Inhibitory effects of Zinc on hyperglycaemia and metabolic disorders in the liver of alloxan-induced diabetic rats

Background: Zinc may participate as a component of the antioxidant defense system. Its deficiency induces oxidative damage to cell components and alterations in antioxidants enzymes in both animal and cells models. There are few studies to provide evidence of the action of zinc in diabetic animal models. Objective: To evaluate the action of oral administration of zinc (Zn) in hyperglycemia and metabolic disorders induced in the liver of alloxan-induced diabetic rats. Materials and method: Wistar rats (age: two months) were used for this study. Inducing diabetes in rats using alloxan, we obtained the diabetic rats after four weeks. The rats were divided into five groups (each n=8): normal (control) rat, diabetic rats before the beginning of treatment (Diab-ref), diabetic rats at the end of the treatment (Diab-Con), diabetic rats treated with zinc gluconate (Diab+Zn), and diabetic rats treated with insulin (Diab+Ins). Zinc was orally administrated in drinking water at dose 150mg/L, and insulin was administrated at 0.5IU/rat/day. Thiobarbituric acid-reactive substances (TBARS) superoxide dismutase (SOD), glutathione peroxidise (GPX), catalase (CAT), transaminase glutanic pyruvic (TGP), transaminase glutanic oxaloacetic (TGO), total bilirubin, total cholesterol (TCh), triglyeerides (TG), high density lipid-cholesterol (HDL-Ch), plasmatic, and liver glucose were determined in blood and liver samples. Results: Zn administration significantly decreased glucose level and glycogen content. Activities of SOD, CAT and GPO were significantly increased by Zn-treatment. In addition, the liver toxicity was prevented by significantly lowering in total bilirubin, TARSs, TGP, and TPO. Conclusion: Zinc supplements may be beneficial for correcting hyperglycemia leading to diabetic complications in the liver.