Vitamin D and diabetes

• Published in: Endocrinology and metabolism clinics of North America Vol. 39; no. 2; p. 419
• Main Authors: Takiishi, Tatiana, Gysemans, Conny, Bouillon, Roger, Mathieu, Chantal
• Format: Journal Article
• Language: English
• Published: United States 01.06.2010
• Subjects: Animals; Diabetes Mellitus, Type 1 - drug therapy; Diabetes Mellitus, Type 1 - prevention & control; Diabetes Mellitus, Type 2 - drug therapy; Diabetes Mellitus, Type 2 - prevention & control; Dietary Supplements; Female; Genetic Predisposition to Disease - genetics; Glucose Intolerance - drug therapy; Humans; Immune System - drug effects; Immune System - metabolism; Insulin - metabolism; Insulin Resistance - genetics; Insulin Secretion; Insulin-Secreting Cells - metabolism; Male; Mice; Pancreatitis - drug therapy; Pancreatitis - prevention & control; Rats; Receptors, Calcitriol - genetics; Receptors, Calcitriol - metabolism; Vitamin D - analogs & derivatives; Vitamin D - blood; Vitamin D - genetics; Vitamin D - metabolism; Vitamin D - therapeutic use; Vitamin D Deficiency - drug therapy; Vitamin D Deficiency - genetics; Vitamin D-Binding Protein - genetics; Vitamin D-Binding Protein - metabolism
• ISSN: 1558-4410
• DOI: 10.1016/j.ecl.2010.02.013

Type 1 (T1D) and type 2 (T2D) diabetes are considered multifactorial diseases in which both genetic predisposition and environmental factors participate in their development. Many cellular, preclinical, and observational studies support a role for vitamin D in the pathogenesis of both types of diabetes including: (1) T1D and T2D patients have a higher incidence of hypovitaminosis D; (2) pancreatic tissue (more specifically the insulin-producing beta-cells) as well as numerous cell types of the immune system express the vitamin D receptor (VDR) and vitamin D-binding protein (DBP); and (3) some allelic variations in genes involved in vitamin D metabolism and VDR are associated with glucose (in)tolerance, insulin secretion, and sensitivity, as well as inflammation. Moreover, pharmacologic doses of 1,25-dihydroxyvitamin D (1,25(OH)(2)D), the active form of vitamin D, prevent insulitis and T1D in nonobese diabetic (NOD) mice and other models of T1D, possibly by immune modulation as well as by direct effects on beta-cell function. In T2D, vitamin D supplementation can increase insulin sensitivity and decrease inflammation. This article reviews the role of vitamin D in the pathogenesis of T1D and T2D, focusing on the therapeutic potential for vitamin D in the prevention/intervention of T1D and T2D as well as its complications.