Tokushima University / Educator and Researcher Directory --- Ohminami, Hirokazu

Personal Web Page

https://researchmap.jp/tokushima0201 (researchmap)

Field of Study

○	Clinical Nutrition, Pathological Nutrition

Subject of Study

○	サルコペニア・フレイルに対する栄養管理法の開発, 心臓リハビリテーション栄養のトランスレーショナルリサーチ, スリーブ状胃切除術の栄養療法

Book / Paper

Book:

1.	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.
2.	Hirokazu Ohminami, Masaki Takikawa, Ayano Kitamura, Mina Matsubara and Yutaka Taketani : Accurate measurement of energy metabolism and its usefulness for dialysis patients, 日本メディカルセンター, Apr. 2023. (Link to Publication Site) ● Publication site (DOI): 10.19020/cd.0000002513 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390014337396806144 ● Search Scopus @ Elsevier (DOI): 10.19020/cd.0000002513 (DOI: 10.19020/cd.0000002513, CiNii: 1390014337396806144)
3.	Hirokazu Ohminami : 栄養科学シリーズNEXT 新・臨床栄養学第2版, 株式会社講談社サイエンティフィク, Tokyo, Mar. 2023.
4.	Hirokazu Ohminami : 動脈硬化性疾患予防ガイドライン2022年版, Jul. 2022.
5.	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)
6.	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.

Academic Paper (Judged Full Paper):

1.	Hirokazu Ohminami : Basics of rehabilitation nutrition, Shikoku Acta Medica, Vol.79, No.5,6, 203-208, 2024. (Keyword) Rehabilitation nutrition / malnutrition / sarcopenia (Link to Publication Site) ● Publication site (DOI): 10.57444/shikokuactamedica.79.5.6_203 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390581091433465728 ● Search Scopus @ Elsevier (DOI): 10.57444/shikokuactamedica.79.5.6_203 (DOI: 10.57444/shikokuactamedica.79.5.6_203, CiNii: 1390581091433465728)
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.	石井亜由美, Takayuki Ise, 西川孝治, Hirokazu Ohminami, Muneyuki Kadota, Shusuke Yagi, Tetsuya Matsuura and Masataka Sata : TAVI後の認知機能低下に関わる因子の検討, 心臓リハビリテーション(JJCR), Vol.29, No.3,4, 242-208, 2023.
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.	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)
14.	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)
15.	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)
16.	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)

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.	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.
3.	Hamamoto Riko, Hirokazu Ohminami, Shu Wakino and Yutaka Taketani : Effectiveness of protein restriction diet on chronic kidney disease: a systematic review, The International Workshop on Gut-kidney Axis and Chronic Kidney Disease, Tokyo, Mar. 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.	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.

Proceeding of Domestic Conference:

