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1 Departments of Kinesiology and Biological Sciences, Diabetes Research Center, University of Southern California, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: turcotte{at}usc.edu.
To determine the role of AMPK activation on the regulation of FA uptake and oxidation, we perfused rat hindquarters with 6 mM glucose, 10 µU/ml insulin, 550 µM palmitate, and [14C]palmitate during rest (R) or electrical stimulation (ES) inducing low intensity (0.1 Hz) muscle contraction either with or without 2 mM AICAR. AICAR treatment significantly increased glucose and FA uptake during R (P<0.05) but had no effect on either variable during ES (P>0.05). AICAR treatment significantly increased total FA oxidation (P<0.05) during both R (0.38±0.11 vs 0.89±0.1 nmol.min-1.g-1) and ES (0.73±0.11 vs 2.01±0.1 nmol.min-1.g-1) which was paralleled in both conditions by a significant increase and significant decrease in AMPK and acetyl-CoA carboxylase (ACC) activity respectively (P<0.05). Low intensity muscle contraction increased glucose uptake, FA uptake and total FA oxidation (P<0.05) despite no change in AMPK (950.5±35.9 vs 1067.7±58.8 nmol.min-1.g-1) or ACC (51.2±6.7 vs 55.7±2.0 nmol.min- 1.g-1) activity from R to ES (P>0.05). When contraction and AICAR treatment were combined, the AICAR-induced increase in AMPK activity (34%) did not account for the synergistic increase in FA oxidation (175%) observed under similar conditions. These results suggest that while AMPK-dependent mechanisms may regulate FA uptake and FA oxidation at rest, AMPK-independent mechanisms predominate during low intensity muscle contraction.
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