| First Author | Ke Y | Year | 2003 |
| Journal | Biochem Biophys Res Commun | Volume | 312 |
| Issue | 4 | Pages | 1165-70 |
| PubMed ID | 14651995 | Mgi Jnum | J:94674 |
| Mgi Id | MGI:3513687 | Doi | 10.1016/j.bbrc.2003.11.053 |
| Citation | Ke Y, et al. (2003) Overexpression of leptin in transgenic mice leads to decreased basal lipolysis, PKA activity, and perilipin levels. Biochem Biophys Res Commun 312(4):1165-70 |
| abstractText | Transgenic mice overexpressing leptin (LepTg) exhibit substantial reductions in adipose mass. Since the binding of leptin to its receptor activates the sympathetic nervous system, we reasoned that the lean state of the LepTg mice could be caused by chronic lipolysis. Instead, the LepTg mice exhibited a low basal lipolysis state and their lean phenotype was not dependent on the presence of beta3-adrenergic receptors. In their white adipose tissue, protein levels of protein kinase A, hormone-sensitive lipase, and ADRP were not impaired. However, compared to normal mice, perilipin, perilipin mRNA, and cAMP-stimulated PKA activity were significantly attenuated. Overall, we demonstrate that the lean phenotype of the LepTg mice does not result in a chronically elevated lipolytic state, but instead in a low basal lipolysis state characterized by a decrease in perilipin and PKA activity in white fat. |
