2012 Fiscal Year Final Research Report

Physiological functions of MIC/TRPM7 channels in white adipocytes

Research Project

Project/Area Number	22790220
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Single-year Grants
Research Field	General physiology
Research Institution	Tokyo Medical University
Principal Investigator	INOUE Hana 東京医科大学, 医学部, 講師 (20390700)
Project Period (FY)	2010 – 2012
Keywords	イオンチャネル / 白色脂肪細胞
Research Abstract	We revealed that white adipocytes isolated from mice as well as differentiated 3T3L1 adipocytes functionally expressed magnesium-inhibited cation (MIC) channel whose molecular identity is thought to be TRPM7. TRPM7 has been reported to be activated by oxidative stress, however, MIC current recorded in adipocytes were inhibited by oxidative stress induced by exposure to hydrogen peroxide and N-methylmaleimide. In the presence of these reagents as well as a conventional TRPM7 inhibitor, 2-aminopyrideine, insulin-dependent glucose uptake was largely inhibited in 3T3L1 adipocytes. Thus, it is suggested that MIC/TRPM7 channel activity is required for the insulin-dependent glucose uptake in adipocytes.

(5 results)