The impact of ACAM/CLMP on the adipocytes differentiation and obesity through the primary ciliary machinery

2016 Fiscal Year Final Research Report

• Project/Area Number: 26461362
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Metabolomics
• Research Institution: Okayama University
• Principal Investigator: Murakami Kazutoshi 岡山大学, 医学部, 客員研究員 (40620753)
• Research Collaborator: WADA JUN 岡山大学, 大学院医歯薬学総合研究科, 教授 ; EGUCHI JUN 岡山大学, 大学病院, 講師 ; NAKATSUKA ATSUKO 岡山大学, 大学病院, 助教
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 脂肪細胞 / メタボリックシンドローム / 肥満症 / 膜蛋白 / 接着分子 / アドヘレンスジャンクション / アクチン

Outline of Final Research Achievements

The excess of lipid accumulation and hypertrophy of adipocytes induces the abnormality of secretion of adipokines and hormones from adipocytes and causes metabolic syndrome and diabetes. We identified ACAM in 2005 from the visceral fat tissue of obese rats. It is a cell adhesion molecule responsible for the homophilic adhesion of the cells. In the transgemic mice overexpressing ACAM in adipocytes fed with a high fat and high sucrose diet were protected from the onset of obesity and diabetes. In transgemnic mice, ACAM is abundantly expressed on plasma membrane of mature adipocytes and associated with formation of Phalloidin-positive polymerized form of cortical actin (F-actin). By electron microscopy, the structure of zonula adherens was formed at interphase of adipocytes. The adhesion of adipocytes and formation of cortical actin prevent the adipocyte hypertrophy and development of obesity and diabetes.

Free Research Field

糖尿病学