Unraveling the mechanisms of exercise-mimicking adiponectin receptor signaling

2016 Fiscal Year Final Research Report

• Project/Area Number: 26713032
• Research Category: Grant-in-Aid for Young Scientists (A)
• Allocation Type: Partial Multi-year Fund
• Research Field: Metabolomics
• Research Institution: The University of Tokyo
• Principal Investigator: Masato Iwabu 東京大学, 医学部附属病院, 特任准教授 (30557236)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 糖尿病 / シグナル伝達 / アディポネクチン

Outline of Final Research Achievements

So far, we have shown that the dramatic upsurge of type 2 diabetes responsible for cardiovascular disease as the leading cause of mortality in Japan is primarily accounted for by the decreased action of adiponectin/adiponectin receptor (AdipoR) signaling and that adiponectin/AdipoR1 are involved in the regulation of mitochondrial functions and exert exercise-mimicking effects in the skeletal muscle. In the process, our research has been instrumental in unraveling potential mechanisms involved in AMPK activation by adiponectin/AdipoR1 through successful conformational analysis of the AdipoRs but also in identifying novel key molecules involved in exercise-mimicking adiponectin/AdipoR1 signaling, thereby unraveling a novel mechanism of metabolic regulation involving AdipoR1.

Free Research Field

糖尿病学