Inhibition of PTP1b in the amygdala reduces food intake, body weight and modulates glycemic homeostasis in obese rats

Abstract

Background The control of food intake depends, in part, of the action and signaling of hormones, such as insulin in hypothalamic neurons. In obesity, inflammatory cytokines activate protein phosphatases, such as protein tyrosine phosphatase 1B (PTP1B). PTP1B interacts with the insulin receptor (IR) and the insulin receptor substrate (IRS1), inhibiting them in hypothalamus. Other brain regions, that are part of the dopaminergic reward system, such as the amygdala, participate of the control of energy balance in parallel to the hypothalamus. Insulin exerts its anorexigenic effect also through the amygdala and, in obesity, this effect is abolished. However, it is not known whether PTP1B is expressed and participates of the regulation of insulin signaling in amygdala.