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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adipose Tissue / pathology
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Animals
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Blood Glucose / analysis
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Body Composition
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Body Height
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Body Weight
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Diabetes Mellitus / etiology
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Diabetes Mellitus, Type 2 / etiology
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Eating
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Energy Metabolism
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Female
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Fertility
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Insulin-Like Growth Factor I / metabolism
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Leptin
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Male
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Mice
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Mice, Mutant Strains
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Mice, Obese
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Neuropeptide Y / deficiency
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Neuropeptide Y / genetics
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Neuropeptide Y / physiology*
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Obesity / pathology
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Obesity / physiopathology*
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Oxygen Consumption
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Proteins / genetics
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Proteins / physiology*
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RNA, Messenger / metabolism
Substances
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Blood Glucose
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Leptin
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Neuropeptide Y
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Proteins
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RNA, Messenger
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Insulin-Like Growth Factor I