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Lack of Adipocyte AMPK Exacerbates Insulin Resistance and Hepatic Steatosis through Brown and Beige Adipose Tissue Function.

Authors: Mottillo, Emilio P  Desjardins, Eric M  Crane, Justin D  Smith, Brennan K  Green, Alex E  Ducommun, Serge  Henriksen, Tora I  Rebalka, Irena A  Razi, Aida  Sakamoto, Kei  Scheele, Camilla  Kemp, Bruce E  Hawke, Thomas J  Ortega, Joaquin  Granneman, James G  Steinberg, Gregory R 
Citation: Mottillo EP, etal., Cell Metab. 2016 Jul 12;24(1):118-29. doi: 10.1016/j.cmet.2016.06.006.
Pubmed: (View Article at PubMed) PMID:27411013
DOI: Full-text: DOI:10.1016/j.cmet.2016.06.006

Brown (BAT) and white (WAT) adipose tissues play distinct roles in maintaining whole-body energy homeostasis, and their dysfunction can contribute to non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes. The AMP-activated protein kinase (AMPK) is a cellular energy sensor, but its role in regulating BAT and WAT metabolism is unclear. We generated an inducible model for deletion of the two AMPK ß subunits in adipocytes (iß1ß2AKO) and found that iß1ß2AKO mice were cold intolerant and resistant to ß-adrenergic activation of BAT and beiging of WAT. BAT from iß1ß2AKO mice had impairments in mitochondrial structure, function, and markers of mitophagy. In response to a high-fat diet, iß1ß2AKO mice more rapidly developed liver steatosis as well as glucose and insulin intolerance. Thus, AMPK in adipocytes is vital for maintaining mitochondrial integrity, responding to pharmacological agents and thermal stress, and protecting against nutrient-overload-induced NAFLD and insulin resistance.


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RGD Object Information
RGD ID: 13673870
Created: 2018-06-23
Species: All species
Last Modified: 2018-06-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.