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    Science. 1996 Dec 6;274(5293):1704-7.

    Attenuation of the obesity syndrome of ob/ob mice by the loss of neuropeptide Y.

    Erickson JC, Hollopeter G, Palmiter RD.

    Source

    Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Box 357370, Seattle, WA 98195-7370, USA.

    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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    PMID:
    8939859
    [PubMed - indexed for MEDLINE]

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