Physiological functions of MIC/TRPM7 channels in white adipocytes
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
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
Keywords | イオンチャネル / 白色脂肪細胞 / TRPM7 / 生理学 / 白色脂肪脂肪細胞 |
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.
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Report
(4 results)
Research Products
(12 results)