Attenuation of the Obesity Syndrome of <i>ob/ob</i> Mice by the Loss of Neuropeptide Y

TLDR

The obesity syndrome of ob/ob mice arises from leptin deficiency, and neuropeptide Y is overproduced in their hypothalamus, implicating it in energy balance. The study generated ob/ob mice lacking NPY to investigate its role in leptin deficiency. The authors created ob/ob mice genetically deficient in NPY. Loss of NPY in ob/ob mice reduces obesity, improves metabolic and reproductive outcomes, and indicates NPY as a central effector of leptin deficiency.

Abstract

The obesity syndrome of ob / ob mice results from lack of leptin, a hormone released by fat cells that acts in the brain to suppress feeding and stimulate metabolism. Neuropeptide Y (NPY) is a neuromodulator implicated in the control of energy balance and is overproduced in the hypothalamus of ob / ob mice. To determine the role of NPY in the response to leptin deficiency, ob / ob mice deficient for NPY were generated. In the absence of NPY, ob / ob mice are less obese because of reduced food intake and increased energy expenditure, and are less severely affected by diabetes, sterility, and somatotropic defects. These results suggest that NPY is a central effector of leptin deficiency.