The Potential Role of Vitamin D Supplementation in Ameliorating the Pathogenesis of Induced Type 2 Diabetes in Rats
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Abstract
Background: Vitamin D act as a pre-hormone in a wide range of skeletal and extra-skeletal functions. The therapeutic potentials of vitamin D cover some very critical areas including diabetes mellitus.
Objectives: The study aimed to assess the role of vitamin D supplementation on glycemic control and insulin resistance in rats with induced type 2 diabetes mellitus (T2DM).
Materials and methods: Sixty male Albino Wistar mature rats, weighing 180±10 g and divided into 5 groups. Normal control group: 10 rats kept on regular diet and received no treatment. Normal + 1000IU vitamin D group: 5 rats kept on regular diet with 1000IU vitamin D supplementation. Diabetic control group: 15 rats with streptozotocin (STZ) induced diabetes mellitus and high fat diet receiving no treatment. Diabetic + 1000IU vitamin D group: 15 rats with STZ induced diabetes mellitus, fed high fat diet and supplemented with 1000IU vitamin D. Diabetic + 2000IU vitamin D group: 15 rats with STZ induced diabetes mellitus, fed high fat diet and supplemented with 2000IU vitamin D.
Results: There was significant reduction of serum glucose, serum insulin and homeostatic model assessment of insulin resistance (HOMA IR), total cholesterol, LDH-c and significant increase of HDL-c in Diabetic + 1000IU Vit. D and Diabetic + 2000IU Vit. D groups, when compared to diabetic group. In pancreatic and hepatic tissues, a significant increase of glucose transporter 2 (GLUT-2), insulin receptor (IR), vitamin D receptors (Vit. DR) gene expressions in diabetic + 1000IU Vit. D and diabetic + 2000IU Vit. D groups, when compared to diabetic rats was noticed (p<0.05). In muscle tissue, a significant increase of gene expression of GLUT-4 in diabetic + 1000IU Vit. D and diabetic + 2000IU Vit. D groups, when compared to diabetic rats. All results of Diabetic + 2000IU Vit. D was significantly better than of Diabetic + 1000IU Vit. D group. Gel Electrophoresis of the polymerase chain reaction (PCR) showed that diabetes mellitus results in increased methylation of GLUT-2 gene which is partially reversed by treatment with 1000IU and 2000IU vitamin D. The same can be implied from amplified GLUT-2 gene electrophoresis of hepatic tissue samples.
Conclusion: Supplementations with vitamin D increased GLUT-2 gene expression in hepatic and pancreatic tissues of diabetic rats by reducing their methylation which was associated with improvement in glycemic state.