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Int J Mol Med ; 35(6): 1779-85, 2015 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-25891365

RESUMEN

With the industrialization of society, the increase in the prevalence of obesity and metabolic disorders has become an important health concern in a number of countries. Quercetin (3,30,40,5,7-pentahydroxyflavone) is well known as a bioactive flavonoid in a variety of biological resources. The aim of the present study was to explore the machanisms responsible for the anti-adipogenic activity of quercetin and its effects on the lipolysis in OP9 mouse stromal cells which rapidly differentiate into adipocytes. The differentiation of OP9 cells into adipocytes was evaluated by the measurement of lipid accumulation by Oil Red O (ORO) staining; lipid accumulation was significantly impaired by treatment with quercetin. Reverse transcription-polymerase chain reaction (RT-PCR) and western blot analysis were used to measure the expression levels of CCAAT/enhancer binding protein α (C/EBPα), proliferator-activated receptor γ (PPARγ), sterol regulatory element-binding protein-1 (SREBP-1) and fatty acid synthase (FAS). The mRNA expression levels of lipases, such as adipose triglyceride lipase (ATGL), hormone sensitive lipase (HSL) and lipoprotein lipase (LPL) were also measured by RT-PCR. Quercetin significantly decreased the expression of transcription factors, including C/EBPα, PPARγ and SREBP-1c both at the protein and mRNA level. The results from the present study demonstrate that quercetin prevents adipogenesis by upregulating ATGL and HSL expression and downregulating FAS, LPL and adipocyte fatty acid-binding protein (aP2) expression, as well as the expression of transcription factors. Our data suggest that quercetin has therapeutic potential by regulating the expression of transcriptional factors and enzymes associated with adipogenesis.


Asunto(s)
Adipogénesis/efectos de los fármacos , Lipasa/metabolismo , Quercetina/farmacología , Factores de Transcripción/metabolismo , Animales , Línea Celular , Lipasa/genética , Ratones , Factores de Transcripción/genética
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