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Am J Physiol Endocrinol Metab (August 23, 2005). doi:10.1152/ajpendo.00096.2005
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Submitted on March 3, 2005
Accepted on August 22, 2005

CHRONIC ROSIGLITAZONE TREATMENT RESTORES AMPK {alpha}2 ACTIVITY IN INSULIN RESISTANT RAT SKELETAL MUSCLE

Sarah J Lessard1, Zhi-Ping Chen1, Matthew J Watt1, Michael Hashem1, Julianne Reid1, Mark A Febbraio1, Bruce E Kemp1, and John A Hawley1*

1 School of Medical Sciences, RMIT University, Bundoora, Victoria, Australia

* To whom correspondence should be addressed. E-mail: john.hawley{at}rmit.edu.au.

Rosiglitazone is an insulin-sensitizing thiazolidinedione (TZD) that exerts PPAR{gamma}-dependent and independent effects. We tested the hypothesis that part of the insulin-sensitizing effect of rosiglitazone is mediated through the action of AMP-activated protein kinase (AMPK). First we determined the effect of acute (30-60 min) incubation of L6 myotubes with rosiglitazone on AMPK regulation and palmitate oxidation. Compared with control (DMSO), 200 µM rosiglitazone increased (P<0.05) AMPK{alpha}1 activity and phosphorylation of AMPK (Thr172). In addition, acetyl Co-A carboxylase (Ser218) phosphorylation and palmitate oxidation were increased (P<0.05) in these cells. To investigate the effects of chronic rosiglitazone treatment on AMPK regulation in skeletal muscle in vivo, obese Zucker rats were randomly allocated into two experimental groups: control and rosiglitazone. Lean Zucker rats were treated with vehicle and acted as a control group for obese Zucker rats. Rats were dosed daily, for 6 wk with either vehicle (0.5% carboxymethylcellulose [CMC], 100 mL/100 g body mass), or 3 mg/kg rosiglitazone. AMPK{alpha}1 activity was similar in muscle from lean and obese animals and was unaffected by rosiglitazone treatment. AMPK{alpha}2 activity was ~25% lower in obese vs. lean animals (P<0.05), but was normalised to control values following rosiglitazone treatment. ACC phosphorylation was decreased with obesity (P<0.05), but was restored to the level of lean controls with rosiglitazone treatment. Our data demonstrate that rosiglitazone restores AMPK signalling in skeletal muscle of insulin resistant obese Zucker rats.




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