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Responses of mice lacking α1AMPK to acute and chronic thermogenic challenges

While activity of α1 isoform of AMP‐activated protein kinase (AMPK) is higher in brown adipose tissue (BAT) than any tissue yet reported, its role in BAT is unknown. Our goal was to elucidate AMPK's in vivo role in BAT, specifically in acute non‐shivering thermogenesis (NST) and chronic (14 days at 4° C) cold‐induced hyperphagia and UCP1 upregulation. C57Bl/6 wild type (WT) and α1AMPK knockout (KO) mice were studied (6–8/group). During acute NST (IP injection of the β3‐adrenergic agonist CL 316,243) core temperature increased similarly (≈0.8°C) in WT and KO mice. Thus α1AMPK is not obligatory for acute NST. In a separate study, chronic cold‐induced hyperphagia was nearly identical in WT and KO mice (≈ 2.5 fold increase in food intake). Chronic cold caused less upregulation of UCP1 in KO (1.9‐fold) than in WT (4‐fold) mice, but did not cause a lower body temperature in KO mice. Therefore α1AMPK is not obligatory for hyperphagia or other adaptations that maintain body temperature near normal during chronic cold exposure. There was little if any compensatory upregulation of α2AMPK in α1AMPK KO mice. Overall our data indicate that high levels of α1AMPK activity in BAT do not play a key role in major aspects of thermoregulation, and instead suggest a currently undefined role for AMPK in BAT physiology.