徳島大学 / 教育研究者総覧 --- 足立雄一郎

専門分野

研究テーマ

著書・論文

著書:

1.	増田真志, 山本浩範, 竹井悠一郎, 中橋乙起, 足立雄一郎, 大西康太, 大南博和, 奥村仙示, 阪上浩, 宮崎淳, 武田英二, 竹谷豊 : All-transレチノイン酸は腸管ナトリウム依存性リン酸トランスポーター遺伝子(Npt2b)の転写を負に制御する, 日本ビタミン学会, 2020年11月. (要約) 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． (キーワード) 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) (出版サイトへのリンク) ● Publication site (DOI): 10.20632/vso.94.11_545 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390571704642711680 ● Search Scopus @ Elsevier (DOI): 10.20632/vso.94.11_545 (DOI: 10.20632/vso.94.11_545, CiNii: 1390571704642711680)

学術論文(審査論文):

1.	Masaki Takikawa, Hirokazu Ohminami, Takayuki Uchida, Ayano Kitamura, Yuichiro Adachi, Yuki Mori, Kohta Ohnishi, Masashi Masuda, Hisami Yamanaka-Okumura and Yutaka Taketani : Dietary combination of sucrose and linoleic acid increases intramyocellular lipid and impairs muscle strength in female Zucker diabetic fatty rats, Journal of Clinical Biochemistry and Nutrition, 76, 3, 271-279, 2025. (キーワード) carbohydrate / 脂肪酸 (fatty acid) / intramyocellular lipid / nutritional interaction / sarcopenic obesity (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.24-229 (文献検索サイトへのリンク) ● Summary page in Scopus @ Elsevier: 2-s2.0-105004057833 (DOI: 10.3164/jcbn.24-229, Elsevier: Scopus)
2.	Anh The Nguyen, Masashi Masuda, Yuki Mori, Yuichiro Adachi, Teppei Fukuda, Airi Furuichi, Masaki Takikawa, Yuki Tsuda, Yuki Hamada, Yusuke Maruyama, Hirokazu Ohminami, Kohta Ohnishi and Yutaka Taketani : All-trans retinoic acid induces lipophagy by reducing Rubicon in Hepa1c1c7 cells., Journal of Lipid Research, 65, 8, 100598, 2024. (要約) All-trans retinoic acid (atRA), a metabolite of vitamin A, reduces hepatic lipid accumulation in liver steatosis model animals. Lipophagy, a new lipolysis pathway, degrades a lipid droplet (LD) via autophagy in adipose tissue and the liver. We recently found that atRA induces lipophagy in adipocytes. However, it remains unclear whether atRA induces lipophagy in hepatocytes. In this study, we investigated the effects of atRA on lipophagy in Hepa1c1c7 cells and the liver of mice fed a high-fat diet (HFD). First, we confirmed that atRA induced autophagy in Hepa1c1c7 cells by Western blotting and the GFP-LC3-mCherry probe. Next, we evaluated the lipolysis in fatty Hepa1c1c7 cells treated with the knockdown of Atg5, an essential gene in autophagy induction. Atg5-knockdown partly suppressed the atRA-induced lipolysis in fatty Hepa1c1c7 cells. We also found that atRA reduced the protein, but not mRNA, expression of Rubicon, a negative regulator of autophagy, in Hepa1c1c7 cells and the liver of HFD-fed mice. Rubicon-knockdown partly inhibited the atRA-induced lipolysis in fatty Hepa1c1c7 cells. In addition, atRA reduced hepatic Rubicon expression in young mice, but the effect of atRA on it diminished in aged mice. Finally, we investigated the mechanism underlying reduced Rubicon protein expression by atRA in hepatocytes. A protein synthesis inhibitor, but not proteasome or lysosomal inhibitors, significantly blocked the reduction of Rubicon protein expression by atRA in Hepa1c1c7 cells. These results suggest that atRA may promote lipophagy in fatty hepatocytes by reducing hepatic Rubicon expression via inhibiting protein synthesis. (キーワード) Animals / Tretinoin / Mice / オートファジー (autophagy) / Lipolysis / Autophagy-Related Proteins / Hepatocytes / Male / Mice, Inbred C57BL / Liver / Cell Line, Tumor / Diet, High-Fat / Autophagy-Related Protein 5 / Intracellular Signaling Peptides and Proteins (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.jlr.2024.100598 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39032560 ● Summary page in Scopus @ Elsevier: 2-s2.0-85202906207 (DOI: 10.1016/j.jlr.2024.100598, PubMed: 39032560, Elsevier: Scopus)
3.	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, 126, 2024. (要約) 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). (キーワード) Mice / Animals / AMP-Activated Protein Kinases / Beclin-1 / Signal Transduction / Lipolysis / Tretinoin / オートファジー (autophagy) / Adipocytes / 3T3-L1 Cells (徳島大学機関リポジトリ) ● Metadata: 2012043 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.jnutbio.2024.109589 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38295886 ● Summary page in Scopus @ Elsevier: 2-s2.0-85185252909 (徳島大学機関リポジトリ: 2012043, DOI: 10.1016/j.jnutbio.2024.109589, PubMed: 38295886, Elsevier: Scopus)
