Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 2002: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
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Research Abstract |
A possible role of nitric oxide (NO) on adipocyte lipolysis was studied in exercise-trained (9 weeks of running) rats. Lipolysis in adipose tissue tended to be greater in trained rats than in control rats. Treatment of adipose tissue with 5 mM N^G -nitro-L-arginine methyl ester (L-NAME) showed that both basal and isoproterenol-stimulated lipolysis were significantly greater in trained rats than in control rats. In contrast, in isolated adipocytes, L-NAME had no effect on lipolysis in either group of rats, although the lipolysis of isolated adipocytes was significantly greater in trained rats than in control rats. Training significantly reduced nitrite/nitrate production in adipocytes but not in tissue. On the other hand, training increased the protein expression of endothelial nitric oxide synthase (eNOS) but not that of inducible NOS (iNOS) in the extracts of tissue homogenates. In tissue homogenates, eNOS activity but not iNOS activity was significantly greater in trained rats than in control rats. In cellular extracts, training significantly reduced the activites of both NOSs, but the mRNA expressions of both NOSs were not different between groups. The NO donor, S-nitroso-N-acetyl-penicillamine (SNAP), significantly inhibited adipocyte lipolysis in response to isoproterenol in both groups. This inhibitory effect of SNAP was greater in the adipocytes of trained rats than in those of the control rats. Thus, it is possible that NO is involved in the regulation of lipolysis and that exercise training enhances the responsiveness of adipocytes to extracellular NO with the reduced production of nitrite/nitrate in adipocytes due to decreased activites of NOSs. On the other hand, it is also possible that exercise increases either the activity or protein expression of eNOS in adipose tissue.
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