The effect of plasminogen activator inhibitor-1 gene 4G/5G polymorphism on glucose and lipid metabolisms in Turkish obese children

• Published in: Clinical endocrinology (Oxford) 2005-05, Vol.62 (5), p.607-610
• Main Authors: Kınık, Sibel Tulgar, Ataç, F. Belgin, Verdi, Hasibe, Çetintaş, Sedat, Şahin, Feride İ., Özbek, Namık
• Format: Article
• Language: English
• Subjects: Adolescent; Biological and medical sciences; Blood Glucose - analysis; Blood Glucose - metabolism; Child; Child, Preschool; Endocrinopathies; Female; Fundamental and applied biological sciences. Psychology; Gene Frequency; Homeostasis; Humans; Insulin - blood; Insulin Resistance; Lipid Metabolism; Lipids - blood; Male; Medical sciences; Obesity - blood; Obesity - genetics; Plasminogen Activator Inhibitor 1 - blood; Plasminogen Activator Inhibitor 1 - genetics; Polymorphism, Genetic; Promoter Regions, Genetic; Turkey; Vertebrates: endocrinology
• ISSN: 0300-0664; 1365-2265
• DOI: 10.1111/j.1365-2265.2005.02268.x

Summary 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. Design and patients 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. Conclusion 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.