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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

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

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.[1]

References

  1. Attenuation of the obesity syndrome of ob/ob mice by the loss of neuropeptide Y. Erickson, J.C., Hollopeter, G., Palmiter, R.D. Science (1996) [Pubmed]
 
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