Vitamin D and type 2 diabetes

•Laboratory studies provide evidence for a relationship between 1,25-dihydroxyvitamin D and insulin release and insulin sensitivity.•Epidemiological studies show associations between vitamin D deficiency and decreased glycemic control and type 2 diabetes mellitus.•Randomized clinical trials on the e...

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Published inThe Journal of steroid biochemistry and molecular biology Vol. 173; pp. 280 - 285
Main Authors Lips, Paul, Eekhoff, Marelise, van Schoor, Natasja, Oosterwerff, Mirjam, de Jongh, Renate, Krul-Poel, Yvonne, Simsek, Suat
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.10.2017
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ISSN0960-0760
1879-1220
DOI10.1016/j.jsbmb.2016.11.021

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Abstract •Laboratory studies provide evidence for a relationship between 1,25-dihydroxyvitamin D and insulin release and insulin sensitivity.•Epidemiological studies show associations between vitamin D deficiency and decreased glycemic control and type 2 diabetes mellitus.•Randomized clinical trials on the effect of vitamin D vs placebo in healthy subjects, individuals with impaired glucose tolerance or type 2 diabetes mellitus show inconsistent results.•Small effects of vitamin D are mainly visible in individuals with vitamin D deficiency and impaired glucose tolerance at baseline.•Meta-analyses of randomized clinical trials did not show significant effects of vitamin D supplementation on glycemic control. Vitamin D deficiency is associated with a decreased insulin release, insulin resistance and type 2 diabetes in experimental and epidemiological studies. Animal studies show that 1α,25–dihydroxyvitamin D3 (1,25(OH)2D3) stimulates the pancreatic β-cell to secrete insulin. The relationship between vitamin D deficiency and insulin resistance could develop through inflammation, as vitamin D deficiency is associated with increased inflammatory markers. In addition, genetic polymorphisms of vitamin D −related genes may predispose to impaired glycemic control and type 2 diabetes. Epidemiologic studies showed an association between low serum 25-hydroxyvitamin D3 (25(OH)D3) concentration and an increased risk for the metabolic syndrome and type 2 diabetes. This may be partly explained by an increased fat mass. A possible causal relationship between vitamin D deficiency and type 2 diabetes should be proven by randomized clinical trials showing that either type 2 diabetes can be prevented or insulin release and insulin sensitivity can be improved by vitamin D supplements. The results of randomized clinical trials on the effect of vitamin D versus placebo, sometimes combined with calcium, in patients with impaired glucose tolerance (“prediabetes”) or type 2 diabetes are inconsistent. Some studies showed a slight decrease of fasting plasma glucose or improvement of insulin resistance, but often only in posthoc analyses. These effects are mainly visible in patients with vitamin D deficiency and impaired glucose tolerance at baseline. Meta-analyses of randomized clinical trials in general did not show significant effects of vitamin D supplementation on glycemic control. Currently, several large scale randomized clinical trials with vitamin D supplementation in doses of 1600–4000IU/d are ongoing with glycemic control or incidence of diabetes mellitus as outcome. Vitamin D deficiency needs to be prevented or cured, but until the results of these trials are published, high-dose vitamin D supplementation cannot be recommended for prevention or amelioration of type 2 diabetes.
AbstractList Vitamin D deficiency is associated with a decreased insulin release, insulin resistance and type 2 diabetes in experimental and epidemiological studies. Animal studies show that 1α,25-dihydroxyvitamin D (1,25(OH) D ) stimulates the pancreatic β-cell to secrete insulin. The relationship between vitamin D deficiency and insulin resistance could develop through inflammation, as vitamin D deficiency is associated with increased inflammatory markers. In addition, genetic polymorphisms of vitamin D -related genes may predispose to impaired glycemic control and type 2 diabetes. Epidemiologic studies showed an association between low serum 25-hydroxyvitamin D (25(OH)D ) concentration and an increased risk for the metabolic syndrome and type 2 diabetes. This may be partly explained by an increased fat mass. A possible causal relationship between vitamin D deficiency and type 2 diabetes should be proven by randomized clinical trials showing that either type 2 diabetes can be prevented or insulin release and insulin sensitivity can be improved by vitamin D supplements. The results of randomized clinical trials on the effect of vitamin D versus placebo, sometimes combined with calcium, in patients with impaired glucose tolerance ("prediabetes") or type 2 diabetes are inconsistent. Some studies showed a slight decrease of fasting plasma glucose or improvement of insulin resistance, but often only in posthoc analyses. These effects are mainly visible in patients with vitamin D deficiency and impaired glucose tolerance at baseline. Meta-analyses of randomized clinical trials in general did not show significant effects of vitamin D supplementation on glycemic control. Currently, several large scale randomized clinical trials with vitamin D supplementation in doses of 1600-4000IU/d are ongoing with glycemic control or incidence of diabetes mellitus as outcome. Vitamin D deficiency needs to be prevented or cured, but until the results of these trials are published, high-dose vitamin D supplementation cannot be recommended for prevention or amelioration of type 2 diabetes.
