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美谷島 克宏 (ミヤジマ カツヒロ) MIYAJIMA Katsuhiro 教授 |
学内職務経歴 【 表示 ／ 非表示 】
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東京農業大学 応用生物科学部 食品安全健康学科 准教授
2016年04月 - 2018年09月
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東京農業大学 応用生物科学部 食品安全健康学科 教授
2018年10月 - 現在
所属学協会 【 表示 ／ 非表示 】
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食品安全委員会農薬専門調査会
2016年04月 - 現在
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日本毒性学会
2001年04月 - 現在
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日本毒性病理学会
1992年12月 - 現在
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日本獣医学会
1992年04月 - 現在
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日本組織細胞化学会
2009年10月 - 現在
論文 【 表示 ／ 非表示 】
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OKI Chika, UNO Kinuko, SASASE Tomohiko, TSUTSUI Takahiro, SEKIGUCHI Keita, YAMAGUCHI Ayane, MANDAI Kouhei, SHINOHARA Masami, SUGIMOTO Miki, MAEKAWA Tatsuya, MIYAJIMA Katsuhiro, OHTA Takeshi
Journal of Veterinary Medical Science 87 ( 2 ) 138 - 146 2025年
記述言語：英語 出版者・発行元：JAPANESE SOCIETY OF VETERINARY SCIENCE
<p>Many genetic and environmental factors are involved in the development and progression of diabetic kidney disease (DKD), and its pathology shows various characteristics. Animal models of DKD play an important role in elucidating its pathogenesis and developing new therapies. In this study, we investigated the pathophysiological features of two DKD animal models: <i>db/db</i> mice (background of hyperglycemia) and KK-Ay mice (background of hyperinsulinemia). Male and female mice were fed a high-fat/high-sucrose (HFS) diet for eight weeks. Two mouse models fed the HFS diet showed increases in urinary protein, kidney weight, and glomerular size, but these changes were pronounced in KK-Ay mice. Pathological examination revealed tubulointerstitial fibrosis in KK-Ay mice fed the HFS diet, but not in <i>db/db</i> mice. In addition, fat accumulation was observed in the macula densa of <i>db/db</i> mice and in the glomeruli of KK-Ay mice fed with the HFS diet. In conclusion, an HFS diet exacerbates renal lesions with tubulointerstitial fibrosis in KK-Ay mice, and KK-Ay mice fed an HFS diet are expected to be useful as a DKD model.</p>
DOI： 10.1292/jvms.24-0313
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Uno Kinuko, Sekiguchi Keita, Suzuki-Kemuriyama Noriko, Ohta Takeshi, Miyajima Katsuhiro
The Journal of Toxicological Sciences 50 ( 7 ) 343 - 350 2025年
記述言語：英語 出版者・発行元：The Japanese Society of Toxicology
<p>Nonalcoholic fatty liver disease (NAFLD) is a lifestyle-related disease. A gut-liver axis is involved in the progression of NAFLD. Disruption of the intestinal barrier function is an exacerbating factor of NAFLD. In this study, we have investigated the interaction between colitis and NAFLD in mouse models of dextran sodium sulfate (DSS)-induced colitis and diet-induced NAFLD-like lesions. Male C57BL/6J mice were provided with a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) and 1.25% DSS water for 3 weeks. The DSS water was administered intermittently. In the large intestine, the DSS-treated groups clearly demonstrated inflammation. Dilation of crypt and goblet cells was observed in the DSS + CDAHFD group. The expression of minor inflammation-related genes was increased in the CDAHFD group. In the liver, the CDAHFD group demonstrated non-alcoholic steatohepatitis (NASH)-like lesions. The number of C-X-C motif chemokine ligand 16 (CXCL16)-positive cells increased in the CDAHFD group and tended to increase in the DSS + CDAHFD group. Toll-like receptor 4 (TLR4)-positive cells were observed mainly in gallbladder epithelial cells in all groups and were more pronounced in the DSS-administered groups. Inflammation-related genes were upregulated in the DSS group. The expression of fibrosis-related genes increased in the DSS + CDAHFD group. DSS-induced colitis and CDAHFD-induced NASH interacted with each other. NAFLD lesions were induced by CDAHFD and exacerbated by TLR4 and CXCL16 in DSS-induced colitis. Colitis is induced by DSS and exacerbated by changes in the intestinal environment due to liver injury. This combined model was useful in analyzing early lesions of liver-gut axis for NAFLD. </p>
