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Articles in PresS, published online ahead of print March 12, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00553.2001
Submitted on December 18, 2001
Accepted on March 5, 2002
1 Department of Kinesiology, University of Southern California, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: ajy{at}usc.edu.
Insulin has been shown to alter long-chain fatty acid (LCFA) metabolism and malonyl-CoA production in muscle. However, these alterations may have been induced in part by the accompanying insulin-induced changes in glucose uptake. Thus to determine the effects of insulin on LCFA metabolism independent of changes in glucose uptake, rat hindquarters were perfused with 600 µM palmitate and [1-14C]palmitate and with either 20 mM glucose and no insulin (G) or 6 mM glucose and 250 µU/ml of insulin (I). As dictated by our protocol, glucose uptake was not significantly different between the G and I groups (11.0±0.5 vs. 11.5±1.2 µmol/g-1/hr-1) (P > 0.05). Total palmitate uptake and oxidation were not significantly different (P > 0.05) between the G (10.1±1.0 and 0.8±0.1 nmol/min-1/g-1) and I (10.2±0.6 and 1.1±0.2 nmol/min-1/g -1) groups. Pre-perfusion muscle triglyceride and malonyl-CoA levels were not significantly different between the G and I groups and did not change significantly during the perfusion (P > 0.05). Similarly, muscle triglyceride synthesis was not significantly different between groups (P > 0.05). These results demonstrate that the presence of insulin under conditions of similar glucose uptake does not alter LCFA metabolism and suggest that cellular mechanisms induced by carbohydrate availability, but independent of insulin, may be important in the regulation of muscle LCFA metabolism.
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