Article

Vitamin D and Diabetes

Laboratory for Experimental Medicine and Endocrinology (LEGENDO), Katholieke Universiteit Leuven, UZ Gasthuisberg, O&N I Herestraat, Leuven, Belgium.
Endocrinology and metabolism clinics of North America (Impact Factor: 2.86). 06/2010; 39(2):419-46, table of contents. DOI: 10.1016/j.ecl.2010.02.013
Source: PubMed

ABSTRACT 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.

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    • "It is also evident that 1,25(OH)2 regulates β cell function. It affects insulin secretion by regulating intracellular levels of calcium, increasing β cell resistance to apoptosis and increasing its replication [24]. Vit D receptor ablation showed abnormal increases in islet renin angiotensin system components, which indicates that the interaction between the islet cells and Vit D is much more complicated than previously assumed [25]. "
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    ABSTRACT: Background Hyperglycemia is a common complication of diabetes melitis (DM) and in the absence of metabolic decompensation is a common finding in the Emergency Department (ED). We aimed to evaluate the 25 OH Vit D [25(OH)D] and procalcitonin (PCT) levels during hyperglycemia and after normalization of blood glucose. Material/Methods The study included 88 patients over the age of 18 years who presented with acute hyperglycemia at the Hacettepe University Department of Emergency Medicine. Euglycemia was obtained within 6–12 hours and serum samples were taken from patients on admission and 6 hours after normalization of blood glucose. Along with plasma glucose, plasma 25(OH)D and PCT levels were measured using ELISA. Results There were 88 (45 males) patients, with a median age of 60.0±13.9 years. Serum 25(OH)D levels increased in all patients after normalization of blood glucose, and serum PCT levels decreased in the whole group. This decrease was independent of type of diabetes or presence of infection. Conclusions We demonstrated an increase in 25(OH)D after normalization of blood glucose, and a decrease in PCT in patients with hyperglycemia. This effect was independent of the type of diabetes and presence of infection. Further studies are needed to evaluate the faster link between metabolic abnormalities, vitamin D, PCT, and inflammation.
    Medical science monitor: international medical journal of experimental and clinical research 04/2013; 19:264-8. DOI:10.12659/MSM.883880 · 1.22 Impact Factor
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    • "In addition, 1,25-dihydroxyvitamin D protects β-cells from detrimental immune attacks, directly by its action on β-cells, but also indirectly by acting on different immune cells, including inflammatory macrophages, dendritic cells, and a variety of T cells. Macrophages, dendritic cells, T lymphocytes, and B lymphocytes can synthesize 1,25-dihydroxyvitamin D, all contributing to the regulation of local immune responses [43]. The potential role of vitamin D deficiency in insulin resistance is shown in Table 1. "
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    ABSTRACT: Vitamin D is characterized as a regulator of homeostasis of bone and mineral metabolism, but it can also provide nonskeletal actions because vitamin D receptors have been found in various tissues including the brain, prostate, breast, colon, pancreas, and immune cells. Bone metabolism, modulation of the immune response, and regulation of cell proliferation and differentiation are all biological functions of vitamin D. Vitamin D may play an important role in modifying the risk of cardiometabolic outcomes, including diabetes mellitus (DM), hypertension, and cardiovascular disease. The incidence of type 2 DM is increasing worldwide and results from a lack of insulin or inadequate insulin secretion following increases in insulin resistance. Therefore, it has been proposed that vitamin D deficiency plays an important role in insulin resistance resulting in diabetes. The potential role of vitamin D deficiency in insulin resistance has been proposed to be associated with inherited gene polymorphisms including vitamin D-binding protein, vitamin D receptor, and vitamin D 1alpha-hydroxylase gene. Other roles have been proposed to involve immunoregulatory function by activating innate and adaptive immunity and cytokine release, activating inflammation by upregulation of nuclear factor κB and inducing tumor necrosis factor α, and other molecular actions to maintain glucose homeostasis and mediate insulin sensitivity by a low calcium status, obesity, or by elevating serum levels of parathyroid hormone. These effects of vitamin D deficiency, either acting in concert or alone, all serve to increase insulin resistance. Although there is evidence to support a relationship between vitamin D status and insulin resistance, the underlying mechanism requires further exploration. The purpose of this paper was to review the current information available concerning the role of vitamin D in insulin resistance.
    BioMed Research International 09/2012; 2012:634195. DOI:10.1155/2012/634195 · 2.71 Impact Factor
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    • "The observed increase in fracture risk is likely to be related to impaired bone quality rather than to bone mineral density. The related mechanisms, due at least in part to hyperglycemia, neuropathy, and higher incidence of hypovitaminosis D, are not yet fully understood [9]. However, disease progression is associated with low bone turnover, suggesting potential influences of antidiabetic agents on bone density and fracture rates. "
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    ABSTRACT: Novel incretin-based drugs, such as glucagon-like peptide-1 receptor agonists (GLP-1 RA) and dipeptidyl peptidase-4 inhibitors (DPP-4i), have been last introduced in the pharmacological treatment of type 2 diabetes. In the last few years, the interest on the relationship of gut hormones with bone metabolism in diabetes has been increasing. The aim of present paper is to examine in vitro and in vivo evidence on the connections between incretin hormones and bone metabolism. We also discuss results of clinical trials and metaanalysis, explore the effects of incretin drugs in vitro on osteogenic cells and osteoclasts, and speculate on the possibility of different effects of GLP-1 RA and DPP-4i on the risk of bone fractures risk in humans. Although existing preliminary evidence suggests a protective effect on the bone, at least for DPP-4i, further controlled, long-term studies with measurement of bone markers, bone density, and clinical fractures rates are needed to substantiate and confirm those findings.
    Experimental Diabetes Research 06/2012; 2012:519784. DOI:10.1155/2012/519784 · 3.54 Impact Factor
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