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Department of Kinesiology, University of Southern California, Los Angeles, California 90089
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 independently 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 (10.3 ± 0.6 vs. 11.0 ± 0.5 µmol · g
1 · h1;
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 · min1 · g1) and I
(10.2 ± 0.6 and 1.1 ± 0.2 nmol · min1 · g1) groups.
Preperfusion 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.
malonyl-coenzyme A; fatty acid oxidation; fatty acid uptake; triglyceride synthesis; intramuscular triglycerides; long-chain fatty acids
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