| First Author | Seoane-Collazo P | Year | 2018 |
| Journal | Diabetes | Volume | 67 |
| Issue | 11 | Pages | 2213-2226 |
| PubMed ID | 30104247 | Mgi Jnum | J:265904 |
| Mgi Id | MGI:6206187 | Doi | 10.2337/db17-1538 |
| Citation | Seoane-Collazo P, et al. (2018) SF1-Specific AMPKalpha1 Deletion Protects Against Diet-Induced Obesity. Diabetes 67(11):2213-2226 |
| abstractText | AMPK is a cellular gauge that is activated under conditions of low energy, increasing energy production and reducing energy waste. Current evidence links hypothalamic AMPK with the central regulation of energy balance. However, it is unclear whether targeting hypothalamic AMPK has beneficial effects in obesity. Here, we show that genetic inhibition of AMPK in the ventromedial nucleus of the hypothalamus (VMH) protects against high-fat diet (HFD)-induced obesity by increasing brown adipose tissue (BAT) thermogenesis and subsequently energy expenditure. Notably, this effect depends upon the AMPKalpha1 isoform in steroidogenic factor 1 (SF1) neurons of the VMH, since mice bearing selective ablation of AMPKalpha1 in SF1 neurons display resistance to diet-induced obesity, increased BAT thermogenesis, browning of white adipose tissue, and improved glucose and lipid homeostasis. Overall, our findings point to hypothalamic AMPK in specific neuronal populations as a potential druggable target for the treatment of obesity and associated metabolic disorders. |
