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J Physiol Volume 580, Number 2, 677-684, April 15, 2007 DOI: 10.1113/jphysiol.2007.128652
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Upregulation of AMPK during cold exposure occurs via distinct mechanisms in brown and white adipose tissue of the mouse

 Jacob D. Mulligan1, Asensio A. Gonzalez2, Annette M. Stewart1, Hannah V. Carey3 and Kurt W. Saupe1,4

1 Department of Medicine, University of Wisconsin, Madison, WI 53706, USA
2 Blood Transfusion Service, Belfast City Hospital, Belfast, UK
3 Department of Comparative Biosciences, University of Wisconsin, Madison, WI 53706, USA
4 Department of Physiology, University of Wisconsin, Madison, WI 53706, USA

AMPK (adenosine monophosphate-activated protein kinase), a key regulator of cellular energy metabolism and whole-body energy balance, is present in brown adipose tissue but its role in regulating the acute metabolic state and chronic thermogenic potential of this metabolically unique tissue is unknown. To address this, the AMPK signalling system in brown and white adipose tissue was studied in C57Bl/6 mice under control conditions, during acute and chronic cold exposure, and during chronic adrenergic stimulation. In control mice AMPK activity in brown adipose tissue was higher than in any tissue yet reported (3-fold the level in liver) secondary to a high level of expression of the {alpha}1 isoform. During the first day of cold, a time of intense non-shivering thermogenesis, AMPK activity remained at basal levels. However, chronic (>7 days) cold caused a progressive increase in brown adipose tissue AMPK activity secondary to increased expression of the {alpha}1 isoform. To investigate the signalling pathway involved, noradrenaline (norepinephrine) and the beta3-adrenergic-specific agonist CL 316, 243 were given for 14 days. This increased uncoupling protein-1 content in brown adipose tissue, but not AMPK activity. In white adipose tissue 15 days of cold increased {alpha}1 AMPK activity 98 ± 20%, an effect reproduced by chronic noradrenaline or CL 316 243. We conclude that chronic cold not only increases AMPK activity in brown and white adipose tissue, but that it does so via distinct signalling pathways. Our data are consistent with AMPK acting primarily as a regulator of chronic thermogenic potential in brown adipose tissue, and not in the acute activation of non-shivering thermogenesis.

(Received 19 January 2006; accepted after revision 29 January 2007; first published online 1 February 2007)
Corresponding author K. W. Saupe: 1630 Medical Sciences Center, 1300 University Ave., Madison, WI 53706, USA.  Email: kws{at}medicine.wisc.edu






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