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2023 Fiscal Year Final Research Report

Roles of four FoxO isoforms on insulin resistance and longevity

Research Project

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Project/Area Number 21K08570
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 54040:Metabolism and endocrinology-related
Research InstitutionChiba University

Principal Investigator

Ono Hiraku  千葉大学, 大学院医学研究院, 准教授 (10570616)

Project Period (FY) 2021-04-01 – 2024-03-31
Keywords加齢 / インスリン抵抗性 / マウス
Outline of Final Research Achievements

Center of the pathology of type 2 diabetes (T2D) is hyperglycemia due to insulin resistance. T2D usually occurs in mid-age, thus aging is believed to enhance insulin resistance. In contrast to this popular theory, in the present study we found that the insulin resistance once occurred in mid-age later disappears in presenile to old age in mice. Part of this biphasic insulin resistance is explained by obesity, but some part of the amelioration of insulin resistance during the presenile to old age period is independent from body weight or fat deposition in tissues, suggesting that aging in later life itself improves insulin sensitivity. This natural improvement of insulin resistance in later life may exist even in human, elucidation of whose mechanism may be clue to find new drugs.

Free Research Field

代謝学

Academic Significance and Societal Importance of the Research Achievements

日本では加齢に伴い疾患が生じ,また健康状態が自然に悪化するという先入観が強い。しかし,それはすべての身体機能において証明されているわけではない。本研究において我々は,2型糖尿病の病態生理の本体であるインスリン抵抗性は,少なくともマウスにおいては,中年では悪化するものの老年期において自然に回復することを証明した。振り返って臨床の現場でも,中年期に発症した2型糖尿病が老年期に悪化してゆく患者は必ずしも多くない。ヒトにおいてもある年齢を過ぎると,加齢そのものが体重や肥満度とは無関係にインスリンの感受性を回復させる可能性を持つことが推測され,その仕組みを見出すことで創薬の手掛かりとなる可能性を持つ。

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Published: 2025-01-30  

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