title: The effect of plasminogen activator inhibitor-1 gene 4G/5G polymorphism on glucose and lipid metabolisms in Turkish obese children.
abstract: OBJECTIVE
  Obesity is a metabolic disorder that is associated with increased plasminogen activator inhibitor-1 (PAI-1) concentration in the circulation. This increase is related to insulin resistance, dyslipidaemia and cardiovascular disease. Some studies have demonstrated a relationship between plasma PAI-1 concentrations and the 4G/5G gene polymorphism in the PAI-1 gene, while other studies have not. It is well known that plasma PAI-1 levels are increased in obesity; however, the relationship between the polymorphism and obesity remains unclear. In this study, we aimed to elucidate the effect of the PAI-1 4G/5G polymorphism on glucose and lipid metabolism parameters in Turkish obese children.
  
  
  METHODS
  Ninety children with obesity (37 male, 53 female; mean age 11.1 +/- 3.4 years; range 5.8-17.6 years) were included in the study. The children were divided into three groups according to the PAI-1 promoter 4G/5G polymorphism (4G/4G, 4G/5G and 5G/5G). These groups were compared for age, body mass index (BMI), serum glucose, lipid and insulin levels, and homeostasis model assessment of insulin resistance (HOMA-IR) score.
  
  
  RESULTS
  The genotype distribution was 52% (47/90) 4G/4G, 25% (22/90) 4G/5G and 23% (21/90) 5G/5G. No statistically significant differences among genotype groups were found with respect to age, BMI, serum levels of glucose, lipid and insulin, and HOMA-IR score.
  
  
  CONCLUSIONS
  Although the frequency of the 4G/4G genotype was higher in subjects in the current study than in subjects reported in the literature, in our study group we observed no influence of the PAI-1 4G/4G polymorphism on lipid and glucose metabolism.
authors.affiliation: Department of Paediatrics, Division of Paediatric Endocrinology, Baskent University Faculty of Medicine, Ankara, Turkey. stkinik@hotmail.com
authors.forename: Sibel Tulgar
authors.initials: ST
authors.lastname: Kinik
authors.forename: F Belgin
authors.initials: FB
authors.lastname: Ataç
authors.forename: Hasibe
authors.initials: H
authors.lastname: Verdi
authors.forename: Sedat
authors.initials: S
authors.lastname: Cetintaş
authors.forename: Feride I
authors.initials: FI
authors.lastname: Sahin
authors.forename: Namik
authors.initials: N
authors.lastname: Ozbek
mesh_terms: D000293:Adolescent; D001786:Blood Glucose / Q000032:analysis / Q000378:metabolism*; D002648:Child; D002675:Child, Preschool; D005260:Female; D005787:Gene Frequency; D006706:Homeostasis; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood / Q000235:genetics*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood / Q000235:genetics*; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic; D014421:Turkey
chemical_list: D001786:Blood Glucose; D007328:Insulin; D008055:Lipids; D017395:Plasminogen Activator Inhibitor 1