Glucose intolerance due to heavy metals intoxication in the rat

Data of the current study show that intraperitoneal (i.p.) injection of cadmium chloride (CdCl2) (5 mg/kg) into male albino rats was found to induce a deterioration in glucose tolerance 24 hr post-treatment, which was accompanied by a reduced elevation in serum insulin levels inresponse to the glucose challenge. CdCl2 produced a significant decrease in the liver content of both glutathione and protein contents 24 hours post CdCl2 treatment while a significant elevation in liver thiobarbeturic acid (TBA)-reactants was observed. A significant decrease in serum total proteins was noticed due to CdCl2 treatment while the serum levels of the two aminotransferases enzymes AST & ALT were in significantly changed affected by cadmium intoxication. The present study suggest that the glucose intolerance observed due to CdCl2 intoxication could be due to the elevation of lipid peroxidation (induced by cadmium) which may affect the rate of glucose transport into the cells. Impaired insulin synthesis and the inactivation of the glucose metabolizing enzymes which could be secondary effects to the glutathione depleting effects of cadmium, were also suggested to be contributing mechanisms to the deterioration of glucose tolerance in cadmium intoxicated rats. The present study throw more light on one of the most serious phases of cadmium toxicity which emphasizes the importance of performing more studies to explore all the consequences of heavy metals pollution. This could be a gate way to determine means for protection against this pollution.