Model rats fructose -induced metabolic syndrome allopurunol the renal function on protective effect

Metabolic syndrome, hyperglycemia, dyslipidemia, hypertension, and abdominal obesity, and metabolic disorders simultaneously. In the world and in our country, change of dietary habits, increased abdominal obesity and sedentary life is becoming a serious problem as a result of more MS every day. Hyperuricaemia obesity, dyslipidemia, metabolic syndrome components, such as the relationship between hyperglycemia and hypertension have been identified. Large epidemiological studies showed an increase in serum uric acid levels according to the degree of MS prevalence reported tapestry Diabetes, obesity, kidney fat low-grade inflammation state are associated with macrophage infiltration. Increased adipose tissue, adipokines, and to trigger the release of reactive oxygen species via synthesis leads to renal damage. A number of studies indicated that fructose consumption; Hyperuricemia is associated with albuminuria, and progressive renal injury in the arterial endothelium at a rate of uric acid xanthine oxidase involved in limiting step in smooth muscle cells and have been shown. Uric acid produced locally has been suggested to also cause endothelial damage by increasing free radical production. Allopurinol, hypoxanthine analog is a drug prevents collapse resulting purine bases responsible for the conversion of hypoxanthine to uric acid occurring xanthine oxidase activity by inhibiting the formation of uric acid. The aim of this study was experimental metabolic syndrome model created with fructose rats, the renal function of allopurinol, a xanthine oxidase inhibitor, to evaluate plasma lipid levels and potentially protective effect of certain yücr intra pathway markers. 8-week study, 28 were female Wistar albino rats. These rats were randomly divided into 4 groups; 1 control group (group fed a standard diet), group 2 fructose group (fructose-rich diet (60% fructose) fed group), group 3 allopurinol group (fed with a standard diet and drinking water allopurinol (20 mg / kg / day) treated group), group 4 fructose and allopurinol group (fructose-rich diet (60% fructose) and enalapril fed with drinking water (20 mg / kg / day) treated group), respectively. The rats were sacrificed after 8 weeks. Blood samples; renal function tests, liver function tests and lipid levels, and renal and liver tissue samples were collected for Western blot analysis and histological applications. In renal tissue TGF-β, TNF-α, NF-kB, IL-6, SMAD-3 protein expression was measured by western blot. High fructose-fed rats allopurinol application of urea, creatinine, HDL, AST, ALT, showed a positive effect on uric acid levels. Total cholesterol, LDL showed no significant effect on glucose and triglyceride allopurinol administration in rats fed a high-fructose.Administration of allopurinol to rats fed high fructose showed a healing effect on hepatocellular necrosis, sinusoidal dilatation, portal inflammation findings in the liver. Tuberculo-vacuolization, tubular dilatation and interstitial inflammation were positively affected in kidney tissue. Allopurinol administration resulted in a significant increase in Smad-3 expression, which significantly reduced TGF-β, IL-6, NF-κB, and TNF-α expressions compared to rats fed only with fructose. As a result, high fructose nutrition has shown worsening and destructive effects on liver and kidney function tests and histopathology, but allopurinol treatment has been shown to improve these effects. It may be concluded that reducing uric acid levels is an important treatment modality in metabolic syndrome. Keywords: Metabolic syndrome, fructose, allopurinol