| First Author | Erickson JC | Year | 1996 |
| Journal | Science | Volume | 274 |
| Issue | 5293 | Pages | 1704-7 |
| PubMed ID | 8939859 | Mgi Jnum | J:37106 |
| Mgi Id | MGI:84534 | Doi | 10.1126/science.274.5293.1704 |
| Citation | Erickson JC, et al. (1996) Attenuation of the obesity syndrome of ob/ob mice by the loss of neuropeptide Y. Science 274(5293):1704-7 |
| abstractText | 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. |
