| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2009: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Research Abstract |
Type 2 diabetes and obesity are characterized by insulin resistance in skeletal muscle. It has been well demonstrated that exercise increase insulin sensitivity in skeletal muscle. However, it remains still unclear how a single bout exercise enhance subsequent insulin sensitivity. Recently, it has been reported that macrophages, at least partly, regulate insulin sensitivity in several insulin target organs. We, therefore, hypothesized that macrophages are involved in the mechanisms of exercise-induced enhancement of insulin sensitivity in skeletal muscle. To test this hypothesis, we injected saline (SAL) or clodronate liposome (CL), a macrophage suppressor, to C57BL6J mice. Then, mice were subjected to a single bout of treadmill running. Twenty-four hour after exercise, we measured ex-vivo insulin-stimulated 2-deoxy glucose (DG) uptake in skeletal muscle. We observed that a single bout exercise enhanced macrophage accumulation and insulin-stimulated 2-DG uptake in plantaris muscle in SAL group. However, CL treatment completely abolished these changes. We also observed that phosphorylation state of Akt, AS160 and AMPK were not changed by CL treatment. From these results, we conclude that macrophages are involved in the mechanisms of exercise-induced enhancement of insulin sensitivity in skeletal muscle, independent of Akt and AMPK phosphorylation states.
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