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Publication : Adipose tissue-specific knockout of AMPKα1/α2 results in normal AICAR tolerance and glucose metabolism.

First Author  Choi RH Year  2019
Journal  Biochem Biophys Res Commun Volume  519
Issue  3 Pages  633-638
PubMed ID  31540695 Mgi Jnum  J:291828
Mgi Id  MGI:6443730 Doi  10.1016/j.bbrc.2019.09.049
Citation  Choi RH, et al. (2019) Adipose tissue-specific knockout of AMPKalpha1/alpha2 results in normal AICAR tolerance and glucose metabolism. Biochem Biophys Res Commun 519(3):633-638
abstractText  AMP-activated protein kinase (AMPK) is a member of Ser/Thr kinases that has been shown to regulate energy balance. Although recent studies have demonstrated the function of AMPK in adipose tissue using different fat-specific AMPK knockout mouse models, the results were somewhat inconsistent. For this study, we tested the hypothesis that AMPK in adipose tissue regulates whole body glucose metabolism. To determine the role of adipose tissue AMPK in vivo, we generated fat-specific AMPKalpha1/alpha2 knockout mice (AMPKFKO) using the Cre-loxP system. Body weights of AMPKFKO mice were not different between 8 and 27 weeks of age. Furthermore, tissue weights (liver, kidney, muscle, heart and white and brown adipose tissue) were similar to wild type littermates and DEXA scan analysis revealed no differences in percentages of body fat and lean mass. Knockout of AMPKalpha1/alpha2 in adipose tissue abolished basal and AICAR-stimulated phosphorylation of AMPK and Acetyl-CoA Carboxylase, a downstream of AMPK. Despite of the ablation of AICAR-stimulated AMPK phosphorylation, the blood glucose-lowering effect of AICAR injection (i.p.) was normal in AMPKFKO mice. In addition, AMPKFKO displayed normal fasting blood glucose concentration, glucose tolerance, insulin tolerance, and insulin signaling, indicating normal whole body glucose metabolism. These data demonstrate that adipose tissue AMPK plays a minimum role in whole body glucose metabolism on a chow diet.
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