Evidence suggests that low levels of the active vitamin D metabolite 25-hydroxyvitamin D are associated with type 1 and type 2 diabetes, as well as obesity. This may be explained by a role for vitamin D in the function of the insulin receptor, perhaps through regulation of intracellular calcium levels. Calcium is an important intracellular signal messenger, and evidence suggests that chronically low levels of 25-hydroxyvitamin D may decrease plasma levels of calcium and at the same time increase intracellular levels. The high levels of cellular calcium may negatively affect the second messenger functions of the cell and disrupt normal cellular homeostasis. The association between low levels of plasma 25-hydroxyvitamin D and insulin resistance have been reported, with insulin resistance negatively affecting correct blood glucose regulation. Low levels of 25-hydroxyvitamin D may also deteriorate the function of the beta cells of the pancreas resulting in further deteriorations in blood glucose regulation.
Researchers have measured the association between plasma levels of 25-hydroxyvitamin D and insulin sensitivity1. Subjects were over 30 years of age and showed clinical symptoms of the metabolic syndrome and insulin resistance from the results of an oral glucose tolerance test, but were clinically free from type 2 diabetes. The results of the analysis showed that plasma levels of 25-hydroxyvitamin D were independently associated with insulin sensitivity in the subjects. In addition, the 25-hydroxyvitamin D levels of the subjects were also associated with β-cell function. These results therefore support other studies that show that associations exist between vitamin D status and blood glucose regulation in otherwise healthy subjects. The ability of vitamin D to regulate calcium metabolism, and the role played by calcium in cell signalling may explain the association between vitamin D and the modulation of blood glucose. In the absence of sunlight current recommendations are to supplement with vitamin D.
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