title: Association of lipoprotein lipase gene variation with the physiological components of the insulin-resistance syndrome in the population of the San Luis Valley, Colorado.
abstract: OBJECTIVE
  To cross-sectionally evaluate the presence of clustering of the insulin-resistance syndrome components. Tests were conducted for association of the HindIII restriction site polymorphism at the lipoprotein lipase locus with clustering of the physiological components of the insulin resistance syndrome.
  
  
  METHODS
  DNA samples of 370 normoglycemic Hispanics and 520 normoglycemic non-Hispanic whites from the San Luis Valley, Colorado, were amplified by the polymerase chain reaction. Lipids and glucose were determined by the standard procedures. Cross-tabulation and chi 2 analysis were used.
  
  
  RESULTS
  The insulin-resistance syndrome components (elevated fasting insulin, reduced high-density lipoprotein cholesterol, and elevated triglycerides) appeared together in individuals of this population sample more often than expected by chance. Individuals in the population with the (+/+) lipoprotein lipase-HindIII restriction of fragment-length polymorphism genotype were more likely to have elevated fasting insulin and triglycerides and a reduced high-density lipoprotein-cholesterol level than subjects with the (+/-) genotype (odds ratio = 2.3, 95% confidence interval 1.38-3.98).
  
  
  CONCLUSIONS
  As expected from the physiological function of lipoprotein lipase, the primary association of lipoprotein lipase genotypes is with triglyceride and high-density lipoprotein-cholesterol levels. This appears to be the first reported genetic association with the insulin-resistance syndrome and may reflect genotype specific differences in the regulation of lipoprotein lipase by insulin.
authors.affiliation: Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, PA 15261.
authors.forename: Y I
authors.initials: YI
authors.lastname: Ahn
authors.forename: R E
authors.initials: RE
authors.lastname: Ferrell
authors.forename: R F
authors.initials: RF
authors.lastname: Hamman
authors.forename: M I
authors.initials: MI
authors.lastname: Kamboh
mesh_terms: D001483:Base Sequence; D001786:Blood Glucose / Q000032:analysis; D008076:Cholesterol, HDL / Q000097:blood; D003120:Colorado; D003430:Cross-Sectional Studies; D004247:DNA / Q000235:genetics; D014644:Genetic Variation / Q000235:genetics*; D005838:Genotype; D006630:Hispanic or Latino / Q000235:genetics; D006801:Humans; D007328:Insulin / Q000097:blood / Q000502:physiology; D007333:Insulin Resistance / Q000235:genetics* / Q000502:physiology*; D008071:Lipoprotein Lipase / Q000235:genetics* / Q000378:metabolism / Q000502:physiology; D008969:Molecular Sequence Data; D005810:Multigene Family; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D013577:Syndrome; D014280:Triglycerides / Q000097:blood; D044465:White People / Q000235:genetics
chemical_list: D001786:Blood Glucose; D008076:Cholesterol, HDL; D007328:Insulin; D014280:Triglycerides; D004247:DNA; D008071:Lipoprotein Lipase