1.	Takayuki Ise, 石井亜由美, 西川幸治, Muneyuki Kadota, Rie Ueno, Shusuke Yagi, Hirokazu Ohminami, Yutaka Taketani and Masataka Sata : 進歩するSHDに対する治療と心臓リハビリテーション, 第30回日本心臓リハビリテーション学会学術集会, Jul. 2024.
2.	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.
3.	西川幸治, Takayuki Ise, 石井亜由美, Hirokazu Ohminami, Muneyuki Kadota, Shusuke Yagi and Masataka Sata : 心不全を伴う若年の高度肥満患者に対する心臓リハビリテーションの経験, 日本心臓リハビリテーションン学会第7回四国支部地方会, Mar. 2024.
4.	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.
5.	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.
6.	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.
7.	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.
8.	石井亜由美, 西川幸治, Muneyuki Kadota, Kenya Kusunose, Shusuke Yagi, Hirokazu Ohminami, 内藤紘一, Yutaka Taketani and Masataka Sata : 情報発信WEB 「リカバルクラブ」を用いた多職種患者教育の取り組み, 第71回日本心臓病学会学術集会，2023年9月8日(金)∼10日(日)，東京, Sep. 2023.
9.	Hirokazu Ohminami : 知っておきたいリハビリテーション栄養のキホン, 第267回徳島医学会学術集会市民公開シンポジウム, Aug. 2023.
10.	Takayuki Ise, 石井亜由美, 西川幸治, 上野理恵, Muneyuki Kadota, Shusuke Yagi, Hirokazu Ohminami, 内藤紘一, Yutaka Taketani and Masataka Sata : 遠隔伴走型心リハ「リカバル」による新たな在宅心リハの取り組み, 第29回日本心臓リハヒリテーション学会学術集会, Jul. 2023.
11.	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.
12.	石井亜由美, Takayuki Ise, 西川幸治, Hirokazu Ohminami, Muneyuki Kadota, Shusuke Yagi, Tetsuya Matsuura and Masataka Sata : 心リハ専従看護師としての働き方, 第29回日本心臓リハビリテーション学会学術集会, Jul. 2023.
13.	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.
14.	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.
15.	Hirokazu Ohminami : 高血圧改善のための食事管理∼減塩を中心に∼, 世界高血圧の日市民公開講座 in 徳島, May 2023.
16.	Takayuki Ise, 石井亜由美, 西川幸治, Muneyuki Kadota, Shusuke Yagi, Hirokazu Ohminami, Yutaka Taketani and Masataka Sata : 遠隔伴走型心臓リハヒリテーション「リカバル」を用いた新たな取り組み, 日本心臓リハヒリテーション学会第6回四国支部地方会, Mar. 2023.
17.	西川幸治, Takayuki Ise, 石井亜由美, Hirokazu Ohminami, Muneyuki Kadota, Shusuke Yagi and Masataka Sata : 心不全を伴う若年の高度肥満患者に対する心臓リハヒリテーションの経験, 日本心臓リハヒリテーション学会第6回四国支部地方会, Mar. 2023.
18.	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.
19.	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.
20.	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.
21.	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.
22.	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.
23.	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.
24.	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.
25.	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.
26.	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.
27.	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.
28.	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.
29.	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.
30.	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.
31.	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.
32.	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.
33.	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.
34.	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.
35.	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.
36.	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.
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.
38.	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.
39.	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.
40.	Takayuki Ise, 石井亜由美, 西川幸治, Muneyuki Kadota, 鈴木佳子, Hirokazu Ohminami, Shusuke Yagi and Masataka Sata : 大動脈狭窄症に対するTAVI後認知機能の変化, 第11回日本脳血管・認知症学会総会, Aug. 2021.
41.	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.
42.	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.
43.	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.
44.	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.
45.	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.
46.	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.
47.	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.
48.	石井亜由美, Takayuki Ise, 西川幸治, 鈴木佳子, Hirokazu Ohminami, Muneyuki Kadota, Shusuke Yagi, 加藤真介 and Masataka Sata : 心臓リハビリテーションの日独比較 ∼ドイツ心リハ研修から∼, 第4回日本心臓リハビリテーション学会四国支部地方会, Mar. 2021.
49.	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.
50.	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.
51.	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.
52.	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.
53.	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.
54.	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.
55.	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.
56.	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.
57.	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.
58.	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.
59.	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.
60.	西川幸治, Takayuki Ise, 石井亜由美, 鈴木佳子, Hirokazu Ohminami, Muneyuki Kadota, Shusuke Yagi, Shinsuke Katoh and Masataka Sata : TAVI後の認知機能低下に関連する因子の検討, 第26回日本心臓リハビリテーション学会学術集会, Jul. 2020.
61.	Muneyuki Kadota, Shusuke Yagi, Takayuki Ise, 石井亜由美, 西川幸治, 鈴木佳子, Hirokazu Ohminami, Shinsuke Katoh and Masataka Sata : イハブラジン導入前後の運動耐容能の推移を観察した虚血性心筋症の一例, 第26回日本心臓リハビリテーション学会学術集会, Jul. 2020.
62.	石井亜由美, Takayuki Ise, 西川幸治, Yukako Honma, 鈴木佳子, Hirokazu Ohminami, Muneyuki Kadota, Takeshi Tobiume, Shusuke Yagi, Yasunobu Hayabuchi, Shinsuke Katoh and Masataka Sata : 心配停止をきたしQT延長症候群と診断されS-ICD植込みとなった5歳児に対する心リハの経験, 第26回日本心臓リハビリテーション学会学術集会, Jul. 2020.
63.	Hirokazu Ohminami, 伊勢孝之, 八木秀介, 門田宗之, 西川幸治, 石井亜由美, 鈴木佳子, 竹谷豊, 加藤真介 and 佐田政隆 : 回復期における運動耐容能の向上は脂質パラメータと相関する, 第26回日本心臓リハビリテーション学会学術集会, Jul. 2020.
64.	石井亜由美, Takayuki Ise, 西川幸治, Yukako Honma, 鈴木佳子, Hirokazu Ohminami, Muneyuki Kadota, Shusuke Yagi, Yasunobu Hayabuchi, Shinsuke Katoh and Masataka Sata : 小児に関する心臓リハビリテーションの取り組みと症例から学んだこと, 第26回日本心臓リハビリテーション学会学術集会, Jul. 2020.
65.	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.
66.	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.
67.	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.
68.	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.
69.	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
70.	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
71.	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
72.	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
73.	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.
74.	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.
75.	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.
76.	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.
77.	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.
78.	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.
79.	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.
80.	田村行識, 堀川陽子, 川勝美里, 中原晴未, 那須楓, 塩山佳奈, 内藤梨都, 松田夏美, Hirokazu Ohminami and 佐々木康人 : ラットにおける蛋白質摂取量の違いがショ糖嗜好性および糖・脂質代謝に及ぼす影響, 第50回日本動脈硬化学会総会・学術集会, Jul. 2018.
81.	田村行識, 赤木里衣, 吉本和樹, 武内風香, 水野善教, 森本満里奈, 堀川陽子, Hirokazu Ohminami and 佐々木康人 : 糖尿病マウスにおける筋骨格系の異常に対する亜鉛投与の効果, 第50回日本動脈硬化学会総会・学術集会, Jul. 2018.

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 )
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 )
Possible interaction of dietary carbohydrate and lipid in the prevention of obesity-related disorders (Project/Area Number: 18K17946 )
Search by Researcher Number (90803057)

Assistant Professor : Ohminami, Hirokazu

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