IMBECU   20882
INSTITUTO DE MEDICINA Y BIOLOGIA EXPERIMENTAL DE CUYO
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
(-)-Epicatechin mitigates metabolic syndrome-associated insulin resistance in rats
Autor/es:
BETTAIEB, A; VAZQUEZ PRIETO, MA; HAJ, FG; FRAGA, CG; OTEIZA, PI
Lugar:
Buenos Aires
Reunión:
Congreso; International Conference of Polyphenols and Healths; 2013
Resumen:
The urgent need for alternative strategies to prevent the emerging global epidemic of metabolic syndrome (MetS) led to the identification of new potential plant products-based therapies. The present study investigated the ability of dietary supplementation of (-)-epicatechin (EC) to prevent high fructose (HFr)-induced insulin resistance and the underlying mechanisms in a rat model of HFr-induced MetS. Adolescent rats were provided with drinking water with or without (HFr) fructose 10% (w/v) for 8 w. A subgroup of HFr rats was supplemented with EC in the diet (20 mg EC/d/kg BW).  Adipose and liver lysates from Rats receiving fructose alone exhibited (1) a significant alteration in the insulin signaling pathway (insulin receptor (IR), IRS-1, Akt and ERK1/2), (2) activation of ER stress pathways, as evidenced by increased PERK (Thr980), eIF2á (Ser51) and IRE1á (Ser724) phosphorylation, and (3) increased inflammation as evidenced by increased activation of the NF-êB pathway. Importantly, EC supplementation attenuated HFr-induced ER stress in liver and adipose tissue. Similarly, EC mitigated HFr-induced activation of NF-êB. In addition, insulin signaling was enhanced in EC-treated rats. In summary, these findings demonstrate that EC is a natural modulator of HFr-induced MetS and a potential target for mitigating MetS-associated complications.