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Impact of rosiglitazone and metformin on serum pro‐inflammatory molecules and adipocytokines in rats with chronic fructose diet
Author(s) -
Sigrist-Flores Santiago,
Pardo Juan Pablo,
Murguía-Romero Miguel,
Villalobos-Molina Rafael,
Jimenez-Flores Rafael
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1120.8
Subject(s) - medicine , endocrinology , metformin , rosiglitazone , adipokine , hyperuricemia , dyslipidemia , leptin , adiponectin , uric acid , metabolic syndrome , fructose , inflammation , adipose tissue , insulin resistance , diabetes mellitus , chemistry , obesity , biochemistry
Metabolic syndrome is a pathological condition involving metabolic abnormalities: abdominal obesity, hyperinsulinemia, dyslipidemia, impaired glucose uptake, all of them linked with increased risk for DM2, and CVD. Those alterations are closely related to a chronic inflammation promoting endothelial dysfunction, and other reactants of acute and chronic phases. Adipose tissue produces adipokines that integrate endocrine, autocrine and paracrine signals, contributing to inflammation. We aimed to explore the in vivo effect of metformin and rosiglitazone in fructose‐fed rats. We evaluated sICAM‐1, TNF‐α, IL‐6, IL‐1β, C‐Reactive Protein, leptin, adiponectin, and glucose, triglycerides, uric acid, HDL‐C and LDL‐C. Drugs were administered alone or combined for 3 mo, in rats fed 30% fructose for 4 mo. At month 6 with fructose diet, altered glucose, triglycerides and uric acid, were observed. Fructose induced changes in IL‐6 and IL‐1β at month 7, not observed in rats treated with metformin. Combined therapy decreased weight and normalized leptin and IL‐1β. Thus, increase in IL‐6 and IL‐1β after fructose intake, evidence inflammation, normalized by the combined effect of metformin and rosiglitazone, and harmonizes with decreased leptin and weight loss. Supported in part by grant PICDS08‐69 from ICyT‐G.D.F., México.