Effect of apolipoprotein C3 and apolipoprotein A1 polymorphisms on postprandial response to a fat overload in metabolic syndrome patients

被引:10
作者
Clemente-Postigo, M. [1 ]
Queipo-Ortuno, M.
Valdivielso, P. [2 ]
Tinahones, F. J. [3 ]
Cardona, F. [1 ]
机构
[1] Hosp Virgen de la Victoria Malaga, Fdn IMABIS, Lab Invest, Malaga, Spain
[2] Hosp Virgen de la Victoria, Lipids Unit, Malaga, Spain
[3] Hosp Virgen de la Victoria Malaga, Serv Endocrinol & Nutr, Malaga, Spain
关键词
APOA1; APOC3; Postprandial hypertriglyceridemia; Metabolic syndrome; Polymorphism; GENE-CLUSTER; I GENE; NONFASTING TRIGLYCERIDES; APO-CIII; RISK; HYPERTRIGLYCERIDEMIA; CHOLESTEROL; PROMOTER; EXPRESSION; MUTATION;
D O I
10.1016/j.clinbiochem.2010.08.014
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Objectives: Apolipoprotein C-III (APOC3) is a component of triglyceride rich lipoproteins, and Sstl polymorphism has been associated with hypertriglyceridemia. Apolipoprotein A-I (APOA1) is the major component of HDL and Mspl polymorphism has been associated with APOA1 and HDL-C levels. Thus, we study the influence of these polymorphisms in the postprandial response in metabolic syndrome (MS). Design and methods: 73 MS patients and 21 healthy subjects underwent a fat overload, with measurements of their fasting and postprandial lipid profile. The APOC3 Sstl and the APOA1 Mspl polymorphisms were genotyped. Results: No significant differences were found in the lipid profile with respect to the Mspl genotype. Patients with the S2S2 APOC3 genotype had significantly higher fasting and postprandial triglyceride levels and postprandial APOC3 and chylomicron-triglyceride levels compared with the other Sstl APOC3 genotypes. Conclusions: Homozygosity for the minor allele of the APOC3 Sstl polymorphism was associated to a worse postprandial response in MS patients. (C) 2010 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:1300 / 1304
页数:5
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