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山东大学学报(医学版) ›› 2014, Vol. 52 ›› Issue (8): 39-42.doi: 10.6040/j.issn.1671-7554.0.2014.135

• 临床医学 • 上一篇    下一篇

外周血单核细胞甘油三酯水解酶的表达与代谢综合征的相关性

靳成伟1, 李葵2, 赵静1, 岳欣1, 尚嫄嫄1, 韩露1, 张运1, 张薇1, 马骁3, 钟明1   

  1. 1. 教育部和卫生部心血管重构和功能研究重点实验室, 山东大学齐鲁医院心内科, 山东 济南 250012;
    2. 山东电力中心医院内科, 山东 济南 250001;
    3. 济南军区第456医院心内科, 山东 济南 250031
  • 收稿日期:2014-03-13 修回日期:2014-06-10 出版日期:2014-08-10 发布日期:2014-08-10
  • 通讯作者: 钟明。E-mail:zhongming2@medmail.com.cn;马骁。E-mail:xmajn@163.com E-mail:zhongming2@medmail.com.cn;xmajn@163.com
  • 基金资助:
    山东省自然科学基金(BS2013YY017);国家自然科学基金(81100605,81270352,81270287);山东大学自主创新基金(2012JC034)

Relationship between the mRNA expression of adipose triglyceride lipase in peripheral blood mononuclear cells and metabolic syndrome

JIN Chengwei1, LI Kui2, ZHAO Jing1, YUE Xin1, SHANG Yuanyuan1, HAN Lu1, ZHANG Yun1, ZHANG Wei1, MA Xiao3, ZHONG Ming1   

  1. 1. Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Public Health, Department of Cardiology, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China;
    2. Department of Internal Medicine, Shandong Electric Power Central Hospital, Jinan 250001, Shandong, China;
    3. Department of Cardiology, the 456th Hospital of PLA, Jinan 250031, Shandong, China
  • Received:2014-03-13 Revised:2014-06-10 Online:2014-08-10 Published:2014-08-10

摘要: 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月于我院心内科住院及门诊就诊的MS患者56 例,同时选取我院健康查体志愿者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。

关键词: 代谢综合征, 甘油三酯水解酶, 颈动脉, 动脉粥样硬化

Abstract: 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; 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 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.

Key words: Metabolic syndrome, Adipose triglyceride lipase, Carotid artery, atherosclerosis

中图分类号: 

  • R589.2
[1] Zimmermann R, Strauss J G, Haemmerle G, et al. Fat mobilization in adipose tissue is promoted by adipose triglyceride lipase[J]. Science, 2004, 306(5700):1383-1386.
[2] Jenkins C M, Mancuso D J, Yan W, et al. Identification, cloning, expression, and purification of three novel human calcium-independent phospholipase A2 family members possessing triacylglycerol lipase and acylglycerol transacylase activities[J]. J Biol Chem, 2004, 279(47):48968-48975.
[3] Smirnova E, Goldberg E B, Makarova K S, et al. ATGL has a key role in lipid droplet/adiposome degradation in mammalian cells[J]. EMBO Rep, 2006, 7(1):106-113.
[4] Lass A, Zimmermann R, Oberer M, et al. Lipolysis-a highly regulated multi-enzyme complex mediates the catabolism of cellular fat stores[J]. Prog Lipid Res, 2011, 50(1):14-27.
[5] Charrière G, Cousin B, Arnaud E, et al. Preadipocyte conversion to macrophage evidence of plasticity[J]. J Biol Chem, 2003, 278(11):9850-9855.
[6] 周一然, 宋建国. 脂肪组织的免疫功能[J]. 生物化学与生物物理进展, 2004, 31(8):679-683.
[7] Kassi E, Pervanidou P, Kaltsas G, et al. Metabolic syndrome: definitions and controversies[J]. BMC Med, 2011, 9(1):48.
[8] Livak K J, Schmittgen T D. Analysis of relative gene expression data using real-time quantitative pcr and the 2(-delta delta c(t)) method[J]. Methods, 2001, 25(4):402-408.
[9] 梁琳琅. 代谢综合征的诊断[J]. 中国实用内科杂志, 2008, 28(11):910-911.
[10] Koutsari C, Mundi M S, Ali A H, et al. Systemic free fatty acid disposal into very low-density lipoprotein triglycerides[J]. Diabetes, 2013, 62(7):2386-2395.
[11] Salgin B, Ong K K, Thankamony A, et al. Higher fasting plasma free fatty acid levels are associated with lower insulin secretion in children and adults and a higher incidence of type 2 diabetes[J]. J Clin Endocrinol Metab, 2012, 97(9):3302-3309.
[12] Rachek L I. Free fatty acids and skeletal muscle insulin resistance[J]. Prog Mol Biol Transl Sci, 2014, 121: 267-292. doi: 10.1016/B978-0-12-800101-1.00008-9.
[13] Boden G, Shulman G I. Free fatty acids in obesity and type 2 diabetes: defining their role in the development of insulin resistance and β-cell dysfunction[J]. Eur J Clin Invest, 2002, 32(3):14-23.
[14] Villena J A, Roy S, Sarkadi-Nagy E, et al. Desnutrin, an adipocyte gene encoding a novel patatin domain-containing protein, is induced by fasting and glucocorticoids: ectopic expression of desnutrin increases triglyceride hydrolysis[J]. J Biol Chem, 2004, 279(45):47066-47075.
[15] Festa A, D'Agostino R Jr, Howard G, et al. Chronic subclinical inflammation as part of the insulin resistance syndrome: The insulin resistance atherosclerosis study (iras)[J]. Circulation, 2000, 102(1):42-47.
[16] de Groot E, Hovingh G K, Wiegman A, et al. Measurement of arterial wall thickness as a surrogate marker for atherosclerosis[J]. Circulation, 2004, 109(23 suppl 1):33-38.
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