Effect of vitamin D on zinc status, carbohydrate metabolism, and activities of some enzymes in alloxan-diabetic rats fed on a zinc deficient diet

Objective: This study was carried out to investigate the effect of vitamin D on experimental diabetes in albino (Wistar) rats fed on a zinc deficient diet.

Methods: Male alloxan-diabetic albino (Wistar) rats of ten weeks of age were divided into three groups. The first group was fed on a zinc adequate diet (AZ containing 5.4 mg zinc/100g). The second group was given a zinc deficient diet (ZD containing 0.12 mg zinc/100g), and the third group received a zinc deficient diet and was treated orally with vitamin D (12.5µg/kg) (ZD + VD). Body weight gain was recorded regularly during the experimental period. After three weeks, the animals were sacrificed and blood glucose, serum cholesterol, serum triglycerides, serum total protein, serum urea, serum zinc, liver zinc, kidney zinc, pancreatic zinc, femur zinc, liver glutathione concentrations, serum glutamic oxalic transaminase (GOT), serum glutamic pyruvic transaminase (GPT) and serum alkaline phosphatase activities were determined.

Results: The body weight gain of the zinc deficient diabetic animals at the end of three weeks of dietary manipulation was significantly lower than that of the zinc adequate diabetic animals. The zinc deficient diet significantly increased the blood glucose, serum cholesterol, serum triglycerides, and serum urea of the zinc deficient diabetic rats as compared to their counterparts fed on an adequate zinc diet. Meanwhile serum zinc, femur zinc, pancreatic zinc, liver zinc, kidney zinc, serum total protein, and liver glutathione levels were diminished. The consumption of a zinc deficient diet led also to an increase in GOT and GPT and a decrease of serum alkaline phosphatase activities. However, vitamin D treatment ameliorated all of the previous physiological and biochemical parameters.

Conclusion: In conclusion, this study demonstrated that vitamin D reduced the severity of diabetes development caused by zinc deficiency. In other words, vitamin D probably increased zinc absorption which led to insulin synthesis and secretion and improvement of insulin activity.