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Science 6 December 1996:
Vol. 274. no. 5293, pp. 1704 - 1707
DOI: 10.1126/science.274.5293.1704
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Reports

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

Jay C. Erickson, Gunther Hollopeter, Richard D. Palmiter *

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.

Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Box 357370, Seattle, WA 98195-7370, USA.
*   To whom correspondence should be addressed.

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Physiolog