Laboratory of Biochemical Genetics and Metabolism, The Rockefeller University, Box 179, New York, NY 10065, USA.
Arterioscler Thromb Vasc Biol. 2012 Oct;32(10):2510-5. doi: 10.1161/ATVBAHA.112.254110. Epub 2012 Sep 4.
Vitamin D deficiency is common and associated with dyslipidemia. However, it is unclear whether oral vitamin D supplementation improves the lipid profile. Therefore, we conducted a randomized, placebo-controlled trial to determine the short-term effects of vitamin D repletion on the lipid profile.
One hundred fifty-one vitamin D-deficient (25-hydroxyvitamin D <20 ng/mL) adults with elevated risk for cardiovascular disease were randomized to receive either 50 000 IU of vitamin D3 weekly for 8 weeks or placebo. The primary outcome was the change in small low-density lipoprotein (LDL) particle number. Secondary outcomes included changes in other nuclear magnetic resonance-based and chemical lipid fractions. Vitamin D failed to improve the lipid profile. Compared with the placebo, vitamin D repletion did not change small LDL particle number (mean change, +18 nmol/L; 95% CI [-80 to +116 nmol/L]; P=0.63). There were also no changes in the chemical lipid profile: total cholesterol (+5.8 mg/dL, 95% CI [-1.4 to +13.0 mg/dL], P=0.14); LDL cholesterol (+3.8 mg/dL, 95% CI [-2.5 to +10.2 mg/dL], P=0.13); high-density lipoprotein cholesterol (+0.4 mg/dL 95% CI [-1.6 to +2.6 mg/dL], P=0.71); and triglycerides (+7.9 mg/dL 95% CI [-6.5 to +22.3 mg/dL]). In the vitamin D repletion group, exploratory multivariate regression analysis demonstrates that changes in LDL cholesterol were positively correlated with the changes in serum calcium (P<0.001) and inversely with the changes in serum parathyroid hormone (P=0.02).
In contrast to the association between low 25-hydroxyvitamin D levels and dyslipidemia, correcting vitamin D deficiency in the short-term does not improve the lipid profile. Repletion of 25-hydroxyvitamin D levels raised serum calcium levels and decreased serum parathyroid hormone levels. These expected physiological responses to vitamin D therapy were correlated with a significant increase in LDL cholesterol. Clinical Trial Registration- URL: http://www.clinicaltrials.gov. Unique identifier: NCT01008384.
维生素 D 缺乏很常见，且与血脂异常有关。然而，口服维生素 D 补充剂是否能改善血脂谱尚不清楚。因此，我们进行了一项随机、安慰剂对照试验，以确定维生素 D 补充对血脂谱的短期影响。
151 名维生素 D 缺乏症（25-羟维生素 D<20ng/mL）且心血管疾病风险增加的成年人被随机分为两组，分别接受每周 50000IU 的维生素 D3 治疗 8 周或安慰剂。主要结局是小而密低密度脂蛋白（LDL）颗粒数的变化。次要结局包括基于核磁共振和化学脂质的其他指标的变化。维生素 D 未能改善血脂谱。与安慰剂相比，维生素 D 补充并未改变小 LDL 颗粒数（平均变化，+18nmol/L；95%CI[-80 至+116nmol/L]；P=0.63）。化学脂质谱也没有变化：总胆固醇（+5.8mg/dL，95%CI[-1.4 至+13.0mg/dL]，P=0.14）；LDL 胆固醇（+3.8mg/dL，95%CI[-2.5 至+10.2mg/dL]，P=0.13）；高密度脂蛋白胆固醇（+0.4mg/dL，95%CI[-1.6 至+2.6mg/dL]，P=0.71）；和甘油三酯（+7.9mg/dL，95%CI[-6.5 至+22.3mg/dL]）。在维生素 D 补充组中，探索性多元回归分析表明，LDL 胆固醇的变化与血清钙的变化呈正相关（P<0.001），与甲状旁腺激素的变化呈负相关（P=0.02）。
与低 25-羟维生素 D 水平与血脂异常的相关性相反，短期内纠正维生素 D 缺乏并不能改善血脂谱。25-羟维生素 D 水平的补充提高了血清钙水平，降低了血清甲状旁腺激素水平。这些对维生素 D 治疗的预期生理反应与 LDL 胆固醇的显著增加有关。
