Vitamin D is a steroid hormone, and not a true vitamin, as it is synthesised in the skin by the action of ultraviolet light on cholesterol. The traditional view is that vitamin D is required to prevent the development of rickets in children and osteomalacia in adults and in this regard vitamin D has important functions in the absorption and metabolism of calcium. However, more recently the physiological functions of vitamin D and its metabolites 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D have been widened to include a wide range of cellular responses. One of the novel functions of vitamin D may relate to its ability to regulate insulin sensitivity. The involvement of vitamin D with the insulin system explains to some extent the association between vitamin D plasma levels and the risk of developing type 1 and type 2 diabetes. Observational studies also show that low levels of vitamin D are associated with glucose intolerance, insulin resistance and metabolic syndrome.
Clinical trials have investigated the effects of vitamin D on the insulin system using randomised and placebo controlled studies. Such studies have generally shown beneficial effects for supplementation of vitamin D with regard to glucose and insulin homeostasis, supporting the observations from epidemiology. For example, in one study1 researcher selected a population of subjects with 25-hydroxyvitamin D (the accepted biomarker of vitamin D status) below 50 nmol/L (20 ng/ml). The subjects were then administered 500 mg per day of calcium as calcium carbonate as well as 1200 IU of vitamin D3 (cholecalciferol) or a placebo for 16 weeks. The 25-hydroxyvitamin D status of those subjects receiving the vitamin D supplement increased significantly compared to the placebo group such that at week 16 the vitamin D group had 25-hydroxyvitamin D plasma concentrations that were ~38 nmol/L higher than the placebo group (~60 nmol/L in the treatment group and ~23 nmol/L in the control group (rounded figures)).
The researchers then assessed the insulin function of the subjects. Including the subjects with diabetes in the analysis prevented statistical significance between the treatment and control groups being obtained for measures of insulin function. However, excluding these subjects showed that the vitamin D supplements had improved the insulin sensitivity, glucose tolerance and β-cell function of the subjects in the treatment group compared to the control group. These effects were only apparent in the subjects who managed to obtain plasma 25-hydroxyvitamin D concentrations above 60 nmol/L (24 ng/mL). Therefore the insulin sensitising effects of vitamin D appear to become apparent at plasma levels above 60 nmol/L which suggests that below this level, vitamin D status is insufficient. In this study the vitamin D showed no side effects and was well tolerated by the subjects. However, the 1200 IU dose given to the subjects was below the 2000 IU dose recommended for adults in the absence of moderate to strong sunlight.
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