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Attenuation of the Obesity Syndrome of ob/ob Mice by the Loss of Neuropeptide Y
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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Metadata
- Authors
- Erickson, J. C., Hollopeter, G., & Palmiter, R. D.
- Venue
- Science
- Published
- 1996-12-06
- Volume
- 274
- Issue
- 5293
- Pages
- 1704-1707
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2125312207
- Cited by
- 801
- References
- 8
- FWCI
- 19.08
- Type
- journal article
- Language
- en
- Open access
- closed
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