DOI： 10.2131/jts.50.343
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Ryoke Katsunori, Ishizuka Kana, Yasui Yuzo, Kondo Kazuma, Suzuki-Kemuriyama Noriko, Maekawa Tatsuya, Miyajima Katsuhiro
Fundamental Toxicological Sciences 11 ( 4 ) 159 - 168 2024年
記述言語：英語 出版者・発行元：The Japanese Society of Toxicology
<p>Titin is a giant protein that is specifically expressed in striated muscle and essential for the maintenance of sarcomere structure and function. Recently, the N-terminal fragment of the Titin (N-titin) has been reported to show high levels in human urine in patients with muscular diseases and is expected to serve as a diagnostic biomarker for these diseases. In this study, we examined the utility of N-titin as a biomarker to detect muscle atrophy in mice. Male BALB/c mice (6 weeks of age, n=5 per group) were given 10 mg/L dexamethasone (DEX) dissolved in drinking water for 4 weeks. The gastrocnemius muscle (GAS) weight was significantly decreased and mRNA levels of muscle atrophy-related genes (Atrogin-1 and MuRF-1) were increased in the GAS after 4 weeks of DEX treatment. Although there were no degenerative/necrotic changes in the histopathological examination, the muscle fiber cross-sectional area significantly decreased in the GAS. On the other hand, there were no DEX treatment-related changes in the muscle weights and the muscle fiber cross-sectional area in the soleus muscle. These results suggest that 4-week of DEX treatment preferentially caused atrophy of fast-dominant muscle. Under the condition of this study, urinary N-titin/CRN ratio markedly increased from Week 2 of the DEX treatment. From the above results, the urinary N-titin/CRN ratio could be a biomarker for monitoring skeletal muscle atrophy in mice.</p>
DOI： 10.2131/fts.11.159
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Sano Ryuhei, Ryu Kanjiro, Sasase Tomohiko, Shinozaki Yuichi, Teoh Soon Hui, Yamaguchi Ayane, Uno Kinuko, Maekawa Tatsuya, Ohta Takeshi, Miyajima Katsuhiro
The Journal of Toxicological Sciences 48 ( 11 ) 597 - 606 2023年
記述言語：英語 出版者・発行元：The Japanese Society of Toxicology
<p>Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease (ESRD). Although current therapeutic strategies for DKD, including sodium-glucose cotransporter-2 inhibitors and mineralocorticoid receptor antagonists, have shown some degree of efficacy, they have failed to completely halt the progression of DKD to ESRD owing to the complexity of DKD pathogenesis. Elucidating the pathophysiological mechanism of DKD is essential for the development of novel therapeutic strategies. In this study, we investigated the pathophysiological characteristics of uninephrectomized (UNx) KK-Ay mice and examined the effects of salt supplementation on the acceleration of renal injury in these mice. UNx KK-Ay mice exhibited pathophysiological renal abnormalities with glomerular and tubulointerstitial fibrosis. Additionally, salt supplementation exacerbated renal injury, particularly tubular injury. These results suggest that UNx KK-Ay mice are useful models for advanced DKD and that salt exacerbates tubular damage in DKD.</p>
DOI： 10.2131/jts.48.597
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Ｊｏｕｒｎａｌ ｏｆ Ｔｏｘｉｃｏｌｏｇｉｃ Ｐａｔｈｏｌｏｇｙ 36 ( 1 ) 1 - 10 2023年
記述言語：英語 出版者・発行元：日本毒性病理学会
委員歴 【 表示 ／ 非表示 】
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食品安全委員会農薬専門調査会 専門委員
2016年04月 - 現在
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日本毒性学会 日本毒性学会認定トキシコロジスト
2005年10月 - 現在
団体区分：学協会
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日本毒性学会 評議員
2016年07月 - 現在
団体区分：学協会
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日本毒性病理学会 日本毒性病理学会認定毒性病理学専門家
1999年10月 - 現在
団体区分：学協会
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日本毒性病理学会 評議員
2014年04月 - 現在
団体区分：学協会