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Preventive effect of biotin in the hypothalamus and pancreatic islets on the development of type 2 diabetes

Research Project

Project/Area Number 15K00825
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Eating habits
Research InstitutionUniversity of Niigata Prefecture

Principal Investigator

Sone Hideyuki  新潟県立大学, 人間生活学部, 教授 (90398511)

Research Collaborator KAMIYAMA Shin  新潟県立大学, 人間生活学部, 准教授 (70525401)
Project Period (FY) 2015-04-01 – 2019-03-31
Project Status Completed (Fiscal Year 2018)
Budget Amount *help
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Keywordsビオチン / 摂食抑制 / 肥満 / 脂質代謝亢進 / 高脂肪食 / 2型糖尿病 / glucokinase / 視床下部 / 膵島細胞 / 膵β細胞 / グルコキナーゼ
Outline of Final Research Achievements

In the present study, we investigated the preventive effect of biotin on the development of type 2 diabetes. We showed that biotin suppressed food intake and body weight gain and increased pancreatic islet cell division. Additionally, biotin elevated the expression of glucokinase gene in both the hypothalamus and pancreatic islets. Glucokinase leads to excitation of the glucose-responsible neuron in hypothalamus which resulted in satiety, and to activation of the IRS-2 pathway which further resulted in the promotion of pancreatic islet cell division to preserve normal function. Moreover, biotin strongly suppressed body weight gain in high-fat diet induced obesity mice via the acceleration of fat catabolism. These findings suggest that biotin prevents obesity and hyperglycemia via the suppression of food intake by inducing satiety, elevation of fat metabolism, and the maintenance of normal pancreatic islet function, leading to the prevention of the development of type 2 diabetes.

Academic Significance and Societal Importance of the Research Achievements

本研究は、ビオチンが高血糖に応答する共通分子としてグルコキナーゼを介し膵島細胞と視床下部を調節することにより、日本人2型糖尿病(非肥満型)を予防するといった新たな発想に基づいている。ビオチンは過剰症の心配のない水溶性のビタミンであり、生体にとってより安全な使用が可能である。また、過食と膵β細胞の量的不足は多くの2型糖尿病に共通する発症要因であり、疾病予防・改善の両面で応用範囲が広く有効性も高いと考えられる。本研究の中核的な課題の1つであるビオチンによるエピゲノム制御は、栄養素による2型糖尿病の新たな予防・治療法の先行研究として多くの注目を集め、今後の研究・教育面において幅広く活用できる。

Report

(5 results)
  • 2018 Annual Research Report   Final Research Report ( PDF )
  • 2017 Research-status Report
  • 2016 Research-status Report
  • 2015 Research-status Report
  • Research Products

    (3 results)

All 2018 2016

All Journal Article (1 results) (of which Peer Reviewed: 1 results,  Acknowledgement Compliant: 1 results) Presentation (2 results)

  • [Journal Article] Biotin augments acetyl CoA carboxylase 2 gene expression in the hypothalamus, leading to the suppression of food intake in mice2016

    • Author(s)
      Hideyuki Sone, Shin Kamiyama, Mutsumi Higuchi, Kaho Fujino, Shizuka Kubo, Masami Miyazawa, Saya Shirato, Kota Shiowaza
    • Journal Title

      Biochemical and Biophysical Research Communications

      Volume: 476 Issue: 3 Pages: 134-139

    • DOI

      10.1016/j.bbrc.2016.04.152

    • Related Report
      2016 Research-status Report
    • Peer Reviewed / Acknowledgement Compliant
  • [Presentation] リポタンパク質を介したビオチンの新規体内輸送経路について2018

    • Author(s)
      曽根英行、野上咲絵、塩沢浩太、神山伸
    • Organizer
      微量栄養素学会
    • Related Report
      2018 Annual Research Report
  • [Presentation] ビオチンによる摂食抑制作用と視床下部ACC-βの遺伝子発現調節について2016

    • Author(s)
      曽根英行、神山伸
    • Organizer
      日本ビタミン学会
    • Place of Presentation
      富山
    • Year and Date
      2016-06-17
    • Related Report
      2016 Research-status Report

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Published: 2015-04-16   Modified: 2020-03-30  

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