| Budget Amount *help |
¥16,600,000 (Direct Cost: ¥16,600,000)
Fiscal Year 2004: ¥4,300,000 (Direct Cost: ¥4,300,000)
Fiscal Year 2003: ¥12,300,000 (Direct Cost: ¥12,300,000)
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| Research Abstract |
In order to clarify the mechanism(s) behind either exercise- or exercise training-induced suppression of fat mass, the following studies were performed in rat adipocytes : (1)effects of exercise on apoptotic and anti-apoptotic signals, (2)effects of exercise and diet on several genes related with lipid metabolism, (3)effects of exercise on tumor necrosis factor-α (TNF-α)-induced apoptotic and anti-apoptotic signals, (4)effect of exercise training on insulin secretion from pancreatic islets, (5)alterations in exercise-induced β-adrenergic receptors and G proteins. As a result, the following findings were obtained. Exercise increased the Bcl2/Bax ratio in retroperitoneal and inguinal adipose tissue, but decreased its ratio in epididymal adipose tissue. Starvation reduced the expressions of some lipogenic genes, and re-feeding enhanced these expressions. Exercise after re-feeding blocked re-feeding-induced enhancement of some lipogenic genes expressions. Exercise training enhanced TNF-α signaling directed toward the expressions of survival signals and the suppression of fatty acid synthase gene expression. The mechanism behind exercise training-induced reduction of insulin secretion may involve an enhanced expression of neuronal nitric oxide synthase and a decreased expression of Gαi-2 protein. Acute exercise altered the expression of Giα2 protein via the ubiquitin-proteasome pathway, and the mechanism underlying the increased density of β_2-AR after exercise may involve alterations in a multi-step event involving the coordinate interaction among proteins mediating β_2-AR trafficking, e.g. G-protein-coupled receptor kinase-2 and β-arrestin-2. Thus, the data obtained in this grant will become helpful to understand more exact mechanism behind exercise training-induced suppression of fat mass.
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