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

      Science (New York, N.Y.)

      Adipose Tissue, pathology, Animals, Blood Glucose, analysis, Body Composition, Body Height, Body Weight, Diabetes Mellitus, etiology, Diabetes Mellitus, Type 2, Eating, Energy Metabolism, Female, Fertility, Insulin-Like Growth Factor I, metabolism, Leptin, Male, Mice, Mice, Mutant Strains, Mice, Obese, Neuropeptide Y, deficiency, genetics, physiology, Obesity, physiopathology, Oxygen Consumption, Proteins, RNA, Messenger

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          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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