4.	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, 326, 3, F411-F419, 2024. (要約) 収集根拠 : 博士論文(自動収集) (キーワード) Humans / Rats / Animals / Phosphates / 高リン血症 (hyperphosphatemia) / Zinc / Renal Insufficiency, Chronic / Nephrectomy / Intestinal Absorption (徳島大学機関リポジトリ) ● Metadata: 2012041 (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajprenal.00310.2023 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38234299 ● CiNii @ 国立情報学研究所 (CRID): 1910585658881299840 ● Summary page in Scopus @ Elsevier: 2-s2.0-85185726165 (徳島大学機関リポジトリ: 2012041, DOI: 10.1152/ajprenal.00310.2023, PubMed: 38234299, CiNii: 1910585658881299840, Elsevier: Scopus)
5.	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, 73, 3, 198-204, 2023. (要約) , 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. (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.23-11 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37970550 ● Summary page in Scopus @ Elsevier: 2-s2.0-85176444768 (DOI: 10.3164/jcbn.23-11, PubMed: 37970550, Elsevier: Scopus)
6.	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, 106, 109017, 2022. (要約) 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. (キーワード) 3T3-L1 Cells / AMP-Activated Protein Kinases / Adipocytes, White / Animals / オートファジー (autophagy) / Autophagy-Related Protein-1 Homolog / Isothiocyanates / Lipolysis / Mice / シグナル伝達 (signal transduction) / Sulfoxides / TOR Serine-Threonine Kinases (徳島大学機関リポジトリ) ● Metadata: 2010246 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.jnutbio.2022.109017 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 2010246, DOI: 10.1016/j.jnutbio.2022.109017, PubMed: 35461903)
7.	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, 5, 7, 2022. (要約) 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. (キーワード) Animals / Gene Expression Regulation / MAP Kinase Signaling System / Mice / Muscle Fibers, Skeletal / Protein Phosphatase 1 / RNA, Messenger / Transcription Factors / Tretinoin (徳島大学機関リポジトリ) ● Metadata: 2010245 (出版サイトへのリンク) ● Publication site (DOI): 10.26508/lsa.202101345 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35318262 ● Summary page in Scopus @ Elsevier: 2-s2.0-85126899851 (徳島大学機関リポジトリ: 2010245, DOI: 10.26508/lsa.202101345, PubMed: 35318262, Elsevier: Scopus)
8.	Masashi Masuda, Hironori Yamamoto, Yuichiro Takei, Otoki Nakahashi, Yuichiro 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, 477, 4, 817-831, 2020. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 2007373 (出版サイトへのリンク) ● Publication site (DOI): 10.1042/BCJ20190716 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32016357 ● Summary page in Scopus @ Elsevier: 2-s2.0-85081075194 (徳島大学機関リポジトリ: 2007373, DOI: 10.1042/BCJ20190716, PubMed: 32016357, Elsevier: Scopus)
9.	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, 67, 2, 179-187, 2020. (要約) <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> (キーワード) skeletal muscle atrophy / endoplasmic reticulum stress / chronic kidney disease / stearoyl-CoA desaturase / saturated fatty acid (徳島大学機関リポジトリ) ● Metadata: 2007653 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.20-24 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33041516 ● CiNii @ 国立情報学研究所 (CRID): 1390566775163696384 ● Search Scopus @ Elsevier (PMID): 33041516 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.20-24 (徳島大学機関リポジトリ: 2007653, DOI: 10.3164/jcbn.20-24, PubMed: 33041516, CiNii: 1390566775163696384)

国際会議:

1.	Yuichiro Adachi, Williams M Allison, Masashi Masuda, Yutaka Taketani, Anderson J Paul and Ivanov Pavel : Stress granules at the crossroad of acute and chronic stress, RNA granule meeting, Oct. 2023.
2.	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.
3.	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.
4.	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, Oct. 2018.

