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Modulation of lipogenesis and glucose metabolism in HepG2 cells and C2C12 myotubes by hydroxycinnamic acid / 国际药学研究杂志
Journal of International Pharmaceutical Research ; (6): 693-698, 2017.
Artigo em Chinês | WPRIM | ID: wpr-668088
ABSTRACT
Objective To investigate the effects and potential mechanism of hydroxycinnamic acid(HYD)on lipogenesis and glucose consumption in HepG2 cells and C2C12 myotubes. Methods The function of HYD on oleic acid(OA)elicited lipid ac-cumulation was measured by oil red O staining. Intracellular quantification of total cholesterol(TC)and triglycerides(TG)in HepG2 cells,and cell viability were observed by MTT assay. Additionally,glucose metabolic action of HYD was tested by glucose consump-tion in HepG2 cells and glucose uptake in C2C12 myotubes. The expression of glucose and lipid metabolism-related genes were detect-ed by real-time quantitative PCR(RT-PCR). Results Treatment with HYD significantly inhibited lipid accumulation in HepG2 cells in a dose-dependent manner without influence on cell viability. Meanwhile,HYD had the capability to increase glucose consumption in HepG2 cells and glucose uptake in C2C12 myotubes. Furthermore,RT-PCR revealed that the beneficial effect of HYD was associat-ed with the down-regulation of sterol regulatory element-binding proteins-1a,-1c,-2(SREBP-1a,SREBP-1c,and SREBP-2),fatty acid synthase(FAS),acetyl-CoA carboxylase(ACC),and hydroxyl methyglutaryl CoA reductase(HMGR),and up-regulation of per-oxisome proliferator-activated receptorα(PPARα). Conclusion HYD is an effective regulator of lipogenesis and glucose consump-tion. Up-regulation of PPAR may partially,if not wholly,participate in its beneficial effect.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of International Pharmaceutical Research Ano de publicação: 2017 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of International Pharmaceutical Research Ano de publicação: 2017 Tipo de documento: Artigo