Based on basic and animal studies, vitamin D and calcium have also been suspected as modifiers of diabetes risk. Vitamin D insufficiency has long been suspected as a risk factor for type 1 diabetes based on animal and human observational studies (Mathieu C, Badenhoop K 2005 Vitamin D and type 1 diabetes mellitus: state of the art. Trends Endocrinol Metab 16:261–266).
More recently, there is accumulating evidence to suggest that altered vitamin D and calcium homeostasis may also play a role in the development of type 2 Diabetes Mellitus.
Animal and in vitro studies provide compelling evidence that vitamin D may play a functional role in the preservation of glucose tolerance through its effects on insulin secretion and insulin sensitivity.
Vitamin D deficient rabbits and mice present with impaired insulin secretion, and supplementation with vitamin D corrects the defect [C. Cade and A. W. Norman, “Vitamin D3 improves impaired glucose tolerance and insulin secretion in the vitamin D-deficient rat in vivo,” Endocrinology, vol. 119, no. 1, pp. 84–90, 1986].
Vitamin D deficiency may influence its effects on insulin secretion and sensitivity via its effects on intracellular calcium [A. G. Pittas, J. Lau, F. B. Hu, and B. Dawson-Hughes, “The role of vitamin D and calcium in type 2 diabetes. A systematic review and meta-analysis,” Journal of Clinical Endocrinology and Metabolism, vol. 92, no. 6, pp. 2017–2029, 2007].
Elevated intracellular calcium impairs post-receptor binding insulin action, such as the dephosphorylation of glycogen synthase and of insulin regulatable glucose transporter (GLUT-4). Vitamin D deficiency results in elevated parathyroid hormone (PTH), which in turn is known to elevate intracellular calcium.
Vitamin D deficiency inhibits the pancreatic secretion of insulin
