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1 Department of Surgical Science and Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden
2 Department of Kinesiology, University of Wisconsin-Madison, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: gcartee{at}umich.edu.
Exposing isolated rat skeletal muscle to 5-aminoimidazole-4-carboxamide-1-
-D-ribofuranoside
(AICAR, a pharmacological activator of AMP-activated protein kinase,
AMPK) plus serum leads to a subsequent increase in insulin-stimulated glucose transport
(Fisher et al. Am. J. Physiol. 282: E18-E23, 2002). Our goal was to determine if
preincubation of primary human skeletal muscle cells with human serum and AICAR
(Serum+AICAR) would also induce a subsequent elevation in insulin-stimulated glucose
uptake. Cells were preincubated for 1 h under 4 conditions: 1) without AICAR or serum
(Control), 2) with serum, 3) with AICAR, or 4) with Serum+AICAR. Some cells were
then collected for immunoblot analysis to assess phosphorylation of AMPK (pAMPK)
and its substrate acetyl CoA carboxylase (ACC). Other cells were incubated for 4
additional h without AICAR or serum and then used to measure basal or insulinstimulated
2-deoxyglucose (2-DG) uptake. Level of pAMPK was increased (P<0.01) for
myotubes exposed to Serum+AICAR vs. all other groups. The phosphorylated ACC
(pACC) levels were higher for both Serum+AICAR (P<0.05) and AICAR (P<0.05) vs.
Control and Serum groups. Basal (P<0.05) and 1.2 nM insulin-stimulated (P<0.005) 2-
DG uptake was higher for Serum vs. all other preincubation conditions at equal insulin
concentration. Regardless of insulin concentration (0, 1.2, or 18 nM), 2-DG was
unaltered in cells preincubated with Serum+AICAR vs. Control cells. In contrast to
results with isolated rat skeletal muscle, increasing the pAMPK and pACC in human
myocytes via preincubation with Serum+AICAR was insufficient to lead to a subsequent
enhancement in insulin-stimulated glucose uptake.
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