ISSN No. 1606-7754                   Vol.12 No.1&2  April-August 2004

Effect of zinc deficiency and experimental diabetes on glutamate oxaloacetate, glutamate pyruvate aminotransferases and alkaline phosphatase activities in rats
Z Kechrid and N Bouzerna
Department of Biochemistry, Faculty of Sciences, University of Annaba, PO BOX 12, Annaba 23000, Algeria

Abstract

The aim of this study was to investigate the effect of low dietary zinc intake and experimental diabetes on transaminases and alkaline phosphatase activities in rats. 8 week old male normal albino (Wistar) rats were fed diets containing either adequate (54 mg/kg) or deficient (1 mg/kg) quantities of zinc for one week. Ten rats from each group (n = 20) were injected with alloxan to induce diabetes. Control and alloxan rats were fed for three weeks and food intake and body weight gain were recorded daily and twice weekly, respectively. On day 28 the animals were killed and blood glucose, serum zinc, pancreatic zinc, serum glutamate oxalate transaminase (GOT), serum glutamate pyruvate transaminase (GPT) and serum alkaline phosphatase were determined after an overnight fast. Body weight gain of diabetic animals at the end of four weeks of dietary manipulation was significantly lower than those of the non-diabetic animals. Diabetic rats had higher food intake and lower serum and pancreatic zinc concentrations compared with non-diabetic rats. Dietary zinc intake significantly altered the body weight gain, food intake and serum zinc concentration of diabetic or non-diabetic rats. Serum GOT and GPT were significantly higher in alloxan-induced diabetic rats than in normal rats while the level of serum alkaline phosphatase was lower. The consumption of low-Zn diet led to increase in GOT and GPT, and decrease in serum alkaline phosphatase. In conclusion, the combination of zinc deficiency and diabetes affects the activities of GOT, GPT and alkaline phosphatase, and it appears that zinc deficiency may lead to the development of severe diabetes.

Keywords : Diabetes Mellitus, rats, alloxan, GOT, GPT, alkaline phosphatase

Introduction

It is well known that zinc forms an integral part of crystalline insulin.1 Pancreatic zinc content of diabetic animals has been found to be strikingly reduced.2 In addition, hyperzincuria has been demonstrated in many diabetic subjects.3 Diabetic children have been shown to have low hair zinc levels, which return to normal after insulin administration.4 Experimental diabetes can be produced by intravenous administration of dithisone5 or by intraperitoneal injection of alloxan.6 Experimental animals show a triphasic change in blood sugar levels, initial hyperglycaemia, hypoglycaemia, and finally hyperglycaemia, after the administration of alloxan. The development of such phases in alloxan diabetes is mainly due to insulin deficiency, insulin surplus and then the absence of insulin secretion, respectively.7

Many research workers reported a significant elevation in glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT) activities in diabetic human8 and animals.7 Raised and decreased levels of alkaline phosphatase were also recorded in patients with diabetes.9, 10

In view of the relationship between zinc and diabetes, and the alteration of GOT, GPT and alkaline phosphatase associated with the diabetic state, this work was carried out to determine the effect of reduced dietary zinc on metabolic changes in alloxan-induced diabetes.

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