(-)-Epicatechin mitigates high-fructose-associated insulin resistance by modulating redox signaling and endoplasmic reticulum stress

Ahmed Bettaieb, Marcela A. Vazquez Prieto, Cecilia Rodriguez Lanzi, Roberto M. Miatello, Fawaz Haj, César G. Fraga, Patricia I. Oteiza

Research output: Contribution to journalArticle

66 Scopus citations

Abstract

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. 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, IRS1, Akt, and ERK1/2) was impaired, whereas 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 that contribute to insulin resistance: HFr-associated increased expression and activity of NADPH oxidase, activation of redox-sensitive signals, expression of NF-κB-regulated proinflammatory 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 for defining interventions that can prevent/mitigate MetS-associated insulin resistance.

Original languageEnglish (US)
Pages (from-to)247-256
Number of pages10
JournalFree Radical Biology and Medicine
Volume72
DOIs
StatePublished - 2014

Keywords

  • Endoplasmic reticulum stress
  • Epicatechin and flavonoids
  • Free radicals
  • Insulin resistance
  • Metabolic syndrome
  • NADPH oxidase
  • Redox signaling

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)
  • Medicine(all)

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