Effect of 1,25-dihydroxy vitamin D3 (1,25(OH)2D3 ) on hexavalent chromium (Cr (VI)) induced alteration of glucose homeostasis in Wistar rats

Background: 1,25-dihydroxy vitamin D3(1,25(OH)2D3) is a fat-soluble known antioxidant vitamin to protect cardiovascular health. Hexavalent chromium (Cr (VI)) as a heavy metal has adverse effects on vascular system. Aim and Objectives: To evaluate the possible protective effects of 1,25(OH)2D3 supplementation on Cr (VI) induced altered glucose regulation. Materials and Methods: Twenty-four adult Wistar male rats were divided into four groups (n=6 in each group) as following: Group-1 (control); Group-2 received K2Cr2O7 5.0 mg/kg body weight intraperitoneally for 10 dosages on every alternate day for 20 days; Group-3 received 1,25(OH)2D3 12.5μg/kg/d, orally daily till 20 days; and Group-4 received both K2Cr2O7 and 1,25(OH)2D3 with dosages as above. At the end of 10th dosage after overnight fasting i.e. (on day 21) blood samples were collected from tail vein of all the rats. Oral Glucose Tolerance Test (OGTT), serum glucose and insulin concentrations were estimated. Insulinogenic index was also calculated. Liver glycogen concentrations were assessed after sacrificing the animals. Results: OGTT showed an increase of fasting blood glucose levels in Cr (VI) treated Group-2 rats till at the end of 2.0 hrs. The Cr (VI) treated and simultaneously supplemented with 1,25(OH)2D3 Group-4 rats showed lesser elevation of blood glucose level till 2.0 hrs. A decrease in plasma insulin level and increase in insulinogenic index were also found in Cr (VI) treated Group-2 rats but in case of vitamin D supplemented Group-4 rats, both plasma insulin levels and insulinogenic index were found to be improved remarkably. Liver glycogen concentrations in K2Cr2O7 treated rats were also found to be reduced significantly but 1,25(OH)2D3 supplemented Group-4 rats showed improvement in liver glycogen concentrations. Conclusion: 1,25(OH)2D3 is found to be beneficial against hexavalent chromium induced alteration of glucose homeostasis.