Elucidation of the mechanism of GPCR-mediated regulation of Adiponectin in intestinal cells to its anti-diabetic effects.

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K11532
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 59040:Nutrition science and health science-related
• Research Institution: 株式会社レオロジー機能食品研究所
• Principal Investigator: Niwase Shamim 株式会社レオロジー機能食品研究所, 未登録, 基礎研究部長 (40647707)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: GPCR61 / Plasmalogens / Adiponectin / Fatty liver / Intestinal cells / Central nervous system

Outline of Final Research Achievements

GPCR61 showed to regulate the expression of Adiponectin in intestinal cells and the oral ingestion of plasmalogens (Pls), which is the ligands of GPCR61 induced expression of Apiponectin, suggesting that Pls-GPCR61 signaling enhance adiponectin to reduce diabetic syndrome such as fat-deposition in the tissues including liver. WE successfully generated GPCR61 knockout (KO) mice which showed increased body weight marked with fatty liver. Next generation sequencing (RNASeq) data using the GPCR61 revealed a comprehensive mechanism of GPCR61 signaling in mice tissues including brain and immune cells. Our present research provided important clues in understanding the role of GPCR61 not only in the intestine but also in the brain tissues and immune cells.

Free Research Field

Molecular mechanism of diseases

Academic Significance and Societal Importance of the Research Achievements

This research provides a possible mechanism how we are susceptible to diabetes and other diseases during aging process when GPCR61 and plasmalogens are reduced. Therefore, this study could help in finding future therapeutics to cure various aging-related diseases including diabetes.