Fatty acid dynamics as insulin secretion capacity regulating factor: analysis in human islets

2019 Fiscal Year Final Research Report

• Project/Area Number: 17KK0184
• Research Category: Fund for the Promotion of Joint International Research (Fostering Joint International Research)
• Allocation Type: Multi-year Fund
• Research Field: Experimental pathology
• Research Institution: Tohoku University
• Principal Investigator: Asai Akira 東北大学, 農学研究科, 特任准教授 (30500011)
• Project Period (FY): 2018 – 2019
• Keywords: インスリン分泌 / ヒト膵島 / β細胞 / 脂肪毒性 / 糖尿病 / モデル動物

Outline of Final Research Achievements

Based on the differences in the expression levels of molecules involved in metabolism and transport of fatty acids and lipids in pancreatic islets of diabetes-prone (Prone) and diabetes-resistant (Resistant) mice, we examined whether similar findings were observed in human islets. The expression level of CD36 (also known as fatty acid translocase), which is higher in Prone mouse than in Resistant mice, was found to be higher in obese individuals with type 2 diabetes than those with normal glucose tolerance. In addition, as well as in mice, CD36 was expressed on the cell surface of pancreatic beta cells in humans.

Free Research Field

代謝学

Academic Significance and Societal Importance of the Research Achievements

Prone系とResistant系の両系統マウスは、多遺伝子性の遺伝的要因と環境的要因との相互作用というヒトにおける2型糖尿病発症基盤を反映して作出されたモデル動物である。両系統マウス間で遺伝的なインスリン分泌能の差異を規定する可能性のある候補因子について、マウスとヒトとの類似性を示した本研究の成果は、両系統マウスの「2型糖尿病発症における膵島病理基盤モデル」としての有用性を確かなものとし、新たな糖尿病予防・治療法開発に繋がる基礎的知見となるものと考えられる。