| First Author | Cheng A | Year | 2002 |
| Journal | Dev Cell | Volume | 2 |
| Issue | 4 | Pages | 497-503 |
| PubMed ID | 11970899 | Mgi Jnum | J:75969 |
| Mgi Id | MGI:2178164 | Doi | 10.1016/s1534-5807(02)00149-1 |
| Citation | Cheng A, et al. (2002) Attenuation of Leptin Action and Regulation of Obesity by Protein Tyrosine Phosphatase 1B. Dev Cell 2(4):497-503 |
| abstractText | Common obesity is primarily characterized by resistance to the actions of the hormone leptin. Mice deficient in protein tyrosine phosphatase 1B (PTP1B) are resistant to diabetes and diet-induced obesity, prompting us to further define the relationship between PTP1B and leptin in modulating obesity. Leptin-deficient (Lep(ob/ob)) mice lacking PTP1B exhibit an attenuated weight gain, a decrease in adipose tissue, and an increase in resting metabolic rate. Furthermore, PTP1B-deficient mice show an enhanced response toward leptin-mediated weight loss and suppression of feeding. Hypothalami from these mice also display markedly increased leptin-induced Stat3 phosphorylation. Finally, substrate-trapping experiments demonstrate that leptin-activated Jak2, but not Stat3 or the leptin receptor, is a substrate of PTP1B. These results suggest that PTP1B negatively regulates leptin signaling, and provide one mechanism by which it may regulate obesity. |
