Title of article :
Impaired glucose tolerance in vitamin d deficiency can be corrected by calcium
Author/Authors :
Ayesha Ismail، نويسنده , , Raghuramulu Namala، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2000
Abstract :
Vitamin D3, via its active metabolite 1α,25-dihydroxyvitamin D3, helps maintain normal calcium levels in the body. Apart from the maintenance of calcium homeostasis, the active form of vitamin D3 is now known to be involved in a number of other functions including that of pancreatic β cells. Low serum insulin levels and impaired glucose tolerance in a vitamin D-deficient state have been reported in experimental animals. Hypocalcemia is a major consequence of vitamin D deficiency. Whether the impairment observed is due to vitamin D deficiency per se or is secondary to low calcium is still a matter of controversy. The present study was conducted to delineate the roles of vitamin D and calcium in glucose intolerance associated with vitamin D deficiency in vivo. It was found that supplementation with either vitamin D3 or high calcium alone to vitamin D-deficient rats could correct the defects. In addition, insulin sensitivity was found to be enhanced in the vitamin D-deficient group compared with vitamin D control or calcium-supplemented groups. Hence the present study demonstrates that calcium per se in the absence of vitamin D increases insulin secretion and normalizes intolerance to glucose seen in vitamin D deficiency.
Keywords :
25-hydroxyvitamin D3 (25-OH-D3) , glucose tolerance , insulin tolerance , Area under the curve (AUC) , Vitamin D3
Journal title :
The Journal of Nutritional Biochemistry
Journal title :
The Journal of Nutritional Biochemistry