Article

Vitamin D and Diabetes

Laboratory of Experimental Medicine and Endocrinology (LEGENDO), Catholic University of Leuven, Herestraat 49, 3000, Leuven, Belgium.
Diabetologia (Impact Factor: 6.67). 08/2005; 48(7):1247-57. DOI: 10.1007/s00125-005-1802-7
Source: PubMed

ABSTRACT

Vitamin D deficiency predisposes individuals to type 1 and type 2 diabetes, and receptors for its activated form-1alpha,25-dihydroxyvitamin D3-have been identified in both beta cells and immune cells. Vitamin D deficiency has been shown to impair insulin synthesis and secretion in humans and in animal models of diabetes, suggesting a role in the development of type 2 diabetes. Furthermore, epidemiological studies suggest a link between vitamin D deficiency in early life and the later onset of type 1 diabetes. In some populations, type 1 diabetes is associated with certain polymorphisms within the vitamin D receptor gene. In studies in nonobese diabetic mice, pharmacological doses of 1alpha,25-dihydroxyvitamin D3, or its structural analogues, have been shown to delay the onset of diabetes, mainly through immune modulation. Vitamin D deficiency may, therefore, be involved in the pathogenesis of both forms of diabetes, and a better understanding of the mechanisms involved could lead to the development of preventive strategies.

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Available from: Conny Gysemans, Sep 16, 2014
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    • "Recently it has been postulated that inflammatory and innate immune activation could be linked to the pathogenesis of T2D and its complications (Pickup, 2004). It has been suggested that low levels of vitamin D may be a risk factor for the development of T2D (Mathieu et al., 2005). At present, important Meta Gene 7 (2016) 1–6 ⁎ Corresponding author at: Av. "
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    ABSTRACT: Introduction: FokI polymorphism has been associated with obesity and type 2 diabetes (T2D) in some populations. Objective: To investigate the frequencies of a genetic polymorphism of Vitamin D receptor (FokI) in patients with T2D and control subjects and investigate the role of 1,25(OH)2D3 in the expression of pro-inflammatory markers in peripheral blood mononuclear cells (PBMCs). Methods: The case-control study was conducted in 160 patients with T2D and 160 control subjects, men and women (30-74years old). The genotype and allele frequency of FokI polymorphisms were determined in these subjects. Subsequently a subgroup of 40 subjects was included from which PBMCs were removed. In vitro, the culture medium was supplemented with two different concentrations of 1,25(OH)2D3(10-8M and 10-10M). The expression profiles of TNFα and mRNA were analysed by qPCR, and GAPDH and β-actin were used as housekeeping genes. Results: The control subjects have an increased frequency of the FF genotype. In subjects with T2D, the ff genotype was associated with higher HOMA-IR values than individuals with genotype Ff (p=0.021). In vitro study in PBMCs showed differential expression of TNFα mRNA by FokI genotype, with a lower expression of this marker of inflammation in FF genotype subjects at a concentration of 10-8M of 1,25(OH)2D3. Conclusion: Our data suggest that VDR FokI polymorphism is associated with T2D, and the genotypes Ff and ff of this variant show a reduced response or resistance to the anti-inflammatory action of VitD, which could indicate a functional role of FokI polymorphism of VDR.
    Full-text · Article · Oct 2015 · Meta Gene
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    • "Results of studies which have been conducted for some years confirm that vitamin D deficiency is a risk factor for MS disorders , including obesity, arterial hypertension, diabetes. On the other hand, there are justified assumptions that these disorders greatly contribute to the deficiency of vitamin D123. Vitamin D is provided to the body per os and is generated in the skin by ultraviolet radiation B (UVB)456. "
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    ABSTRACT: Vitamin D deficiency is a risk factor for metabolic syndrome disorders and the occurrence of these disorders greatly contributes to the deficiency of vitamin D. Postmenopausal women are particularly prone to that deficiency. The aim of the study was to assess vitamin D concentration in the plasma of pre- and postmenopausal women, with or without metabolic syndrome. The study included 141 women aged 26-77 (the mean age 58.74 years old), divided into 4 groups depending on the pre- or postmenopausal period and diagnosed or not with metabolic syndrome according to the International Diabetes Federation criteria (2005). Vitamin D concentration was assessed by LIAISON(®) test using chemiluminescent immunoassay (CLIA) technology. The mean vitamin D concentration was the highest among premenopausal women without metabolic syndrome (24.32 ng/ml), it was insignificantly higher than in postmenopausal women without metabolic syndrome (23.52 ng/ml) and significantly higher than in both groups with metabolic syndrome - premenopausal (19.86 ng/ml) and postmenopausal women (9.32 ng/ml). The recommended plasma 25(OH)D concentration was not found in any of postmenopausal women with diagnosed metabolic syndrome. Postmenopausal women with metabolic syndrome had a significantly lower 25(OH)D vitamin concentration in plasma than postmenopausal women without metabolic syndrome. The frequency of vitamin D deficiency in women with metabolic syndrome was very high, significantly higher than in women without metabolic syndrome.
    Full-text · Article · Oct 2014 · Menopausal Review
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    • "The expression of calbindin-D28K (vitamin D dependent on the union of proteins and calcium) has demonstrated a protective effect on beta cells from cytokine mediated cell death, reducing the risk of T2DM [88]. There are few studies in humans associating vitamin D and chronic inflammatory status of T2DM patients; however, the evidence suggests that vitamin D can improve insulin sensitivity and promote pancreatic β-cell survival by modulating the effects of cytokines and nuclear transcription factors such as NF-κB [90]. "
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    ABSTRACT: Chronic diseases have become one of the most important public health problems, due to their high costs for treatment and prevention. Until now, researchers have considered that the etiology of Type 2 diabetes mellitus (T2DM) is multifactorial. Recently, the study of the innate immune system has offered an explanation model of the pathogenesis of T2DM. On the other hand, there is evidence about the beneficial effect of polyunsaturated fatty acids (PUFA) n-3 and n-6 in patients with chronic inflammatory diseases including diabetes. Furthermore, high vitamin D plasmatic concentrations have been associated with the best performance of pancreatic β cells and the improving of this disease. In conclusion, certain fatty acids in the adequate proportion as well as 25-hydroxivitamin D can modulate the inflammatory response in diabetic people, modifying the evolution of this disease.
    Full-text · Article · Feb 2014 · Journal of Immunology Research
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