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Evidence-Based Complementary and Alternative Medicine
Volume 2013 (2013), Article ID 590376, 12 pages
http://dx.doi.org/10.1155/2013/590376
Research Article

Improvement of Liquid Fructose-Induced Adipose Tissue Insulin Resistance by Ginger Treatment in Rats Is Associated with Suppression of Adipose Macrophage-Related Proinflammatory Cytokines

1Faculty of Basic Medical Sciences, Chongqing Medical University, Chongqing 400016, China
2The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China
3College of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, China
4Endocrinology and Metabolism Group, Sydney Institute of Health Sciences, Sydney, NSW 2000 , Australia
5Pharmafood Institute, Kyoto 602-8136, Japan

Received 31 October 2012; Revised 25 December 2012; Accepted 12 January 2013

Academic Editor: Wen-Chin Yang

Copyright © 2013 Jianwei Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Adipose tissue insulin resistance (Adipo-IR) results in excessive release of free fatty acids from adipose tissue, which plays a key role in the development of “lipotoxicity.” Therefore, amelioration of Adipo-IR may benefit the treatment of other metabolic abnormalities. Here we found that treatment with the alcoholic extract of ginger (50 mg/kg/day, by oral gavage) for five weeks attenuated liquid fructose-induced hyperinsulinemia and an increase in the homeostasis model assessment of insulin resistance (HOMA-IR) index in rats. More importantly, ginger reversed the increases in the Adipo-IR index and plasma nonesterified fatty acid concentrations during the oral glucose tolerance test assessment. Adipose gene/protein expression profiles revealed that ginger treatment suppressed CD68 and F4/80, two important macrophage accumulation markers. Consistently, the macrophage-associated cytokines tissue necrosis factor alpha and interleukin-6 were also downregulated. In contrast, insulin receptor substrate (IRS)-1, but not IRS-2, was upregulated. Moreover, monocyte chemotactic protein (MCP)-1 and its receptor chemokine (C-C motif) receptor-2 were also suppressed. Thus these results suggest that amelioration of fructose-induced Adipo-IR by ginger treatment in rats is associated with suppression of adipose macrophage-related proinflammatory cytokines.