Effect of quercetin on perirenal adipose tissue adiponectin and resistin levels in rats with metabolic syndrome induced by high fructose-diet

Authors : Emine Kılıç Toprak, Melek Tunç Ata

Pages : 347-357

Doi:10.31362/patd.1398168

View : 49 | Download : 86

Publication Date : 2024-04-01

Article Type : Research Paper

Abstract :Purpose: Metabolic syndrome (MetS) is a cluster of risk factors for developing heart disease, stroke, and type 2 diabetes. Visceral adiposity and insulin resistance are crucial mechanisms of MetS. The increase in adipose tissue observed in MetS causes proinflammatory and anti-inflammatory cytokine imbalance. Accumulating evidence on quercetin, one of the antioxidants frequently used in MetS treatment, suggests that quercetin has significant anti-obesity and lipid-lowering effects simultaneously. Our aim is to investigate the effects of quercetin supplementation on MetS parameters and adipose tissue adipokine levels in rats fed high fructose. Materials and methods: Sprague Dawley rats, 8-10 weeks of age, were divided into 4 groups, including a control group (C), high fructose (HF) group, quercetin (Q) group, and high fructose+quercetin (HF+Q) group. Fructose was administered to HF groups as a 20% solution in drinking water for 10 weeks. The rats in the Q groups were given 50 mg quercetin per kg BW by gavage for the last 4 weeks of experiment. The body weight, triglyceride (TG), high density lipoprotein (HDL), fasting insulin, fasting glucose, and HOMA-IR were determined in rats. Adiponectin and resistin levels were determined by ELISA assay from perirenal adipose tissue homogenates. Results: We showed that quercetin acts to improve TG, fasting glucose and insulin resistance in high fructose-fed rats. In this study, we found no effect of quercetin on perirenal adipose tissue adiponectin and resistin levels. Conclusion: These results showed that high fructose could induce MetS in rats, while quercetin could favorably affect these parameters.
Keywords : Metabolik sendrom, quercetin, perirenal adipoz doku, adiponektin, resistin