Association between angiotensin-1 converting enzyme gene olymorphism and the metabolic syndrome in a Mexican opulation.
- Author:
Cleto ALVAREZ-AGUILAR
1
;
Maria Lucia ENRIQUEZ-RAMIREZ
;
Benigno FIGUEROA-NUNEZ
;
Anel GOMEZ-GARCIA
;
Ernesto RODRIGUEZ-AYALA
;
Cristina MORAN-MOGUEL
;
Victor Manuel FARIAS-RODRIGUEZ
;
Dolores MINO-LEON
;
Joel Edmundo LOPEZ-MEZA
Author Information
1. Unidad de Investigacion en Epidemiologia Clinica, Hospital General Regional No. 1, Morelia, Michoacan, Mexico. calvareza@yahoo.com.mx
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
metabolic syndrome X;
obesity;
peptidyl-dipeptidase A;
polymorphism, genetic;
renin-angiotensin system;
risk factors
- MeSH:
Aged;
Cross-Sectional Studies;
Female;
*Genetic Predisposition to Disease;
Humans;
Male;
Metabolic Syndrome X/*genetics;
Mexico;
Middle Aged;
Peptidyl-Dipeptidase A/*genetics;
*Polymorphism, Genetic;
Population Groups/genetics;
Risk Factors
- From:Experimental & Molecular Medicine
2007;39(3):327-334
- CountryRepublic of Korea
- Language:English
-
Abstract:
Metabolic Syndrome (MS) is recognized as a cluster of cardiovascular risk factors. All components of MS have a genetic base. Genes of the renin angiotensin system are potential candidate genes for MS. We investigated whether angiotensin converting enzyme (ACE) gene polymorphism increases susceptibility to MS as an entity in a Mexican population. In a cross-sectional study, 514 individuals were studied including 245 patients with MS and 269 subjects without MS criteria. ACE gene polymorphism was detected using PCR. MS was defined according to The National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) criteria, except that the raised fasting plasma glucose >or=100 mg/dl criterion for identification of intolerance fasting glucose was modified in accordance with the suggestion of the American Diabetes Association. Patients with MS were significantly different from subjects without MS in relation to mean body mass index (BMI), waist circumference (WC), systolic blood pressure, diastolic blood pressure, glucose, total cholesterol (C), triglycerides, HDL-C, and LDL-C (P<0.0001). The differences in the mean BMI, WC, glucose, total cholesterol, triglycerides, LDL-C, and HDL-C were maintained in patients with the MS and DD genotypes (P<0.01). The DD genotype was strongly associated with MS (adjusted OR=5.48, 95% CI 3.20-9.38, P<0.0001). We concluded that the DD genotype increases susceptibility to MS in a Mexican population. These results indicate that pharmacological and non-pharmacological treatment and a reduction in body fat will have important therapeutic implications in this disease.
