Investigation of the role of entero-pancreatic endocrine cells on high-carbohydrate-induced body weight gain

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K09823
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Metabolomics
• Research Institution: Fujita Health University (2018-2019); Nagoya University (2017)
• Principal Investigator: Seino Yusuke 藤田医科大学, 医学部, 講師 (80534833)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: ショ糖 / スターチ / GIP / インスリン / β細胞量 / 肥満 / 餌スイッチ / KATP チャネル

Outline of Final Research Achievements

Mice fed a high-sucrose diet show resistance to body weight gain, in comparison with mice fed a high-starch diet (ST) or control diet, which is due to increased energy expenditure. In mice fed ST, GIP plays a minor role while excessive insulin secretion plays an important role in body weight gain. ST also increases beta-cell mass (BCM) in a KATP channel-dependent manner, which is mediated through upregulation of cyclinD2 expression. Furthermore, short term loading to ST induces an increase in BCM in a manner independent of body weight gain, which is mediated through upregulation of cyclinA2 expression. In addition, 2 weeks of control diet feeding is sufficient for reversal of the morphological changes induced in islets by ST feeding.

Free Research Field

代謝・栄養学

Academic Significance and Societal Importance of the Research Achievements

ショ糖とでんぷん（スターチ）では同じ糖質でも糖代謝・体重に全く異なる影響を及ぼすことが明らかとなった。また脂質やでんぷんの過剰摂取は肥満を引き起こすが、脂質においてはGIPがでんぷんにおいてはインスリンが肥満に関与することを明らかにした。本研究で明らかとなった機序が、糖尿病・肥満患者に対する栄養指導や薬物療法の向上に貢献できると考えられた。