Vitamin D deficiency is associated with a decreased insulin release, insulin resistance and type 2 diabetes in experimental and epidemiological studies. Animal studies show that 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) stimulates the pancreatic β-cell to secrete insulin. The relationship between vitamin D deficiency and insulin resistance could develop through inflammation, as vitamin D deficiency is associated with increased inflammatory markers. In addition, genetic polymorphisms of vitamin D -related genes may predispose to impaired glycemic control and type 2 diabetes. Epidemiologic studies showed an association between low serum 25-hydroxyvitamin D3 (25(OH)D3) concentration and an increased risk for the metabolic syndrome and type 2 diabetes. This may be partly explained by an increased fat mass. A possible causal relationship between vitamin D deficiency and type 2 diabetes should be proven by randomized clinical trials showing that either type 2 diabetes can be prevented or insulin release and insulin sensitivity can be improved by vitamin D supplements. The results of randomized clinical trials on the effect of vitamin D versus placebo, sometimes combined with calcium, in patients with impaired glucose tolerance ("prediabetes") or type 2 diabetes are inconsistent. Some studies showed a slight decrease of fasting plasma glucose or improvement of insulin resistance, but often only in posthoc analyses. These effects are mainly visible in patients with vitamin D deficiency and impaired glucose tolerance at baseline. Meta-analyses of randomized clinical trials in general did not show significant effects of vitamin D supplementation on glycemic control. Currently, several large scale randomized clinical trials with vitamin D supplementation in doses of 1600-4000IU/d are ongoing with glycemic control or incidence of diabetes mellitus as outcome. Vitamin D deficiency needs to be prevented or cured, but until the results of these trials are published, high-dose vitamin D supplementation cannot be recommended for prevention or amelioration of type 2 diabetes.
•Laboratory studies provide evidence for a relationship between 1,25-dihydroxyvitamin D and insulin release and insulin sensitivity.•Epidemiological studies show associations between vitamin D deficiency and decreased glycemic control and type 2 diabetes mellitus.•Randomized clinical trials on the effect of vitamin D vs placebo in healthy subjects, individuals with impaired glucose tolerance or type 2 diabetes mellitus show inconsistent results.•Small effects of vitamin D are mainly visible in individuals with vitamin D deficiency and impaired glucose tolerance at baseline.•Meta-analyses of randomized clinical trials did not show significant effects of vitamin D supplementation on glycemic control. Vitamin D deficiency is associated with a decreased insulin release, insulin resistance and type 2 diabetes in experimental and epidemiological studies. Animal studies show that 1α,25–dihydroxyvitamin D3 (1,25(OH)2D3) stimulates the pancreatic β-cell to secrete insulin. The relationship between vitamin D deficiency and insulin resistance could develop through inflammation, as vitamin D deficiency is associated with increased inflammatory markers. In addition, genetic polymorphisms of vitamin D −related genes may predispose to impaired glycemic control and type 2 diabetes. Epidemiologic studies showed an association between low serum 25-hydroxyvitamin D3 (25(OH)D3) concentration and an increased risk for the metabolic syndrome and type 2 diabetes. This may be partly explained by an increased fat mass. A possible causal relationship between vitamin D deficiency and type 2 diabetes should be proven by randomized clinical trials showing that either type 2 diabetes can be prevented or insulin release and insulin sensitivity can be improved by vitamin D supplements. The results of randomized clinical trials on the effect of vitamin D versus placebo, sometimes combined with calcium, in patients with impaired glucose tolerance (“prediabetes”) or type 2 diabetes are inconsistent. Some studies showed a slight decrease of fasting plasma glucose or improvement of insulin resistance, but often only in posthoc analyses. These effects are mainly visible in patients with vitamin D deficiency and impaired glucose tolerance at baseline. Meta-analyses of randomized clinical trials in general did not show significant effects of vitamin D supplementation on glycemic control. Currently, several large scale randomized clinical trials with vitamin D supplementation in doses of 1600–4000IU/d are ongoing with glycemic control or incidence of diabetes mellitus as outcome. Vitamin D deficiency needs to be prevented or cured, but until the results of these trials are published, high-dose vitamin D supplementation cannot be recommended for prevention or amelioration of type 2 diabetes.
Author Krul-Poel, Yvonne
Lips, Paul
Oosterwerff, Mirjam
Simsek, Suat
de Jongh, Renate
Eekhoff, Marelise
van Schoor, Natasja
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  fullname: Oosterwerff, Mirjam
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  fullname: Simsek, Suat
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Keywords Type 2 diabetes
Vitamin D deficiency
Impaired fasting glucose
Vitamin D supplementation
Insulin resistance
β-cell function
Impaired glucose tolerance
Language English
License Copyright © 2016 Elsevier Ltd. All rights reserved.
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Publisher_xml – name: Elsevier Ltd
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Snippet •Laboratory studies provide evidence for a relationship between 1,25-dihydroxyvitamin D and insulin release and insulin sensitivity.•Epidemiological studies...
Vitamin D deficiency is associated with a decreased insulin release, insulin resistance and type 2 diabetes in experimental and epidemiological studies. Animal...
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SubjectTerms Animals
Blood Glucose - analysis
Blood Glucose - metabolism
Diabetes Mellitus, Type 2 - blood
Diabetes Mellitus, Type 2 - drug therapy
Diabetes Mellitus, Type 2 - etiology
Diabetes Mellitus, Type 2 - metabolism
Humans
Impaired fasting glucose
Impaired glucose tolerance
Insulin - metabolism
Insulin resistance
Randomized Controlled Trials as Topic
Type 2 diabetes
Vitamin D - metabolism
Vitamin D - therapeutic use
Vitamin D deficiency
Vitamin D Deficiency - blood
Vitamin D Deficiency - complications
Vitamin D Deficiency - drug therapy
Vitamin D Deficiency - metabolism
Vitamin D supplementation
Vitamins - metabolism
Vitamins - therapeutic use
β-cell function
Title Vitamin D and type 2 diabetes
URI https://dx.doi.org/10.1016/j.jsbmb.2016.11.021
https://www.ncbi.nlm.nih.gov/pubmed/27932304
https://www.proquest.com/docview/1847889332
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