**1. Introduction**

Vitamin D (VD) is a unique bioregulatory molecule as it can be synthesized in the skin in addition to its dietary sources. VD in its metabolically active form, 1,25(OH)2D (calcitriol), is a secosteroid hormone produced after hepatic (at carbon atom 25) and, not exclusively, kidney (at carbon atom 1) hydroxylations. The wellstudied function of VD is associated with its ability to regulate metabolic processes in skeletal tissue by affecting mineralization, maintaining a balance between the formation and resorption of bone tissue, and thereby contributing to the prevention of osteoporosis and the occurrence of fractures. In addition to being involved in calcium-phosphate metabolism, the variety of physiological effects of VD also extends to extra-skeletal tissues, since the vast majority of their species possesses vitamin D receptor (VDR). Furthermore, most of these tissues also express the cytochrome P450 enzyme, CYP27B1, responsible for converting 25-hydroxyvitamin D (25OHD), the main circulating metabolite of VD, to hormonally active

form–1,25(OH)2D. 1,25(OH)2D through VDR controls the expression of both those genes that participate in mineral homeostasis and bone remodeling, and genes (about 500) that participate in various cellular pathways that affect physiological and cellular mechanisms, such as immunomodulation, hormone secretion, inhibition of cell proliferation, and induction of cell differentiation.

Recent epidemiological studies have indicated the association between VD deficiency and both type 1 (T1D) and type 2 (T2D) diabetes mellitus. Moreover, impaired glucose tolerance and diabetes have been shown to ameliorate in VD-deficient individuals after VD supplementation. Vitamin D deficiency, which may be a key factor for diabetes development, is prevalent around the globe, with an estimated one billion people being vitamin D deficient. The role of VD in diabetes became clearer after the discovery of VDR in the pancreas, adipose tissue, skeletal muscle cells, and immune cells, which indicates a regulatory effect of VD on glucose homeostasis. Vitamin D can directly enhance insulin synthesis and its release from pancreatic β-cells as well as increase the expression of the insulin receptor in peripheral tissues. It can also indirectly exert an antidiabetic effect by acting on cells of the immune system that secrete pro-inflammatory cytokines as mediators affecting weight gain, systemic inflammation (contributes to insulin resistance), and autoimmune-mediated destruction of pancreatic β-cells. These findings suggested that VD deficiency probably has a causal relationship with diabetes mellitus. Some studies have also reported that VD deficiency was not the cause, but the result of diabetes. Regardless of whether this deficiency is one of the causes of diabetes or its consequence, it is obvious that low levels of VD are closely associated with poor regulation of diabetes and its complications; however, the extent of this relationship and its clinical relevance are not well established.

The aim of the present chapter is to summarize the latest evidence linking VD insufficiency/deficiency with the development of T1D and T2D and their complications. We also analyzed different intervention studies with VD supplements to determine their influence on glucose metabolism and delineated the underlying mechanisms. Previous reviews on the role of VD in diabetes mellitus have been published in recent years. Here, priority was given to the most recent and convincing available evidence.
