title: A Pro 12 Ala substitution in the PPARγ2 polymorphism may decrease the number of diseased vessels and the severity of angiographic coronary artery.
abstract: OBJECTIVE
  Peroxisome proliferator-activated receptor γ (PPARγ) is a ligand-activated transcription factor that regulates the gene expression of the key proteins involved in lipid metabolism, vascular inflammation, and proliferation. PPARγ may contribute toward attenuation of atherogenesis. We investigated the relationship of the Pro 12 Ala PPARγ2 polymorphism with the presence and severity of coronary artery disease (CAD) assessed by Gensini score (Gs).
  
  
  METHODS
  A total of 239 patients and 244 control individuals were investigated for clinical, biochemical, anthropometric, and angiographic information. Standard definitions were used to diagnose patients with acute coronary syndrome. The Gs system was used to calculate the severity of CAD. The computer model Homeostatic Model Assessment (HOMA) 2 was used to determine β-cell function (HOMA-β), insulin sensitivity (HOMA-S), and insulin resistance (HOMA-IR). PCR-RFLP was performed for DNA genotyping for Pro 12 Ala in the PPARγ2 polymorphism.
  
  
  RESULTS
  Allele frequencies were 0.842 for the Pro allele and 0.158 for the Ala allele. The diseased vessel number was lower in patients with the Ala allele than others. The Gs tended to be lower in patients with the Ala allele than in others [10 (8-16) vs. 24 (16-32), P<0.001]. Patients with Pro/Pro had a significantly higher glycemia, insulinemia, and HOMA-IR, and reduced HOMA-β and HOMA-S than Pro/Ala and Ala/Ala individuals.
  
  
  CONCLUSIONS
  The Ala 12 Ala genotype of the PPARγ2 gene may decrease the number of diseased vessels and the severity of CAD, which could be because of a direct antiatherogenic effect of this polymorphism as well as an indirect effect through its association with a lower level of inflammatory parameters and insulin resistance.
authors: Research Unit 05/UR/09-12: Genetic and Biological Factors of Atherosclerosis, Medicine Faculty, University of Monastir, Monastir, Tunisia. youssef_sarraj@yahoo.fr
authors: Sarraj Mohamed
authors: SM
authors: Youssef
authors: Najah
authors: N
authors: Mohamed
authors: Slimani
authors: S
authors: Afef
authors: Ben H
authors: BH
authors: Khaldoun
authors: Neffati
authors: N
authors: Fadoua
authors: Najjar M
authors: NM
authors: Fadhel
authors: Slimane M
authors: SM
authors: Naceur
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000409:Alanine; D019943:Amino Acid Substitution; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging* / Q000235:genetics*; D003331:Coronary Vessels / Q000000981:diagnostic imaging*; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000235:genetics; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D047495:PPAR gamma / Q000235:genetics*; D010641:Phenotype; D011110:Polymorphism, Genetic; D011237:Predictive Value of Tests; D011392:Proline; D012307:Risk Factors; D012720:Severity of Illness Index
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D007328:Insulin; D047495:PPAR gamma; D011392:Proline; D000409:Alanine