回大会, Jun. 2017.
100.	伊美友紀子, 矢引紀江, Abuduli Maerjianghan, Masashi Masuda, Hisami Okumura and Yutaka Taketani : 高リン食による白色脂肪組織量の減少, 日本ビタミン学会第69回大会, Jun. 2017.
101.	Yutaka Taketani, 福田詩織, Hisami Okumura and Masashi Masuda : リンと心血管疾患:リン制限は寿命を延伸する?, 第17回日本抗加齢医学会総会, Jun. 2017.
102.	Hironori Yamamoto, 香川知博, 中橋乙起, 石黒真理子, Masashi Masuda and Eiji Takeda : 生体ビタミンD代謝の日内リズムの制御機構の解明, 第71回日本栄養・食糧学会大会, May 2017.
103.	新井田祐樹, Masashi Masuda, 吉澤和香, Yimamu Ilimulati, 吉田里沙, 甲谷芹奈, Hisami Okumura, Yoshichika Kawai, Yutaka Taketani and Hironori Yamamoto : 骨格筋脂質代謝異常が慢性腎臓病に伴うProtein Energy Wasting (CKD-PEW) を誘発する, 第71回日本栄養・食糧学会大会, May 2017.
104.	織田奈央子, 杉原康平, 吉本亜由美, Takashi Uebanso, Masashi Masuda, Hisami Okumura and Yutaka Taketani : 高リン食摂取は腸内環境を変化させる, 日本栄養食糧学会, 322, May 2017.
105.	竹内綾乃, 石田陽子, Masashi Masuda, Yutaka Taketani, 羽田尚彦, 小笠原明恵 and Hisami Okumura : 抗がん剤誘発性の悪心・嘔吐に対するホウレンソウ由来グリセロ糖脂質の抑制効果, 第71回日本栄養・食糧学会大会, May 2017.
106.	山口智勢, Hisami Okumura, 江角遥佳, Masashi Masuda and Yutaka Taketani : 血糖値・血清インスリン濃度及び嗜好性に影響を与える脂質負荷量の検討, 日本病態栄養学会年次学術集会, Jan. 2017.
107.	新井田裕樹, Masashi Masuda, 吉澤和香, Hisami Okumura and Yutaka Taketani : 慢性腎臓病に伴う脂質代謝異常がProtein Eneregy Wastingに与える影響, 日本栄養・食糧学会中国・四国支部大会, Nov. 2016.
108.	山口智勢, Hisami Okumura, 江角遥佳, Masashi Masuda and Yutaka Taketani : 生体や嗜好性に影響を与える脂質負荷量の検討, 日本栄養・食糧学会中国・四国支部, Nov. 2016.
109.	Hiroshi Tatano, Hisami Okumura, Daisuke Kajiura, 近藤千佳, 平山明由, Kazuaki Mawatari, Yoshichika Kawai, Masashi Masuda and Yutaka Taketani : GC-MSを用いた肉の種類別の摂取バイオマーカーの探索, 第10回メタボロームシンポジウム, Oct. 2016.
110.	Masashi Masuda and 宮崎淳 : 飽和脂肪酸と血管石灰化, 日本脂質栄養学会第25回大会, Sep. 2016.
111.	杉原康平, Masashi Masuda, 中尾真理, Abuduli Maerjianghan, 石田陽子, Hironori Yamamoto, Eiji Takeda and Yutaka Taketani : リンの過剰摂取はDSS誘発性大腸炎を悪化させる, 第19回日本病態栄養学会年次学術集会，パシフィコ横浜，神奈川県横浜市，2016年1月9日~10日, Jan. 2016.
112.	多々納浩, Hisami Okumura, Yutaka Taketani and Masashi Masuda : 生活習慣病の要:栄養教育と実践, 第62回日本栄養改善学会学術総会, Sep. 2015.
113.	中橋乙起, Hironori Yamamoto, 田中更紗, Masashi Masuda, Yutaka Taketani, Ken-ichi Miyamoto, 加藤茂明 and Eiji Takeda : Fibroblast Growth Factor15遺伝子の発現に及ぼす食餌性リン及び活性型ビタミンD3の影響, 第64回日本栄養・食糧学会大会, May 2010.

Et cetera, Workshop:

1.	Aika Yoshizawa, 中尾真理, Yukiko Imi, 矢引紀江, Yuuki Niida, Masashi Masuda, Hisami Okumura and Yutaka Taketani : 慢性腎臓病に伴う骨ミネラル代謝異常(CKD-MBD)における骨ー筋連関, 第3回日本CKD-MBD研究会学術集会(御茶ノ水ソラシティカンファレンスセンター), Mar. 2019.
2.	Mayu Hayashi, Shiori Tatano, Maki Kishimoto, Masashi Masuda, Hisami Okumura, Hironori Yamamoto and Yutaka Taketani : 妊娠前における食餌性リン負荷が仔のリン・ビタミンD代謝調節系に及ぼす影響, 第3回日本CKD-MBD研究会学術集会(御茶ノ水ソラシティカンファレンスセンター), Mar. 2019.
3.	Masashi Masuda : 小胞体ストレスによる血管石灰化, 第35回 ROD-21研究会, Feb. 2017.
4.	Masashi Masuda : 飽和脂肪酸と血管石灰化, 第16回徳島Bone Forum, Oct. 2016.
5.	Masashi Masuda, Hironori Yamamoto, Yimamu Yilimulati, 大谷彩子, 大西里奈, Eiji Takeda and Yutaka Taketani : 第2回 Neo Vitamin D Workshop 学術集会, Aug. 2016.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

Basis for the research of transgenerational epigenomic nutrition for precision nutrition (Project/Area Number: 23K28019 )
生体内リン代謝と老化を繋ぐ分子機序解明の研究基盤 (Project/Area Number: 21H03359 )
Study for the establishment of new treatment methods using lipoquality for age-related diseases. (Project/Area Number: 20K21761 )
Establishment of molecular basis of rehabilitation nutrition for heart failure targeting cardiac metabolic remodeling (Project/Area Number: 20H04038 )
Elucidation of set-point mechanism for phosphate homeostasis and development of a novel therapeutic target for age-related diseases (Project/Area Number: 19H04053 )
The pathogenesis of sarcopenia induced by abnormal lipid metabolism in chronic kidney disease (Project/Area Number: 17K19910 )
The effects of epigenetic modification on the pathogenesis and the development of chronic kidney disease (Project/Area Number: 17H05061 )
Establishment of a novel research strategy for dietetics based on epigenomics (epigenome dietetics) (Project/Area Number: 16H03046 )
The roll of rapid-phase parathyroid hormone secretion in chronic kidney disease-mineral and bone disorder (Project/Area Number: 15H06442 )
Search by Researcher Number (50754488)

Associate Professor : Masuda, Masashi

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Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)