info:eu-repo/semantics/article
(-)-Epicatechin mitigates high-fructose-associated insulin resistance by modulating redox signaling and endoplasmic reticulum stress
Fecha
2014-07Registro en:
Bettaieb, Ahmed; Vazquez, Marcela Alejandra; Rodriguez Lanzi, Maria Cecilia; Miatello, Roberto Miguel; Haj, Fawaz G.; et al.; (-)-Epicatechin mitigates high-fructose-associated insulin resistance by modulating redox signaling and endoplasmic reticulum stress; Elsevier Science Inc; Free Radical Biology and Medicine; 72; 7-2014; 247-256
0891-5849
CONICET Digital
CONICET
Autor
Bettaieb, Ahmed
Vazquez, Marcela Alejandra
Rodriguez Lanzi, Maria Cecilia
Miatello, Roberto Miguel
Haj, Fawaz G.
Fraga, César Guillermo
Oteiza, Patricia Isabel
Resumen
We investigated the capacity of dietary (-)-epicatechin (EC) to mitigate insulin resistance through the modulation of redox-regulated mechanisms in a rat model of metabolic syndrome (MetS). Adolescent rats were fed a regular chow diet without or with high fructose (HFr) (10% (w/v)) in drinking water for 8 weeks, and a group of HFr-fed rats was supplemented with EC in the diet. HFr-fed rats developed insulin resistance which was mitigated by EC supplementation. Accordingly, the activation of components of the insulin signaling cascade (insulin receptor (IR), IRS-1, Akt and ERK1/2) was impaired, while negative regulators (PKC, IKK, JNK and PTP1B) were upregulated in the liver and adipose tissue of HFr rats. These alterations were partially or totally prevented by EC supplementation. In addition, EC inhibited events which contribute to insulin resistance: HFr-associated increased expression and activity of NADPH oxidase , activation of redox-sensitive signals , expression of NF-kB-regulated pro-inflammatory cytokines and chemokines, and some sub-arms of endoplasmic reticulum stress signaling. Collectively, these findings indicate that EC supplementation can mitigate HFr-induced insulin resistance and are relevant to define interventions that can prevent/mitigate MetS-associated insulin resistance.