Epidemiological evidence suggests that vitamin D status is inversely associated with diabetes risk. A role for vitamin D in the development of type 2 diabetes has been established in animal models that show decreased glucose tolerance and incidence of diabetes in animals restricted of vitamin D. In addition, populations exposed to increased solar radiation in lower latitudes, have a reduced risk of diabetes and higher levels of the vitamin D marker 25(OH)D, compared to populations in higher latitudes. The role of vitamin D in the development of diabetes is of major interest because evidence suggests that large numbers of individuals, particularly those with darker skin in high latitudes, have insufficient circulating levels of 25(OH)D. Recent increases in diabetes cases have highlighted the failure of traditional controls for diabetes, with vitamin D not featuring as part of mainstream treatment for the disease.
Clinical trials investigating the effects of vitamin D supplements on insulin function are few in number. However, those that have been undertaken have confirmed that vitamin D plays a role in the function of the insulin system. For example, researchers1 randomly assigned 92 adults (mean age 57 years, mean body mass index 32kg/m2) at risk of diabetes to receive either 2000IU of vitamin D, 800mg calcium carbonate or a placebo for 16 weeks. The pancreatic β-cell function of the individuals was then assessed by the disposition index after intravenous injection of glucose. The results showed that calcium had no influence on any measured parameters. However, those consuming 2000IU of vitamin D showed an increase in the disposition index which the authors explained by improved insulin secretion. In contrast, those not taking the vitamin D supplement had a decrease in the disposition index.
Short-term supplementation with modest amounts of vitamin D show beneficial effects on pancreatic β-cell function. This study supports other evidence that shows an important role for vitamin D in the aetiology of type 2 diabetes. There is now good evidence that vitamin D can affect both pancreatic function and insulin sensitivity, both of which are present in type 2 diabetes. The vitamin D metabolite 1,25-dihydroxyvitamin D [1,25(OH)2D] may bind to the vitamin D receptor which is expressed in β-cells. The human insulin gene promoter also contains a vitamin D response element which can be transcriptionally activated by 1,25(OH)2D wich supports the evidence to suggest a role for vitamin D in insulin secretion and synthesis. Pancreatic β-cells also contain 25(OH)D-1-α-hydroxylase a P450 enzyme that converts calcidiol [25(OH)D] to calcitriol [1,25(OH)2D]. This suggests that the activated form of vitamin D in needed in β-cells.
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