| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Research Abstract |
In this study, to gain insight into the role of Akt in heart and SKM, we ablated Akt1 and Akt2 by crossing Akt1 and Akt2 floxed mice with MCK-Cre or MLC1-Cre transgenic mice, respectively, resulting in both heart and SKM specific Akt1/Akt2 knockout (M-Akt1/2DKO)mice or SKM specific Akt1/Akt2 knockout (MLC1-Akt1/2DKO) mice. M-Akt1/2DKO mice died within 5 weeks after birth due to heart failure. Quantitative RT-PCR analysis revealed genes regulating oxidative phosphorylation were decreased significantly in the heart of M-Akt1/2DKO mice. In MLC1-Akt1/2DKO mice, the body weight and skeletal muscle volume were decreased at 6 weeks after birth, and showed impaired glucose tolerance and insulin resistance at 32 weeks.
These data suggest that Akt1 and Akt2 play an important role for maintaining heart and SKM growth and function by regulating mitochondrial energy metabolism and controlling quantity and quality of skeletal muscle which are involved in glucose metabolism in whole body.
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