Vitamin D and new insights into pathophysiology of type 2 diabetes
K Vondra, Richard Hampl
Abstract
Abstract Deficiency in vitamin D plays a role in the onset and development of insulin resistance (IR) and type 2 diabetes (T2DM). A normal level of vitamin D is able to reduce low grade inflammation, which is a major process in inducing insulin resistance. It is also engaged in maintaining low resting levels of reactive species and radicals, normal Ca 2+ signaling, a low expression of pro-inflammatory cytokines but increased formation of anti-inflammatory cytokines. Vitamin D is also able to prevent hypermethylation (of DNA) and consequent functional inactivation of many genes, as well as other epigenetic alterations in β cells and in other insulin-sensitive peripheral tissues, mainly liver, adipose tissue and muscle. Vitamin D deficiency thus belongs to key factors accelerating the development of IR and consequently T2DM as well. However, vitamin D supplementation aimed at the control of glucose homeostasis in humans showed controversial effects. As a result, further studies are running to gain more detailed data needed for the full clinical utilization of vitamin D supplementation in the prevention and treatment of T2DM. Until new results are published, supplementation with high doses of vitamin D deficiency is not recommended. However, prevention of vitamin D deficiency and its correction are highly desired.