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. 2007 Apr 15;580(Pt. 2):677-84.
doi: 10.1113/jphysiol.2007.128652. Epub 2007 Feb 1.

Upregulation of AMPK during cold exposure occurs via distinct mechanisms in brown and white adipose tissue of the mouse

Jacob D Mulligan  1 , Asensio A Gonzalez, Annette M Stewart, Hannah V Carey, Kurt W Saupe
Affiliations

V体育官网 - Upregulation of AMPK during cold exposure occurs via distinct mechanisms in brown and white adipose tissue of the mouse

Jacob D Mulligan et al. J Physiol. .

Abstract

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 alpha1 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 alpha1 isoform. To investigate the signalling pathway involved, noradrenaline (norepinephrine) and the beta(3)-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 VSports手机版. In white adipose tissue 15 days of cold increased alpha1 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. .

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Figures

Figure 3
Figure 3. Effect of varying lengths of cold exposure on α1 and α2 AMPK activities in mouse tissue
Mice were housed at 4°C for the indicated times before tissue collection. Each cold-exposure group had its own control group that was maintained at 22°C until being killed. AMPK activity was measured in homogenates of BAT following immunoprecipitation with an α1- or α2-specific antibody. Data are expressed as mean ± s.e.m. for n=5–6 per group, *P ≤ 0.05 relative to control group. Note that the cold-induced increase in AMPK activity is both isoform and tissue specific.
Figure 1
Figure 1. Comparison of AMPK activity in mouse BAT and liver
A, activities of α1 AMPK and α2 AMPK were measured in homogenates of BAT and liver from mice, following immunoprecipitation with isoform-specific antibodies. Activities were determined in the presence of 200 μm AMP. Data are expressed as mean ± s.e.m. for n=5 in each group. B, Western blots were performed on homogenates of BAT and liver from mice. Immunoblots were probed with antibodies directed against α1 AMPK protein.
Figure 2
Figure 2. Western blots on homogenates of mouse BAT and liver
Immunoblots were probed with antibodies directed against phospho-(Ser79)-ACC (A) or total ACC (B). Compared to liver, BAT contains a large amount of total ACC protein, as well as phosphorylated (inhibited) ACC.
Figure 4
Figure 4. Effects of 14 days of treatment with adrenergic agonists on UCP1 protein levels in BAT (A), and α1 AMPK activity in BAT and WAT
(B) Despite the expected increases in BAT UCP-1, α1 AMPK activity in BAT was not increased by β3-adrenergic stimulation. In contrast, both the higher dose of noradrenaline and β3-adrenergic stimulation significantly increased α1 AMPK activity in WAT. Data are expressed as mean ± s.e.m. for n=5–6 per group; *P ≤ 0.05 compared to the control group that received vehicle.
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