Abstract
Background and objectiveThe current systematic review and meta-analysis of randomized controlled trials (RCTs) was conducted to summarize the effect of vitamin D supplementation on endothelial activation among patients with metabolic syndrome and related disorders.MethodsCochrane library, Embase, PubMed, and Web of Science database were searched to identify related RCTs published before 30th April 2018. The heterogeneity among the included studies was assessed using Cochran’s Q test and I-square (I2) statistic. Data were pooled by using the random-effect model and standardized mean difference (SMD) was considered as summary effect size.ResultsFourteen clinical trials that contained a total of 1253 participants were included in the current meta-analysis. Vitamin D supplementation significantly decreased von willebrand factor (vWF) (SMD -0.27; 95% CI, − 0.46, − 0.08; P = 0.006; I2:40.5%). However, we found no significant impact of vitamin D supplementation on intercellular adhesion molecule 1(ICAM-1) (SMD -1.96; 95% CI, − 4.02, 0.09; P = 0.06; I2:97.4%), vascular celladhesion molecule 1 (VCAM-1) (SMD -0.50; 95% CI, − 1.19, 0.19; P = 0.15; I2:91.2%), on E-selectin (SMD -0.04; 95% CI, − 0.36, 0.28; P = 0.81; I2:78.8%) and endothelin (SMD -0.49; 95% CI, − 1.18, 0.19; P = 0.15; I2:90.5%). The pooled data from trials of vitamin D supplementation with dosage of ≤4000 IU/day (− 0.37, 95% CI: -0.65, − 0.10, I2: 73.5%) significantly reduced vWF concentrations, while there was no effect of vitamin D supplementation on vWF concentrations among trials with the dosage of intervention > 4000 IU/day (− 0.17, 95% CI: -0.43, 0.10, I2: 0.0%). VWF concentrations significantly reduced in pooled data from trials with duration study ≤8 weeks (− 0.37, 95% CI: -0.67, − 0.07, I2: 60.6%), but there was no effect of vitamin D supplementation on vWF concentrations among trials with > 8 weeks (− 0.20, 95% CI: -0.45, 0.05, I2: 0.0%). While there was no effect of vitamin D supplementation on vWF concentrations among trials with total sample size of ≤60 patients (− 0.03, 95% CI: -0.42, 0.36, I2: 0.0%), vWF concentrations in trials with more than 60 patients decreased significantly (− 0.34, 95% CI: -0.56, − 0.12, I2: 60.9%).ConclusionsOverall, the current meta-analysis demonstrated that vitamin D supplementation to patients with metabolic syndrome and related disorders resulted in an improvement in vWF, but did not affect ICAM-1, VCAM-1, E-selectin and endothelin levels.
Highlights
Atherosclerosis starts as endothelial activation, and endothelial dysfunction has been proposed to be the ultimate common pathway by which several risk factors result in vascular complications [1]
The pooled data from trials of vitamin D supplementation with dosage of ≤4000 IU/day (− 0.37, 95% CI: -0.65, − 0.10, I2: 73.5%) significantly reduced von willebrand factor (vWF) concentrations, while there was no effect of vitamin D supplementation on vWF concentrations among trials with the dosage of intervention > 4000 IU/day (− 0.17, 95% CI: -0.43, 0.10, I2: 0.0%)
Von willebrand factor (VWF) concentrations significantly reduced in pooled data from trials with duration study ≤8 weeks (− 0.37, 95% CI: -0.67, − 0.07, I2: 60.6%), but there was no effect of vitamin D supplementation on vWF concentrations among trials with > 8 weeks (− 0.20, 95% CI: -0.45, 0.05, I2: 0.0%)
Summary
Atherosclerosis starts as endothelial activation, and endothelial dysfunction has been proposed to be the ultimate common pathway by which several risk factors result in vascular complications [1]. Vitamin D deficiency and/or insufficiency may increase the risk of metabolic syndrome, type 2 diabetes mellitus (T2DM), hypertension, kidney disease and cardiovascular disease (CVD) through activating a pro-inflammatory cascade, which in turn may result in a rise in arterial stiffness and endothelial dysfunction [3, 4]. The main mechanisms of function of vitamin D through which it may influence the atherosclerotic process have not been completely elucidated [14] This may in part be through increased production of nitric oxide (NO), decreased oxidative damage, reduced gene expression of interleukin 6 (IL-6), and decreased circulating levels of vascular cell adhesion molecules (VCAM) and intracellular adhesion molecule (ICAM) [15]. The current systematic review and meta-analysis of randomized controlled trials (RCTs) was conducted to summarize the effect of vitamin D supplementation on endothelial activation among patients with metabolic syndrome and related disorders
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