title: Genetic profiling in healthy subjects from the Stanislas cohort based on 24 polymorphisms: effects on biological variables.
abstract: BACKGROUND
  The association of genetic profiles with biological or clinical assessments is not clearly established especially among apparently healthy subjects.
  
  
  METHODS
  A multivariate statistical analysis was performed on 24 polymorphisms related to the main metabolic pathways involved in cardiovascular diseases (CVDs). They were collected among 1551 healthy subjects of the Stanislas cohort to obtain genetic profiles. Association with biological variables was then studied at baseline (t0) and 5 years later (t5).
  
  
  RESULTS
  Six genetic clusters were identified with relevant profiles and five polymorphisms from the selectin, apolipoprotein C3 and lipoprotein lipase genes (SELE-98G/T, APOC3-3175C/G, APOC3-482C/T, APOC3-1100C/T, LPL-93T/G) were sufficiently characteristic to associate 99.6% of the subjects with their corresponding cluster. A 5-year follow-up showed that clinical and biological measurements in relation to CVD risk factors already differ with triglyceride (p=0.009 for t0 and p=0.005 for t5) and high-density lipoprotein cholesterol (p=0.014 for t0 and p=0.003 for t5) for these previous genetic clusters.
  
  
  CONCLUSIONS
  This study presents the hypothesis that SELE could be protective, whereas APOC3 could be associated with risk. It remains to be seen whether these polymorphisms will be predictive of CVD events among the selected clusters of different metabolic subtypes after a 10-year follow-up.
authors.affiliation: INSERM U525, Nancy University, Nancy, France.
authors.forename: Eliane
authors.initials: E
authors.lastname: Albuisson
authors.forename: Sandy
authors.initials: S
authors.lastname: Maumus
authors.forename: Ndeye-Coumba
authors.initials: NC
authors.lastname: Ndiaye
authors.forename: Bérangère
authors.initials: B
authors.lastname: Marie
authors.forename: Nicolas
authors.initials: N
authors.lastname: Jay
authors.forename: François
authors.initials: F
authors.lastname: Kohler
authors.forename: Gérard
authors.initials: G
authors.lastname: Siest
authors.forename: Sophie
authors.initials: S
authors.lastname: Visvikis-Siest
mesh_terms: D000328:Adult; D053305:Apolipoprotein C-III / Q000235:genetics / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000175:diagnosis / Q000235:genetics*; D002784:Cholesterol / Q000235:genetics / Q000378:metabolism; D015331:Cohort Studies; D005260:Female; D005500:Follow-Up Studies; D005819:Genetic Markers; D006801:Humans; D008071:Lipoprotein Lipase / Q000235:genetics / Q000378:metabolism; D008075:Lipoproteins, HDL / Q000235:genetics / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011110:Polymorphism, Genetic; D012016:Reference Values; D012307:Risk Factors; D019087:Selectins / Q000235:genetics / Q000378:metabolism; D014280:Triglycerides / Q000235:genetics / Q000378:metabolism
chemical_list: D053305:Apolipoprotein C-III; D005819:Genetic Markers; D008075:Lipoproteins, HDL; D019087:Selectins; D014280:Triglycerides; D002784:Cholesterol; D008071:Lipoprotein Lipase