Effect of Vitamin D Supplementation on Some Inflammatory Biomarkers in Type 2 Diabetes Mellitus Subjects: A Systematic Review and Meta-Analysis of Randomized Controlled Trials
The mechanism, by which vitamin D influences inflammatory biomarkers in type 2 diabetes mellitus (T2DM), is not very well known. Thus, a meta-analysis of randomized controlled trials was conducted to assess the effect of vitamin D supplementation on some inflammatory biomarkers in T2DM subjects. We...
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Published in | Annals of nutrition and metabolism Vol. 73; no. 1; p. 62 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
01.01.2018
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Subjects | |
Online Access | Get more information |
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Summary: | The mechanism, by which vitamin D influences inflammatory biomarkers in type 2 diabetes mellitus (T2DM), is not very well known. Thus, a meta-analysis of randomized controlled trials was conducted to assess the effect of vitamin D supplementation on some inflammatory biomarkers in T2DM subjects.
We searched randomized controlled trials from PubMed and the Cochrane Library in October 2017 and conducted a meta-analysis to evaluate the effectiveness of vitamin D supplementation on high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Either a fixed-effects or a random-effects model was used to calculate pooled effects.
We identified 13 studies that met our inclusion criteria. The results indicated that the vitamin D supplementation significant decreased the hs-CRP level by 0.45 μg/mL, whereas the vitamin D supplementation did not influence the TNF-α and IL-6. Subgroup analysis showed that vitamin D significantly lowered hs-CRP by 0.34 μg/mL among trials with a daily vitamin D dose ≤4,000 IU and by 0.31 μg/mL among trials with time of vitamin D supplementation > 12 weeks.
Vitamin D supplementation is beneficial for the reduction of hs-CRP inT2DM subjects but does not have a significant influence on TNF-α and IL-6 in T2DM subjects. |
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ISSN: | 1421-9697 |
DOI: | 10.1159/000490358 |