PAI-1 gene 4G/5G polymorphism, cytokine levels and their relations with metabolic parameters in obese children.
Obesity is associated with the changes of plasminogen activator inhibitor-1 (PAI-1), tumor necrosis factor-alpha (TNFalpha) and transforming growth factor beta (TGFbeta) levels. However, the precise effect of the 4G allele on obesity is still contradictory. Here, we aimed to elucidate the role of the 4G/5G polymorphism of the PAI-1 gene on the PAI-1 level and determine the associations between cytokines, glucose and lipid metabolism parameters in obese children. Thirty-nine obese children (mean age 11.4 +/- 3.3 years) and 38 age-matched healthy control group (mean age 10.3 +/- 3.5 years) were included in the study. In all cases, serum levels of glucose, lipid and insulin were measured, homeostasis model assessment of insulin resistance (HOMA-IR) was calculated, and 4G/5G polymorphism of PAI-1 gene, plasma PAI-1 level and serum TNFalpha and TGFbeta levels were studied. The mean relative body mass index (BMI) and HOMA-IR score, VLDL, TG, insulin, PAI-1, TNFalpha levels were higher, and HDL and TGFbeta levels were lower in the obese group. The frequency of the 4G/4G genotype was considerably higher in obese children than in controls. Also, a positive correlation was found between PAI-1 and TNFalpha levels, and relative BMI, HOMA-IR score, insulin, TG, HDL levels. TGFbeta was inversely correlated only with relative BMI. There was no correlation among three cytokines. In conclusion, childhood obesity contributes to higher PAI-1 and TNFalpha and lower TGFbeta levels. Especially PAI-1 and TNFalpha accompany insulin resistance and dyslipidemia.
Kinik
Sibel Tulgar
ST
Başkent University Faculty of Medicine, 6. Cadde 70/1, 06490 Bahçelievler, Ankara, Turkey. stkinik@hotmail.com
Ozbek
Namik
N
Yuce
Muammer
M
Yazici
Ayse Canan
AC
Verdi
Hasibe
H
Ataç
F Belgin
FB
D000273:Adipose Tissue / Q000378:metabolism; D000293:Adolescent; D001786:Blood Glucose / Q000235:genetics / Q000378:metabolism*; D015992:Body Mass Index; D016022:Case-Control Studies; D002648:Child; D016207:Cytokines / Q000097:blood* / Q000235:genetics; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000235:genetics; D050356:Lipid Metabolism / Q000235:genetics; D008055:Lipids / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood / Q000235:genetics* / Q000378:metabolism; D010641:Phenotype; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood / Q000235:genetics*; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic; D012307:Risk Factors; D016212:Transforming Growth Factor beta / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D001786:Blood Glucose; D016207:Cytokines; D007328:Insulin; D008055:Lipids; D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha