Biopharmanet-Tec Center, University of Parma, Parma, Italy.
Department of Cardiology, Hacettepe University Faculty of Medicine, Ankara, Turkey.
Nutr Metab Cardiovasc Dis. 2018 Aug;28(8):822-829. doi: 10.1016/j.numecd.2018.04.010. Epub 2018 May 12.
Low vitamin D (vitD) has been linked to increased cardiovascular (CV) risk, but the effects of vitD supplementation are not clarified. We evaluated the impact of vitD normalization on HDL cholesterol efflux capacity (CEC), which inversely correlates with CV risk, the proatherogenic serum cholesterol loading capacity (CLC), adipokine profile and subclinical atherosclerosis.
Healthy premenopausal women with vitD deficiency (n = 31) underwent supplementation. Subclinical atherosclerosis was evaluated by flow-mediated dilation (FMD), pulse wave velocity (PWV) and augmentation index (AIx), measured with standard techniques. HDL CEC and serum CLC were measured by a radioisotopic and fluorimetric assay, respectively. Malondialdehyde (MDA) in HDL was quantified by the TBARS assay. Pre-β HDL was assessed by 2D-electrophoresis. Serum adipokines were measured by ELISA. VitD replacement restored normal levels of serum 25-hydroxyvitamin D (25OHD) and significantly improved FMD (+4%; p < 0.001), PWV (-4.1%: p < 0.001) and AIx (-16.1%; p < 0.001). Total CEC was significantly improved (+19.5%; p = 0.003), with a specific increase in the ABCA1-mediated CEC (+70.8%; p < 0.001). HDL-MDA slightly but significantly decreased (-9.6%; p = 0.027), while no difference was detected in pre-β HDL. No change was observed in aqueous diffusion nor in the ABCG1-mediated CEC. Serum CLC was significantly reduced (-13.3%; p = 0.026). Levels of adiponectin were increased (+50.6%; p < 0.0001) and resistin levels were decreased (-24.3%; p < 0.0001). After vitD replacement, an inverse relationship was found linking the ABCA1-mediated CEC with pre-β HDL (r = 0.346; p < 0.001) and resistin (r = 0.220; p = 0.009).
Our data support vitD supplementation for CV risk prevention.
维生素 D(vitD)水平较低与心血管(CV)风险增加有关,但 vitD 补充的效果尚不清楚。我们评估了 vitD 正常化对高密度脂蛋白胆固醇流出能力(CEC)的影响,CEC 与 CV 风险呈负相关,还评估了致动脉粥样硬化的血清胆固醇负荷能力(CLC)、脂联素谱和亚临床动脉粥样硬化。
患有 vitD 缺乏症的健康绝经前妇女(n=31)接受了补充治疗。使用标准技术通过血流介导的扩张(FMD)、脉搏波速度(PWV)和增强指数(AIx)评估亚临床动脉粥样硬化。通过放射性同位素和荧光测定法分别测量 HDL CEC 和血清 CLC。通过 TBARS 测定法定量测定 HDL 中的丙二醛(MDA)。通过 2D-电泳评估前-β HDL。通过 ELISA 测量血清脂联素。vitD 替代恢复了血清 25-羟维生素 D(25OHD)的正常水平,并显著改善了 FMD(+4%;p<0.001)、PWV(-4.1%:p<0.001)和 AIx(-16.1%:p<0.001)。总 CEC 显著提高(+19.5%;p=0.003),其中 ABCA1 介导的 CEC 特异性增加(+70.8%;p<0.001)。HDL-MDA 略有但显著降低(-9.6%;p=0.027),而前-β HDL 无差异。水相扩散和 ABCG1 介导的 CEC 没有变化。血清 CLC 显著降低(-13.3%;p=0.026)。脂联素水平升高(+50.6%;p<0.0001),抵抗素水平降低(-24.3%;p<0.0001)。vitD 替代后,发现 ABCA1 介导的 CEC 与前-β HDL(r=0.346;p<0.001)和抵抗素(r=0.220;p=0.009)呈负相关。
我们的数据支持补充 vitD 以预防 CV 风险。