国内講演発表:

1.	竹谷豊, 足立雄一郎, 山本菜摘, 大南博和, 増田真志 : 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, 2023年9月.
2.	山本菜摘, 増田真志, 足立雄一郎, 春本恵里花, 野邊悠太郎, 大南博和, 山本浩範, 竹谷豊 : 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, 2023年6月.
3.	野邊悠太郎, 増田真志, 佐々木晧平, 足立雄一郎, 大南博和, 竹谷豊 : 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, 2022年10月.
4.	春本恵里花, 増田真志, 佐々木晧平, 足立雄一郎, 森優樹, 大南博和, 山本浩範, 竹谷豊 : 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, 2022年6月.
5.	増田真志, 足立雄一郎, 竹谷豊 : 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, 2022年6月.
6.	佐々木晧平, 増田真志, 足立雄一郎, 春本恵里花, 大南博和, 奥村仙示, 山本浩範, 竹谷豊 : 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, 2022年3月.
7.	野邊悠太郎, 増田真志, 足立雄一郎, 山本菜摘, 大南博和, 奥村仙示, 竹谷豊 : 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, 2021年10月.
8.	足立雄一郎, 増田真志, 榊原伊織, 内田貴之, 大南博和, 奥村仙示, 二川健, 竹谷豊 : 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, 2021年9月.
9.	足立雄一郎, 増田真志, 榊原伊織, 内田貴之, 佐々木皓平, 野邊悠太郎, 大南博和, 大西康太, 奥村仙示, 山本浩範, 二川健, 竹谷豊 : 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, 2021年7月.
10.	佐々木皓平, 増田真志, 足立雄一郎, 森優樹, 野邊悠太郎, 大南博和, 大西康太, 奥村仙示, 山本浩範, 竹谷豊 : 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, 2021年6月.
11.	佐々木晧平, 増田真志, 足立雄一郎, 大西康太, 大南博和, 奥村仙示, 竹谷豊 : 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, 2020年10月.
12.	佐守美穂, 亀井優輝, 大西康太, 足立雄一郎, 増田真志, 大南博和, 奥村仙示, 竹谷豊, 羽田尚彦, 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, 2020年10月.
13.	足立雄一郎, 増田真志, 大西康太, 大南博和, 奥村仙示, 竹谷豊 : 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, 2020年7月.
14.	新井田裕樹, 増田真志, 吉澤和香, 足立雄一郎, 大西康太, 大南博和, 内田貴之, 奥村仙示, 二川健, 山本浩範, 竹谷豊 : 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, 2020年1月.
15.	新井田裕樹, 増田真志, 吉澤和香, 足立雄一郎, 大西康太, 大南博和, 内田貴之, 奥村仙示, 二川健, 山本浩範, 竹谷豊 : 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, 2019年9月.
16.	足立雄一郎, 増田真志, 新井田裕樹, 大西康太, 内田貴之, 奥村仙示, 山本浩範, 二川健, 竹谷豊 : 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, 2019年6月.
17.	佐藤景子, 増田真志, 足立雄一郎, 大西康太, 奥村仙示, 山本浩範, 竹谷豊 : 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, 2019年5月.
18.	足立雄一郎, 増田真志, 新井田裕樹, 大西康太, 内田貴之, 奥村仙示, 二川健, 竹谷豊 : 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, 2018年11月.
19.	吉田里沙, 増田真志, 森優樹, 新井田裕樹, 足立雄一郎, 大西康太, 河合慶親, 二川健, 山本浩範, 竹谷豊 : 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, 2018年9月.
20.	新井田裕樹, 増田真志, 吉澤和香, 足立雄一郎, 内田貴之, 大西康太, 河合慶親, 二川健, 山本浩範, 竹谷豊 : 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), 2018年6月.
21.	吉田里沙, 新井田裕樹, 足立雄一郎, 酒井晶子, 奥村仙示, 大西康太, 内田貴之, 河合慶親, 山本浩範, 二川健, 竹谷豊, 増田真志 : 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), 2018年5月.
22.	甲谷芹奈, 増田真志, 新井田裕樹, 足立雄一郎, 山田あかり, 奥村仙示, 竹谷豊 : 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, 2017年11月.
23.	新井田裕樹, 増田真志, 足立雄一郎, イマムイリムラティ, 奥村仙示, 山本浩範, 竹谷豊 : 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, 2017年9月.

特任助教 : 足立雄一郎

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特任助教 : 足立 雄一郎

研究活動

専門分野

研究テーマ

著書・論文

著書:

学術論文(審査論文):

国際会議:

国内講演発表:

特任助教 : 足立雄一郎