Traditionally, the role for vitamin D in human metabolism has been seen to be one of calcium regulation. Vitamin D is actually a hormone, not a vitamin, and is synthesised endogenously in the skin from the action of ultraviolet light on cholesterol. The resulting vitamin D is then converted first into 25-hydroxyvitamin D [25(OH)D] and then 1,25-dihydroxyvitamin D [1,25(OH2)D], the latter two compounds having different biological activities. Vitamin D plays a role in calcium homeostasis and low levels decrease calcium absorption, which may produce long term changes in bone homeostasis. Novel roles for vitamin D have recently been discovered, and one such role is that of a regulator of blood glucose homeostasis through modulation of the insulin receptor. Epidemiological evidence shows inverse associations for 25(OH)D with obesity, type 1 diabetes, and type 2 diabetes, supporting the theory that vitamin D is involved in some way in regulating glucose metabolism in humans.
A number of prospective studies have been performed to investigate the association between circulating 25(OH)D and glucose homeostasis. In one such study1, researchers measured a number of biochemical parameters relating to blood glucose homeostasis in pre-diabetic and normal healthy subjects. Those with pre-diabetes had significantly lower insulin sensitivity and β-cell function compared to the healthy subjects. Within the pre-diabetic groups, insulin sensitivity was significantly lower in the 25(OH)D group compared to the 25(OH)D sufficient group of pre-diabetic subjects. These results suggest that pre-diabetic subjects with low circulating levels of 25(OH)D are at the highest risk of being insulin resistance. Calcium may be involved in the effects of 25(OH)D on blood glucose because low levels of plasma calcium increase intracellular calcium. This increased intracellular calcium may then interfere with the insulin signal cascade, decreasing insulin sensitivity and causing elevations in blood glucose.
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