Attenuation of the obesity syndrome of ob/ob mice by the loss of neuropeptide Y - PubMed (original) (raw)
Attenuation of the obesity syndrome of ob/ob mice by the loss of neuropeptide Y
J C Erickson et al. Science. 1996.
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.
Comment in
- On raising energy expenditure in ob/ob mice.
Himms-Hagen J. Himms-Hagen J. Science. 1997 May 16;276(5315):1132-3. doi: 10.1126/science.276.5315.1132. Science. 1997. PMID: 9173544 No abstract available.
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