| First Author | Mottillo EP | Year | 2016 |
| Journal | Cell Metab | Volume | 24 |
| Issue | 1 | Pages | 118-29 |
| PubMed ID | 27411013 | Mgi Jnum | J:249879 |
| Mgi Id | MGI:6101081 | Doi | 10.1016/j.cmet.2016.06.006 |
| Citation | Mottillo EP, et al. (2016) Lack of Adipocyte AMPK Exacerbates Insulin Resistance and Hepatic Steatosis through Brown and Beige Adipose Tissue Function. Cell Metab 24(1):118-29 |
| abstractText | 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 beta subunits in adipocytes (ibeta1beta2AKO) and found that ibeta1beta2AKO mice were cold intolerant and resistant to beta-adrenergic activation of BAT and beiging of WAT. BAT from ibeta1beta2AKO mice had impairments in mitochondrial structure, function, and markers of mitophagy. In response to a high-fat diet, ibeta1beta2AKO 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. |
