Effect of thiazolidinedione treatment on progression of subclinical atherosclerosis in premenopausal women at high risk for type 2 diabetes
Effect of thiazolidinedione treatment on progression of subclinical atherosclerosis in premenopausal women at high risk for type 2 diabetes
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DOI：
10.1210/jc.2004-1685
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发表时间：
2005-04-01
影响因子：
5.8
通讯作者：
Buchanan, TA
中科院分区：
文献类型：
--
作者：
Xiang, AH;Peters, RK;Buchanan, TA
我们测试了噻唑烷二酮药物治疗对 2 型糖尿病高危年轻女性颈动脉内膜中层厚度 (CIMT) 进展率的影响以及 CIMT 的一些假定决定因素。共有 266 名非糖尿病、近期患有妊娠期糖尿病的西班牙裔女性被随机分配到安慰剂组或曲格列酮组。 CIMT 测量在基线、每年和研究结束时进行，并在口服葡萄糖耐量测试期间测量肥胖、血脂、葡萄糖和胰岛素水平。在基线和 3 个月后测量胰岛素敏感性（最小模型分析）。分析数据以比较治疗组之间的 CIMT 进展率，并调查 CIMT 进展差异的潜在决定因素。192 名女性在基线和至少一次随访中进行了 CIMT 测量。接受曲格列酮治疗的女性的 CIMT 变化平均率降低了 31% (P = 0.048)。这种组间差异不能用肥胖、血脂、葡萄糖或胰岛素的基线或试验中差异来解释。 CIMT进展的减缓是逐渐发生的，仅发生在胰岛素敏感性增加的女性中，并且与基线时代谢综合征的存在无关。曲格列酮通过涉及循环中或直接在动脉壁中的未测量的动脉粥样硬化介质的机制来减少亚临床动脉粥样硬化的进展。
We tested the effects of treatment with a thiazolidinedione drug on rates of progression of carotid intima-media thickness (CIMT) and some putative determinants of CIMT in young women at high risk for type 2 diabetes. A total of 266 nondiabetic, Hispanic women with recent gestational diabetes were randomized to placebo or troglitazone. CIMT measurements were made at baseline, annually, and at study end, together with measurements of obesity, serum lipids, and glucose and insulin levels during oral glucose tolerance tests. Insulin sensitivity ( minimal model analysis) was measured at baseline and 3 months later. Data were analyzed to compare CIMT progression rates between treatment groups and investigate potential determinants of differences in CIMT progression.One hundred ninety-two women had a CIMT measurement at baseline and at least one follow-up visit. The mean rate of CIMT change was 31% lower in women assigned to troglitazone ( P = 0.048). This intergroup difference was not explained by baseline or on-trial differences in obesity, lipids, glucose, or insulin. The reduction in CIMT progression developed gradually, occurred only in women who had an increase in insulin sensitivity, and was unrelated to the presence of the metabolic syndrome at baseline.Troglitazone reduced the progression of subclinical atherosclerosis via a mechanism that involved unmeasured mediators of atherosclerosis, either in the circulation or directly in the arterial wall.