Emory University School of Medicine, Division of Cardiology, Grady Memorial Hospital/Vascular Research Laboratory, 69 Jesse Hill Drive SE #C247, Atlanta, GA 30303, USA.
J Clin Lipidol. 2007 Dec;1(6):605-13. doi: 10.1016/j.jacl.2007.10.002. Epub 2007 Oct 18.
The mechanisms that link metabolic syndrome to development of atherosclerosis are largely unknown. There is increasing evidence for the role of adipokines in this process. Niacin would appear to be a logical choice in combating the atherogenic dyslipidemia seen in metabolic syndrome, as it remains the most effective agent in raising high-density lipoprotein cholesterol, and also reduces triglycerides. We hypothesized that statin-intolerant patients with insulin resistance would respond to controlled-release niacin with a rise in plasma adiponectin levels.
Fifty patients with the metabolic syndrome (National Cholesterol Education Program/Adult Treatment Panel III criteria) were randomized to either once-daily controlled-release niacin (1000 mg/day) or placebo. Measurements at baseline and after 52 weeks of treatment were made of the carotid intimal media thickness, flow-mediated dilation of the brachial artery, and blood plasma adiponectin levels. These measures were compared to changes in lipoprotein concentrations in plasma.
Changes in high-density lipoprotein cholesterol correlated significantly to changes in flow-mediated vasodilation and carotid artery intima-media thickness, and there was a trend toward correlation with plasma adiponectin levels. There was a significant difference in mean serum levels of adiponectin after the treatment period between placebo and niacin groups (16.3 ± 1.7 and 17.7 ± 1.9 mg/dL, respectively) (P = 0.022).
Treatment with controlled-release niacin for 52 weeks results in sustained improvements in adiponectin levels compared to placebo in patients with metabolic syndrome. No adverse effects of niacin on glycemic control were found.
代谢综合征与动脉粥样硬化发展之间的联系机制在很大程度上尚不清楚。越来越多的证据表明，脂肪因子在这一过程中起作用。烟酸似乎是对抗代谢综合征中出现的动脉粥样硬化性血脂异常的合理选择，因为它仍然是提高高密度脂蛋白胆固醇最有效的药物，同时还降低甘油三酯。我们假设，对他汀类药物不耐受且伴有胰岛素抵抗的患者会对控释烟酸做出反应，使血浆脂联素水平升高。
50 名患有代谢综合征（国家胆固醇教育计划/成人治疗小组 III 标准）的患者被随机分为每日一次控释烟酸（1000mg/天）或安慰剂组。在基线和 52 周治疗后测量颈动脉内膜中层厚度、肱动脉血流介导的扩张以及血浆脂联素水平。将这些测量值与血浆脂蛋白浓度的变化进行比较。
高密度脂蛋白胆固醇的变化与血流介导的血管扩张和颈动脉内膜中层厚度的变化显著相关，并且与血浆脂联素水平呈趋势相关。治疗后，安慰剂组和烟酸组之间血清脂联素的平均水平有显著差异（16.3±1.7 和 17.7±1.9mg/dL，分别）（P=0.022）。
与安慰剂相比，控释烟酸治疗 52 周可使代谢综合征患者的脂联素水平持续升高。未发现烟酸对血糖控制有不良影响。
