目的探讨代谢综合征(MS)患者外周血单核细胞(PBMC)中甘油三酯水解酶(ATGL)的表达与MS的关系。方法选取2010年5月至2011年9月于心内科住院及门诊就诊的MS患者56例(MS组),同时选取健康查体志愿者55例为正常对照组,检测并记录一般资料及血生化指标。采用实时荧光定量PCR检测患者外周血单核细胞ATGL mRNA表达;高频超声检测患者颈动脉内膜中层厚度,测量并计算颈动脉压力弹性系数和颈动脉僵硬度;参数间行Pearson线性相关及多元线性逐步回归分析确定参数之间的变化依存关系。结果与对照组相比,MS组外周血单核细胞ATGL mRNA表达显著增加[(7.04±3.66)vs(2.25±1.69),P〈0.001],多元线性回归结果显示,年龄、甘油三酯(TG)和胰岛素抵抗指数是ATGL mRNA表达增加的独立危险因素;MS组颈动脉内膜中层厚度增加[(0.89±0.19)mm vs(0.56±0.12)mm,P〈0.001]。多元线性回归结果显示,TG升高和ATGL mRNA表达增加是颈动脉内膜中层厚度增加的独立危险因素。结论 MS患者外周血单核细胞中ATGL mRNA的表达与MS发生发展及血管损伤密切相关。
Objective To determine the mRNA expression of adipose triglyceride lipase( ATGL) in peripheral blood mononuclear cell( PBMC),and to explore its role in the vascular injury of metabolic syndrome( MS). Methods ATGL mRNA expression in PBMCs was determined by real time quantitative PCR in 55 controls and 56 MS patients.All subjects underwent carotid ultrasonography to measure the intima-media thickness,pressure-strain elastic modulus and stiffness. Pearson correlation was applied to assess correlation between the mRNA relative expression of ATGL and age,body mass index,blood pressure,levels of triglycerides,high-density lipoprotein cholesterol and HOMA index.Stepwise linear regression analysis was performed to examine the relationship of intima-media thickness to clinical variablesand the relative expression levels of ATGL mRNA. Results Compared with the controls,MS patients had significantly increased mRNA expression of ATGL[( 7. 04 ± 3. 66) vs( 2. 25 ± 1. 69),P〈0. 001]. Multivariate linear regression analysis showed that age,elevated triglycerides and the homeostasis model assessment index were independent risk factors for ATGL mRNA expression. Furthermore,markedly increased intima-media thickness was also found in MS patients[( 0. 89 ± 0. 19) mm vs( 0. 56 ± 0. 12) mm,P〈0. 001]. Multivariate linear regression analysis indicated that the increased triglycerides and ATGL mRNA expression were independent risk factors for intima-media thickness.Conclusion The ATGL mRNA expression in peripheral blood mononuclear is associated with the progression of vascular atherosclerosis in metabolic syndrome.