Vitamin D and diabetes mellitus: an update 2013

Abstract

Vitamin D deficiency and diabetes mellitus are two common conditions and they are widely prevalent across all ages, races, geographical regions, and socioeconomic conditions. Epidemiologic studies have shown association of vitamin D deficiency and increased risk of chronic diseases, such as cancer, cardiovascular disease, type 2 diabetes, and autoimmune diseases, such as multiple sclerosis and type 1 diabetes mellitus. The identification of 1,25(OH) 2 D receptors and 1-α-hydroxilase expression in pancreatic beta cells, in cells of the immune system, and in various others tissues, besides the bone system support the role of vitamin D in the pathogenesis of type 2 diabetes. Observational studies have revealed an association between 25(OH) D deficiency and the prevalence of type 1 diabetes in children and adolescents. This review will focus on the concept of vitamin D deficiency, its prevalence, and its role in the pathogenesis and risk of diabetes mellitus and cardiovascular diseases. RESUMOA deficiência de vitamina D e o diabetes melito são enfermidades comuns na população e são altamente prevalentes em todas as raças, idades, regiões geográficas e situação socioeconômica. Estudos epidemiológicos mostram uma associação entre hipovitaminose D com o aumento do risco de doenças crônicas, tais como câncer, doença cardiovascular, diabetes melito do tipo 2 e doenças autoimunes como a esclerose múltipla e o diabetes mellitus do tipo 1. A identificação de receptores da 1,25(OH) 2 D e da expressão da 1 α-hidroxilase nas células betapancreáticas, em células do sistema imunológico e em uma variedade de células do organismo além do tecido ósseo, suporta o papel da vitamina D na patogênese do diabetes tipo 2 e do tipo 1. Esta revisão apresenta e discute o conceito de deficiência de vitamina D, sua prevalência e seu papel na patogênese e no risco de desenvolvimento do diabetes melito e doenças cardiovasculares. Arq Bras Endocrinol Metab. 2014;58(1):1-8 Descritores Vitamina D; diabetes melito; patogênese

Anti-Hyperglycemic Effect of Different Fractions of Annona Reticulata Leaf

“…The major compounds 9-octadecenamide, (Z)-, ethyl isoallocholate and 9,10-secocholesta-5,7,10(19)-triene-3,24,25-triol, (3α,5Z,7E)-present in ethyl acetate fraction [8] may be considered as compounds responsible for the observed anti-hyperglycemic activity. The compound 9, 10-secocholesta-5, 7, 10(19)-triene-3,24,25-triol, (3α,5Z,7E)-is a hydroxyl derivative of vitamin D3 and vitamin D3 is known to have a positive effect in the management of diabetes [14][15][16]. Hence, the structural derivatives of vitamin D3 may be one of the responsible compounds for the observed anti-hyperglycemic activity.…”

Vitamin D and Diabetes Mellitus: A Review

“…After the translocation to the core of the cell, the complex is connected to VERE (vitamin D's element of response) in the promoter of the gene of the insulin and will activate the transcription of the insulin's gene, which will promote the cell's proliferation, differentiation and the immunomodulation [7] [17]. Recently, studies have suggested that a polymorphism of the RVD gene can confer genetic protection against DM1, and the polymorphism of the CYP27B1 gene has influence in the susceptibility for the DM1 [9] [11].…”

“…New studies based on a larger groups of patients are necessary to show whether the administration of 25-hydroxy vitamin D or 1,25(OH)2D would significantly reduce the risk of DM1, or contribute to the preservation of adequate levels of C peptide after diagnosis (17). As the exact cutoff value of vitamin D3 to protect against de development of DM, if it exists, is not known, most authors suggest that 25-hydroxy vitamin D levels should stay above 30 ng/mL, without a specific consequence in mind besides keeping it within the "normal" range.…”

Obesity, related diseases and their relationship with vitamin D deficiency in adolescents

“…Griz et al (27) suggest that leptin appears to have multiple central and peripherical effects on bone metabolism. Although peripheral leptin has an anabolic effect on bones (with possible inhibition of the osteoclasts) particularly in the appendicular skeleton, the central leptin is deleterious to the axial skeleton, as it seems to activate pathway that inhibits the ability of the kidney to actively synthesize 25(OH) D. Therefore, it seems that the effects of leptin signaling in the bone differ significantly between the axial and appendicular regions.…”