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Asian Journal of Animal Sciences

Year: 2010 | Volume: 4 | Issue: 4 | Page No.: 190-196
DOI: 10.3923/ajas.2010.190.196
Prevention of Alloxan Induced Diabetes Mellitus in Rats by Vitamin a Dietary Supplementation
M.Y. Gwarzo, V.A. Nwachuku and A.O. Lateef

Abstract: The aim of the study was to examine whether vitamin A dietary supplementation can prevent alloxan induced diabetes mellitus. Alloxan was used to destroy the β-cells of pancreas by generation of reactive oxygen species in Wistar albino rats. In this study, the blood glucose level and histological architecture of the pancreatic beta cells were examined. Three groups (n = 5) and were fed on commercial diet as lib. Group one was control diabetic, group two was fed with vitamin A supplementation in the diet (824 IU daily) before and after diabetic induction with alloxan. Group three was control non diabetic. The rats were made diabetic by intra peritoneal injection of 100 mg kg-1 b.wt. with alloxan once per week for three weeks. Fasting blood glucose was measured seven days after diabetic induction to determine the severity of blood glucose elevation. Histochemical analysis using hematoxylin stain (magnification X40) of the vitamin A administered rats revealed remarkable normal pancreatic beta cells, unlike the diabetic rats whose beta cell were necrotic and little in number. Vitamin A effect on serum glucose level was significantly different compared to diabetic control (5.53±0.40 vs. 18.64±3.92 mmol L-1, p<0.0001), respectively. Through treatment with vitamin A for one week after induction did not have any significant effect, but has reduced the serum level by about 3 mmol compared before treatment (16.81±2.88 vs. 19.60±2.95 mmol L-1, p<0.96), respectively. Taken together, the result suggests that Vitamin A protects against alloxan induced diabetes in rats.

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How to cite this article
M.Y. Gwarzo, V.A. Nwachuku and A.O. Lateef, 2010. Prevention of Alloxan Induced Diabetes Mellitus in Rats by Vitamin a Dietary Supplementation. Asian Journal of Animal Sciences, 4: 190-196.

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