期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 72, 期 -, 页码 247-256出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2014.04.011
关键词
Metabolic syndrome; Insulin resistance; Epicatechin and flavonoids; Redox signaling; NADPH oxidase; Endoplasmic reticulum stress; Free radicals
资金
- University of California at Davis, NIFA [CA-D-XXX-7244-H]
- JDRF [1-2009-337]
- NIH USA [R56DK084317, R01DK090492, 1K99DK100736]
- Programa I + D 2010 Universidad Nacional de Cuyo
- PICT
- PIP [11220120100558]
- Ubacyt Argentina [20020120100177]
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, IRSI, Ala, 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 NE-kappa B-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. (C) 2014 Elsevier Inc. All rights reserved.
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