| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
Angiotensin II type 1 receptor (AT1R) is a major player in the signal transduction of renin-angiotensin system, and the overactivation of this signaling contributes to the progression of visceral obesity. AT1R-associated protein (ATRAP) promotes AT1R internalization along with the suppression of overactivation of tissue AT1R signaling. We demonstrated that the enhancement of ATRAP in adipose tissue ameliorated high-fat diet-induced visceral obesity and insulin resistance via the attenuation of overactivated AT1R signaling and adipose inflammation. Furthermore, we revealed that low-dose angiotensin II administration could promote the insulin resistance even in a lean type, and this finding was mainly caused by the dysfunction of glucose uptake in skeletal muscle due to increased oxidative stress. The enhancement of ATRAP in skeletal muscle ameliorated this insulin resistance in a lean type via the attenuation of overactivated AT1R signaling and oxidative stress in skeletal muscle.
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