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Am J Physiol Endocrinol Metab (September 11, 2002). doi:10.1152/ajpendo.00278.2002
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Articles in PresS, published online ahead of print September 10, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00278.2002
Submitted on June 25, 2002
Accepted on August 10, 2002

AMP-Activated Protein Kinase Activates Transcription of the UCP3 and HKII Genes in Rat Skeletal Muscle

James Stoppani1, Audrey L. Hildebrandt2, Kei Sakamoto3, David Cameron-Smith2, Laurie J. Goodyear4, and P. Darrell Neufer1*

1 John B. Pierce Laboratory, New Haven, CT, USA; Department of Cellular and Molecular Physiology, Yale University, New Haven, CT, USA
2 John B. Pierce Laboratory, New Haven, CT, USA
3 Research Division, Joslin Diabetes Center, Boston, MA, USA; Harvard Medical School, Boston, MA, USA
4 Research Division, Joslin Diabetes Center, Boston, MA, USA; Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: dneufer{at}jbpierce.org.

AMP-activated protein kinase (AMPK) has recently emerged as a key signaling protein in skeletal muscle coordinating the activation of both glucose and fatty acid metabolism in response to increased cellular energy demand. To determine whether AMPK signaling may also regulate gene transcription in skeletal muscle, rats were given a single subcutaneous injection (1 mg/g) of the AMP analogue, 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR). AICAR injection activated (P<0.05) AMPK {alpha}2 (~2.5-fold) and transcription of the uncoupling protein-3 (~4-fold, UCP3) and hexokinase II (~10-fold, HKII) genes in both red and white skeletal muscle. However, AICAR injection also elicited (P<0.05) an acute drop (60%) in blood glucose and a sustained (2 hr) increase in blood lactate, prompting concern regarding the specificity of AICAR on transcription. To maximize AMPK activation in muscle while minimizing potential systemic counterregulatory responses, a single-leg arterial infusion technique was employed in fully conscious rats. Relative to saline infused controls, single-leg arterial infusion of AICAR (0.125, 0.5 and 2.5 µg.g-1 for 60 min) induced a dose-dependent increase (2 to 4-fold, P<0.05) in UCP3 and HKII transcription in both red and white skeletal muscle. Importantly, AICAR infusion activated transcription only in muscle from the infused leg and had no effect on blood glucose or lactate levels. These data provide evidence that AMPK signaling is linked to the transcriptional regulation of select metabolic genes in skeletal muscle.




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