Autonomic nerve-mediated regulation of adipose tissue metabolism: parasympathetic nervous system and adiponectin secretion

2023 Fiscal Year Final Research Report

• Project/Area Number: 21K19496
• Research Category: Grant-in-Aid for Challenging Research (Exploratory)
• Allocation Type: Multi-year Fund
• Review Section: Medium-sized Section 54:Internal medicine of the bio-information integration and related fields
• Research Institution: The University of Tokyo
• Principal Investigator: Kubota Naoto 東京大学, 医学部附属病院, 届出研究員 (50396719)
• Co-Investigator(Kenkyū-buntansha): 窪田 哲也 公益財団法人朝日生命成人病研究所, その他部局等, 教授(移行) (60385698) ; 相原 允一 東京大学, 医学部附属病院, 助教 (60779362)
• Project Period (FY): 2021-07-09 – 2024-03-31
• Keywords: アディポネクチン

Outline of Final Research Achievements

Adiponectin has been identified as an insulin-sensitive hormone, and its decrease with obesity is thought to be causes of insulin resistance, but the regulatory mechanism is still not fully understood. In this study, we found that adiponectin is increased in a model of disrupted hypothalamic ventral medial nucleus (VMH) despite the presence of obesity, indicating that adiponectin secretion is regulated by the autonomic nervous system. The expression of PPARγ and FGF21 was upregulated in the adipose tissue of VMH-disrupted mice, suggesting that these molecules regulate adiponectin secretion independently of obesity.

Free Research Field

糖尿病

Academic Significance and Societal Importance of the Research Achievements

インスリン感受性ホルモンであるアディポネクチンが抗糖尿病作用・抗動脈硬化作用を有していることに関しては既に国内外から数多くの報告があったが、その分泌調節機構や病態における破綻のメカニズムについてはなお十分な知見が得られていなかった。本研究は、長年課題とされてきた“アディポネクチンの生理的な分泌調節機構とその破綻の分子メカニズム”の一端を解明し、新規肥満インスリン抵抗性治療開発につながる可能性がある。