IMBECU   20882
INSTITUTO DE MEDICINA Y BIOLOGIA EXPERIMENTAL DE CUYO
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
-(-)Epicatechin and its metabolites on the modulation of the hepatic NADPH oxidase
Autor/es:
CREMONINI E; BETTAIEB A; VAZQUEZ PRIETO MA; CERVELLATI C; HAJ FG; OTEIZA PI
Lugar:
Paris
Reunión:
Congreso; 5ème Symposium Nutrition, Biologie de l`Oxigène et Médicine-Paris; 2013
Resumen:
Excess liver oxidant production can contribute to obesity-associated altered hepatic glucose and lipid homeostasis. Consumption of (-)-epicatechin (EC)-rich foods improves obesity-related metabolic diseases.  This work investigated if EC and its metabolites could inhibit hyperlipidemia-induced hepatic oxidant production through the regulation of NADPH oxidase (NOX)  subunit expression (NOX3, p47, p22) and NOX activity in vivo and in HepG2 cells. Hyperlipidemia was induced in rats by high fructose (HFr) consumption, with/without EC supplementation.  HepG2 cells were treated with palmitate (Pal), in the absence/presence of EC/EC metabolites (ECM).  EC supplementation mitigated HFr-associated hyperlipidemia in rats and the associated NOX3 increased expression, but not that of p22 or p47.  In HepG2 cells, Pal (0.25 mM) caused an increase in cellular oxidants which was prevented by EC and ECM.  Pal increased NOX3, p47 and p22 expression (mRNA, protein). EC and its metabolites (0.25-1 µM) treatment attenuated Pal-induced NOX3, but not p47 and p22 expression.  Pal also caused NOX activation, measured as both enzyme activity, and p47 translocation to the cell membrane. EC and ECM (1 µM) inhibited NOX activation, but not p47 membrane translocation. Results shown that EC modulates NADPH oxidase, both at a level of expression and activity in vivo and in vitro. Thus, treatment with EC could be relevant to the improvement of obesity-associated hepatotoxicity.