Evidence is accumulating to suggest that in the absence of adequate sunlight, dietary vitamin D is required in higher concentrations than was previously thought. Sub-clinical insufficiencies of vitamin D appear to be common at higher latitudes and are associated with a number of diseases including multiple sclerosis, cancer and type 2 diabetes. Evidence from animal studies shows that vitamin D has an influence on insulin metabolism, with research identifying a possible role in both insulin secretion and insulin receptor sensitivity. Researchers are therefore interested in the possible role played by vitamin D in the prevention and treatment of type 2 diabetes in humans. Epidemiological studies suggest that increased calcium and vitamin D are associated with reduced risk of type 2 diabetes. Calcium may improve vitamin D status because in the presence of high calcium intakes less 25-hydroxyvitamin D3 [25(OH)D3], would be needed to converted to 1, 25-hydroxyvitamin D3.
There are a limited numbers of studies researching the affects of vitamin D and calcium supplementation on humans with respect to type 2 diabetes. However, some randomised controlled trials have been performed. For example, researchers1 have investigated the effects of vitamin D and calcium on the glycaemic status in men and women with type 2 diabetes. In the study, 90 diabetic subjects were randomly assigned to receive a plain yoghurt drink (150 mg/250mL calcium), a vitamin D fortified yoghurt drink (500IU vitamin D with 150 mg/250 mL calcium) or a vitamin D and calcium fortified yoghurt drink (500 IU vitamin D with 250 mg/mL calcium). The drinks were consumed twice per day for 12 weeks and fasting serum glucose, glycated haemoglobin, insulin resistance, lipid profiles and percentage fat mass were assessed at baseline and after 12 weeks.
Measurement of the vitamin D status at baseline showed that 70% of the subjects receiving vitamin D or vitamin D plus calcium had suboptimal 25(OH)D3 levels, but after 12 weeks this had fallen to 10% and 20% respectively. Levels rose from 44.4 nmol/L to 77.7 nmol/L in the vitamin D group and from 44.5 nmol/L to 74.6 nmol/L in the vitamin D plus calcium group. In the yoghurt only group the number of subjects with sub-optimal 25(OH)D3 remained at 80% with levels falling from 41.6 nmol/L to 37.2 nmol/L within the 12 week. In addition, fasting serum glucose, glycated haemoglobin, waste circumference and body mass index decreased significantly in the vitamin D supplemented groups, when compared to the control. Interestingly, in the vitamin D supplemented groups, an inverse association was reported for changes in serum 25(OH)D3 with fasting serum glucose and insulin sensitivity.
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