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

Jay C. Erickson, Gunther Hollopeter and Richard D. Palmiter
Science
New Series, Vol. 274, No. 5293 (Dec. 6, 1996), pp. 1704-1707
Stable URL: http://www.jstor.org/stable/2890949
Page Count: 4
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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.

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