FUJITA Hiroki

写真a

Affiliation

Graduate School of Medicine  Doctorial Course in Medicine  Bioregulatory Medicine  Department of Metabolism and Endocrinology
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Research Interests 【 display / non-display 】

  • Extra-pancreatic actions of incretin

  • Diabetic nephropathy and oxidative stress

  • Development of mouse models of diabetic nephropathy

  • Renal protective effect of GLP-1

  • Frailty, sarcopenia, cognitive impairment in older people with diabetes

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Graduating School 【 display / non-display 】

  • 　
    -
    1995.03

    Niigata University   Faculty of Medicine   Graduated

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Graduate School 【 display / non-display 】

  • 　
    -
    2001.03

    Akita University  Graduate School,Division of Medicine  Doctor's Course  Completed

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Campus Career 【 display / non-display 】

  • 2018.04
    -
    Now

    Akita University   Graduate School of Medicine   Doctorial Course in Medicine   Bioregulatory Medicine   Associate Professor  

  • 2007.10
    -
    2018.03

    Akita University   Hospital   Geriatrics   Lecturer  

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Research Areas 【 display / non-display 】

  • Life Science / General internal medicine

  • Life Science / Nephrology

  • Life Science / Metabolism and endocrinology

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Research Achievements 【 display / non-display 】

    ◆Original paper【 display / non-display 】

  • Gastric inhibitory polypeptide receptor antagonism suppresses intramuscular adipose tissue accumulation and ameliorates sarcopenia

    Takahashi Y.

    Journal of Cachexia, Sarcopenia and Muscle ( Journal of Cachexia, Sarcopenia and Muscle )  14 ( 6 ) 2703 - 2718   2023.12  [Refereed]

    Research paper (journal)   Domestic Co-author

    BACKGROUND: Intramuscular adipose tissue (IMAT) formation derived from muscle fibro-adipogenic progenitors (FAPs) has been recognized as a pathological feature of sarcopenia. This study aimed to explore whether genetic and pharmacological gastric inhibitory polypeptide (GIP) receptor antagonism suppresses IMAT accumulation and ameliorates sarcopenia in mice. METHODS: Whole body composition, grip strength, skeletal muscle weight, tibialis anterior (TA) muscle fibre cross-sectional area (CSA) and TA muscle IMAT area were measured in young and aged male C57BL/6 strain GIP receptor (Gipr)-knockout (Gipr-/- ) and wild-type (Gipr+/+ ) mice. FAPs isolated from lower limb muscles of 12-week-old Gipr+/+ mice were cultured with GIP, and their differentiation into mature adipocytes was examined. Furthermore, TA muscle IMAT area and fibre CSA were measured in untreated Gipr-/- mice and GIP receptor antagonist-treated Gipr+/+ mice after glycerol injection into the TA muscles. RESULTS: Body composition analysis revealed that 104-week-old Gipr-/- mice had a greater proportion of lean tissue mass (73.7 ± 1.2% vs. 66.5 ± 2.7%, P < 0.05 vs. 104-week-old Gipr+/+ mice) and less adipose tissue mass (13.1 ± 1.3% vs. 19.4 ± 2.6%, P < 0.05 vs. 104-week-old Gipr+/+ mice). Eighty-four-week-old Gipr-/- mice exhibited increases in grip strength (P < 0.05), weights of TA (P < 0.05), soleus (P < 0.01), gastrocnemius (P < 0.05) and quadriceps femoris (P < 0.01) muscles, and average TA muscle fibre CSA (P < 0.05) along with a reduction in TA muscle IMAT area assessed by the number of perilipin-positive cells (P < 0.0001) compared with 84-week-old Gipr+/+ mice. Oil Red O staining analysis revealed 1.6- and 1.7-fold increased adipogenesis in muscle FAPs cultured with 10 and 100 nM of GIP (P < 0.01 and P < 0.001 vs. 0 nM of GIP, respectively). Furthermore, both untreated Gipr-/- mice and GIP receptor antagonist-treated Gipr+/+ mice for 14 days after glycerol injection into the TA muscles at 12 weeks of age showed reduced TA muscle IMAT area (1.39 ± 0.38% and 2.65 ± 0.36% vs. 6.54 ± 1.30%, P < 0.001 and P < 0.01 vs. untreated Gipr+/+ mice, respectively) and increased average TA muscle fibre CSA (P < 0.01 and P < 0.05 vs. untreated Gipr+/+ mice, respectively). CONCLUSIONS: GIP promotes the differentiation of muscle FAPs into adipocytes and its receptor antagonism suppresses IMAT accumulation and promotes muscle regeneration. Pharmacological GIP receptor antagonism may serve as a novel therapeutic approach for sarcopenia.

    DOI PubMed

  • Efficacy and Safety of 6-Month High Dietary Protein Intake in Hospitalized Adults Aged 75 or Older at Nutritional Risk: An Exploratory, Randomized, Controlled Study

    Shota Moyama, Yuichiro Yamada, Noboru Makabe, Hiroki Fujita, Atsushi Araki, Atsushi Suzuki, Yusuke Seino, Kenichiro Shide, Kyoko Kimura, Kenta Murotani, Hiroto Honda, Mariko Kobayashi, Satoshi Fujita, Koichiro Yasuda, Akira Kuroe, Katsushi Tsukiyama, Yutaka Seino, Daisuke Yabe

    Nutrients     2023.04  [Refereed]

    Research paper (journal)   Domestic Co-author

  • Relationships among Postprandial Plasma Active GLP-1 and GIP Excursions, Skeletal Muscle Mass, and Body Fat Mass in Patients with Type 2 Diabetes Treated with Either Miglitol, Sitagliptin, or Their Combination: A Secondary Analysis of the MASTER Study.

    Masahiro Sato, Hiroki Fujita, Hiroki Yokoyama, Atsushi Mikada, Yohei Horikawa, Yuya Takahashi, Yuichiro Yamada, Hironori Waki, Takuma Narita

    Journal of clinical medicine   12 ( 9 )   2023.04  [Refereed]

    Research paper (journal)  

    DOI PubMed

  • Dual inhibition of SGLT2 and DPP-4 promotes natriuresis and improves glomerular hemodynamic abnormalities in KK/Ta-Ins2<sup>Akita</sup> mice with progressive diabetic kidney disease

    Fujita H.

    Biochemical and Biophysical Research Communications ( Biochemical and Biophysical Research Communications )  635   84 - 91   2022.12  [Refereed]

    Research paper (journal)   Domestic Co-author

    DOI

  • Cases of fulminant type 1 and type 2 diabetes mellitus whose HbA1c levels were unmeasurable due to increased labile HbA1c

    Kato S.

    Diabetology International ( Diabetology International )  13 ( 4 ) 698 - 703   2022.10  [Refereed]

    Research paper (journal)   Domestic Co-author

    DOI

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    ◆Other【 display / non-display 】

  • 腸管がつなぐ栄養・代謝・糖尿病 生体防御の調節因子としてのGLP-1(GLP-1 as a regulator of biological defense)

    佐藤 雄大, 山田 祐一郎, 藤田 浩樹, 清水 辰徳, 加藤 俊祐

    糖尿病 ( (一社)日本糖尿病学会 )  62 ( Suppl.1 ) S - 16   2019.04

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Grant-in-Aid for Scientific Research 【 display / non-display 】

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