The role of ATE1 in feeding behavior and energy metabolism

Abstract

Obesity results from energy imbalance, whereby intake chronically exceeds expenditure. Energy intake is largely regulated by the hypothalamus in response to the hormones leptin and ghrelin. As obesity has been on the rise since the 1960’s, there is an urgent need for a more detailed understanding of energy metabolism at the molecular level. Previously we found that disruption of Ate1 gene function caused loss of fat and resistance to diet-induced obesity in mice. To gain insight into the molecular mechanism of Ate1 function, we compared leptin production and sensitivity between Ate1- containing and Ate1-lacking mice. Here we show that plasma leptin levels are decreased in Ate1-lacking mice but there is no change in leptin responsiveness compared to Ate1- containing mice. This work will elucidate the role of the Ate1 gene in fat and energy metabolism and may provide new therapeutic targets for the pharmacological regulation of obesity.