title: Linkage of high-density lipoprotein-cholesterol concentrations to a locus on chromosome 9p in Mexican Americans.
abstract: High-density lipoproteins (HDLs) are anti-atherogenic lipoproteins that have a major role in transporting cholesterol from peripheral tissues to the liver, where it is removed. Epidemiologic studies have shown that low levels of high-density lipoprotein-cholesterol (HDL-C) are associated with an increased incidence of coronary heart disease and an increased mortality rate, indicating a protective role of high concentrations of HDL-C against atherogenesis and the development of coronary heart disease. HDL-C level is influenced by several genetic and nongenetic factors. Nongenetic factors include smoking, which has been shown to decrease the HDL-C level. Exercise and alcohol have been shown to increase HDL-C levels. Decreased HDL-C is often associated with other coronary heart disease risk factors such as obesity, hyperinsulinemia and insulin resistance, hypertriglyceridemia and hypertension. Although several genes have been identified for rare forms of dyslipidemia, the genes accounting for major variation in HDL-C levels have yet to be identified. Using a multipoint variance components linkage approach, we found strong evidence of linkage (lod score=3.4; P=0.00004) of a quantitative trait locus (QTL) for HDL-C level to a genetic location between markers D9S925 and D9S741 on chromosome 9p in Mexican Americans. A replication study in an independent set of Mexican American families confirmed the existence of a QTL on chromosome 9p.
authors.affiliation: Division of Clinical Epidemiology, Department of Medicine, University of Texas Health Science Center, San Antonio, Texas, USA. arya@uthscsa.edu
authors.forename: Rector
authors.initials: R
authors.lastname: Arya
authors.forename: Ravindranath
authors.initials: R
authors.lastname: Duggirala
authors.forename: Laura
authors.initials: L
authors.lastname: Almasy
authors.forename: David L
authors.initials: DL
authors.lastname: Rainwater
authors.forename: Michael C
authors.initials: MC
authors.lastname: Mahaney
authors.forename: Shelley
authors.initials: S
authors.lastname: Cole
authors.forename: Thomas D
authors.initials: TD
authors.lastname: Dyer
authors.forename: Ken
authors.initials: K
authors.lastname: Williams
authors.forename: Robin J
authors.initials: RJ
authors.lastname: Leach
authors.forename: James E
authors.initials: JE
authors.lastname: Hixson
authors.forename: Jean W
authors.initials: JW
authors.lastname: MacCluer
authors.forename: Peter
authors.initials: P
authors.lastname: O'Connell
authors.forename: Michael P
authors.initials: MP
authors.lastname: Stern
authors.forename: John
authors.initials: J
authors.lastname: Blangero
mesh_terms: D000328:Adult; D000368:Aged; D002318:Cardiovascular Diseases / Q000208:ethnology / Q000235:genetics; D016022:Case-Control Studies; D008076:Cholesterol, HDL / Q000097:blood*; D002874:Chromosome Mapping; D002899:Chromosomes, Human, Pair 9 / Q000235:genetics*; D015897:Comorbidity; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology; D005260:Female; D005787:Gene Frequency; D005819:Genetic Markers; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D006938:Hyperlipoproteinemia Type II / Q000453:epidemiology / Q000208:ethnology / Q000235:genetics*; D008126:Lod Score; D008297:Male; D017058:Mexican Americans / Q000235:genetics*; D008875:Middle Aged; D010641:Phenotype; D019655:Quantitative Trait, Heritable; D012307:Risk Factors; D013781:Texas / Q000453:epidemiology
chemical_list: D008076:Cholesterol, HDL; D005819:Genetic Markers