Updated on 2025/04/22

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MIYAJIMA Katsuhiro

Professor

Title

Professor

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From School 【 display / non-display

  • Kitasato University   Faculty of Veterinary Medicine and Animal Sciences   Graduated

    1986.04 - 1992.03

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    Country:Japan

Degree 【 display / non-display

  • 博士(医学) ( 2010.03   東海大学 )

Employment Record in Research 【 display / non-display

  • Tokyo University of Agriculture   Faculty of Applied Bio-Science   Department of Nutritional Science and Food Safety   Associate Professor

    2016.04 - 2018.09

  • Tokyo University of Agriculture   Faculty of Applied Bio-Science   Department of Nutritional Science and Food Safety   Professor

    2018.10

External Career 【 display / non-display

  • Japan Tobacco Inc.   Central Pharmaceutical Research Institute   Chief Researcher

    1996.04 - 2016.04

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    Country:Japan

Professional Memberships 【 display / non-display

  • 食品安全委員会農薬専門調査会

    2016.04

  • The Japanese Society of Toxicology

    2001.04

  • The Japanese Society of Toxicological Pathology

    1992.12

  • The Japanese Society of Veterinary Science

    1992.04

  • al of the Japan Society of Histochemistry and Cytochem

    2009.10

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Research Areas 【 display / non-display

  • Life Science / Experimental pathology  / Toxicological pathology

  • Life Science / Laboratory animal science  / Toxicology

Papers 【 display / non-display

  • High-fat/high-sucrose diet-induced renal changes in obese diabetic mice: a comparison with <i>db/db</i> and KK-Ay mice

    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

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    Language:English   Publisher: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

    PubMed

  • Utility of urinary N-titin as a muscle atrophy biomarker in dexamethasone-induced muscle atrophy model mice

    Ryoke Katsunori, Ishizuka Kana, Yasui Yuzo, Kondo Kazuma, Suzuki-Kemuriyama Noriko, Maekawa Tatsuya, Miyajima Katsuhiro

    Fundamental Toxicological Sciences   11 ( 4 )   159 - 168   2024

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    Language:English   Publisher: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

  • Effects of <i>Siraitia grosvenorii</i> extract on nonalcoholic steatohepatitis-like lesions in Sprague Dawley rats fed a choline-deficient, methionine-lowered, l-amino acid-defined diet

    Uno Kinuko, Miyajima Katsuhiro, Ogawa Shuji, Suzuki-Kemuriyama Noriko, Nakae Dai

    Journal of Toxicologic Pathology   36 ( 1 )   1 - 10   2023

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    Language:English   Publisher:JAPANESE SOCIETY OF TOXICOLOGIC PATHOLOGY  

    <p><i>Siraitia grosvenorii</i> is the fruit of a cucurbitaceous vine endemic to China. Its extract has been used as a sweetener and exhibits various anti-inflammatory and anticarcinogenic effects mediated via its antioxidant properties. In the present study, we aimed to clarify the preventive or ameliorative effects of <i>S. grosvenorii</i> extract (SGE) on nonalcoholic steatohepatitis-like lesions induced in male Hsd: Sprague Dawley rats fed a choline-deficient, methionine-lowered, <span style="font-variant: small-caps;">l-</span>amino acid-defined diet for 13 weeks. This diet increased hepatotoxicity parameters and upregulated the expression of inflammation- and fibrosis-related genes in the liver, resulting in the progression of hepatic lesions, oxidative stress, hepatocellular apoptosis, and fibrosis. Furthermore, this diet upregulated the expression of phosphorylated nuclear factor-κB (NF-κB) and CD44. SGE administration inhibited these lesions, similar to CD44, a factor that controls hepatic inflammation and fibrosis. These results revealed that SGE impacts the disease stage via antioxidative effects and regulation of CD44 expression. SGE was found to be useful for preventing and treating steatohepatitis.</p>

    DOI: 10.1293/tox.2022-0043

  • Effects of salt supplementation in uninephrectomized KK-Ay mice: Examining the potential of a diabetic kidney disease model

    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

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    Language:English   Publisher: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

    PubMed

  • Important Points at Interpretation ofNongenotoxic-Carcinogenicity Induced by Pesticidesin Rodent Bioassays

    Satoh Hiroshi, Machino Satoshi, Fujii Tatsuya, Yoshida Midori, Asano Satoshi, Yokoyama Yoko, Miyajima Katsuhiro

    Food Hygiene and Safety Science (Shokuhin Eiseigaku Zasshi)   63 ( 1 )   34 - 42   2022.02

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    Language:Japanese   Publisher:Japanese Society for Food Hygiene and Safety  

    <p>Assessment of carcinogenicity is important for human health at dietary risk assessment of pesticide residues. This article indicated important points on interpretation of carcinogenicity in toxicological evaluation of pesticide residues based on principles of risk analysis in foods by CODEX to be a guide for risk assessors. This guidance was referred from the guidance on carcinogenicity evaluation by international and/or national organizations, and the interpretations of Food Safety Commissions of Japan (FSCJ) published in their risk assessment reports. We focused on carcinogenicity obtained from routine carcinogenicity bioassays in rodents. The guidance includes the purpose and usefulness of the bioassay studies, consideration points to be carcinogenicity and influencing factors to carcinogenicity in the test to judge carcinogenic hazard at hazard identification. Considering on human relevance as carcinogenic hazard also was proposed using practical case examples. Next, a carcinogenic hazard is evaluated on dose-response relationship to judge points of departure on carcinogenicity. At the end of this article, we challenged our recommendation on future assessment of carcinogenicity to progress from hazard to risk.</p>

    DOI: 10.3358/shokueishi.63.34

    PubMed

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Committee Memberships 【 display / non-display

  • 食品安全委員会農薬専門調査会   専門委員  

    2016.04   

  • The Japanese Society of Toxicology   Diplomate of the Japanese Society of Toxicology (JSOT)  

    2005.10   

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    Committee type:Academic society

  • The Japanese Society of Toxicology   Councilor  

    2016.07   

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    Committee type:Academic society

  • The Japanese Society of Toxicological Pathology   Diplomate of Japanese Society of Toxicologic Pathology (JSTP)  

    1999.10   

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    Committee type:Academic society

  • The Japanese Society of Toxicological Pathology   Councilor  

    2014.04   

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    Committee type:Academic society

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