کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1949594 | 1537772 | 2010 | 8 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Direct evidence for leptin-induced lipid oxidation independent of long-form leptin receptor Direct evidence for leptin-induced lipid oxidation independent of long-form leptin receptor](/preview/png/1949594.png)
Leptin administration has been shown to enhance muscle lipid oxidation in relation to the energy expenditure. Both long-form (Ob-RL) and short-form leptin receptors (Ob-RS) are expressed in skeletal muscle, but the role of Ob-RS is unclear. In the present study, the role of Ob-RS in leptin-induced lipid oxidation in skeletal muscles was investigated using primary murine myotubes from m/m and db/db mice. Primary myotubes were treated with leptin (0.1, 1, 10, 100 nM) for 24 h. Lipid oxidation was determined by 14CO2 production rate from [1-14C] palmitate. Leptin was found to increase lipid oxidation in a dose- and time-dependent manner in db/db myotubes as well as in m/m myotubes. Leptin significantly increased phosphorylation of JAK2 and STAT3 in both types of myotube. Leptin-induced lipid oxidation was abolished by STAT3 siRNA. To investigate the mechanism underlying leptin-induced lipid oxidation, the effects of pharmacological inhibitors were examined. JAK2 or p38 MAPK inhibitor suppressed leptin-induced lipid oxidation and decreased STAT3 phosphorylation in both types of myotube, respectively. Leptin significantly increased phosphorylation of p38 MAPK, and leptin-induced lipid oxidation was abolished by treatment with p38 MAPK siRNA in both types of myotube. These results suggest that leptin induces lipid oxidation in skeletal muscle through the JAK2/p38 MAPK/STAT3 signaling pathway via not only Ob-RL but also Ob-RS.
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1801, Issue 10, October 2010, Pages 1115–1122