Molecular mechanism of SH2-Bβ in regulating JAK2/STAT3 during development of obesity
10.3760/cma.j.issn.1000-6699.2009.01.027
- VernacularTitle:SH2-Bβ调控JAK2/STAT3在肥胖症发病中的分子机制
- Author:
Chaojun DUAN
;
Cui LI
;
Cane TANG
;
Jing WU
;
Faqing TANG
;
Zhuchu CHEN
;
Zhiqiang XIAO
- Publication Type:Journal Article
- Keywords:
SH2-Bβ;
Obesity;
Leptin signal pathway
- From:
Chinese Journal of Endocrinology and Metabolism
2009;25(1):90-91
- CountryChina
- Language:Chinese
-
Abstract:
The molecular techniques were used to analyse tyrosine phosphorylation of JAK2 and STAT3 in leptin receptor overpression cell lines and SH2-Bβ knockout (SH2-Bβ-/-) mice. The serum level of leptin in SH2-Bβ mice was measured by ELISA. The results showed that SH2-Bβ dramatically enhanced the leptin-stimulated tyrosine phosphorylation of JAK2 and STAT3 in vitro. Leptin-stimulated activation of JAK2 and phosphorylation of STAT3 were significantly impaired in hypothalamus of SH2-Bβ-/- mice. The fasting and postprandial serum levels of leptin and body weight were markedly increased in SH2-Bβ-/- mice. Therefore, SH2-Bβ is an endogenous enhancer of leptin sensitivity and regulates body weight via leptin/ JAK2/STAT3 pathway.