Direct evidence for leptin-induced lipid oxidation independent of long-form leptin receptor.
Biochim Biophys Acta
; 1801(10): 1115-22, 2010 Oct.
Article
em En
| MEDLINE
| ID: mdl-20601111
ABSTRACT
Leptin administration has been shown to enhance muscle lipid oxidation in relation to the energy expenditure. Both long-form (Ob-R(L)) and short-form leptin receptors (Ob-R(S)) are expressed in skeletal muscle, but the role of Ob-R(S) is unclear. In the present study, the role of Ob-R(S) 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, 100nM) for 24h. Lipid oxidation was determined by (14)CO(2) production rate from [1-(14)C] 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-R(L) but also Ob-R(S).
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Leptina
/
Metabolismo dos Lipídeos
/
Receptores para Leptina
Limite:
Animals
Idioma:
En
Revista:
Biochim Biophys Acta
Ano de publicação:
2010
Tipo de documento:
Article
País de afiliação:
Japão