title: The influence of weight loss on fibrinolytic and metabolic parameters in obese children and adolescents.
abstract: We studied i) whether short-term weight loss alters plasminogen activator inhibitor-1 antigen (PAI-1-Ag) and tissue-type plasminogen activator antigen (tPA-Ag) in obese children, and ii) whether changes in body composition and/or abdominal adiposity are responsible for changes in PAI-1 and tPA-Ag. 20 obese boys (mean age 11.9 yr) and 40 obese girls (mean age 12 yr) were studied before and after three weeks of low-caloric diet and physical activity. Body composition was assessed by means of bioelectrical impedance, and the waist-to-hip ratio (WHR) was measured. Blood samples were determined for insulin, glucose, triglycerides, PAI-1-Ag, tPA-Ag, and the fasting insulin resistance index (FIRI) was calculated. Boys had a greater WHR, higher levels of glucose, and a slightly greater FIRI than girls. Estimates of adiposity, insulin, and triglycerides were correlated with PAI-1 and tPA-Ag. WHR was significantly correlated with fibrinolytic parameters only in girls. Insulin and tPA-Ag contributed to PAI-1 (adj. R2 = 0.36, p <0.0001), whereas percentage fat mass and triglycerides contributed to tPA-Ag (adj. R2 = 0.469, p <0.0001). The weight loss program significantly reduced adiposity, abdominal adiposity, and lowered fibrinolytic and metabolic parameters. Initial levels of PAI-1 and changes in body mass contributed to the fall in PAI-1 (adj. R2 = 0.18, p = 0.0016) and initial levels of tPA-Ag contributed significantly to changes in tPA-Ag (adj. R2 = 0.57, p <0.0001). The results suggest that changes in fibrinolytic parameters are associated with the loss in body mass but can occur independently of a concomitant reduction in fatness. Although initial PAI-1 and tPA-Ag predict the changes of these fibrinolytic parameters, the results do not exclude the possibility that the improvement in metabolic state and changes in unmeasured parameters related to physical activity and low-caloric diet could have influenced our findings.
authors.affiliation: Institute of Sport Sciences, Karl-Franzens University, Graz, Austria. Karl.Sudi@kfunigraz.ac.at
authors.forename: K M
authors.initials: KM
authors.lastname: Sudi
authors.forename: S
authors.initials: S
authors.lastname: Gallistl
authors.forename: M
authors.initials: M
authors.lastname: Tröbinger
authors.forename: D
authors.initials: D
authors.lastname: Payerl
authors.forename: G
authors.initials: G
authors.lastname: Weinhandl
authors.forename: W
authors.initials: W
authors.lastname: Muntean
authors.forename: R
authors.initials: R
authors.lastname: Aigner
authors.forename: M H
authors.initials: MH
authors.lastname: Borkenstein
mesh_terms: D000005:Abdomen; D000273:Adipose Tissue; D000293:Adolescent; D001786:Blood Glucose / Q000032:analysis; D001823:Body Composition; D001824:Body Constitution; D002648:Child; D017097:Electric Impedance; D005260:Female; D005342:Fibrinolysis; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008297:Male; D009765:Obesity / Q000097:blood* / Q000628:therapy*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012044:Regression Analysis; D012727:Sex Characteristics; D010959:Tissue Plasminogen Activator / Q000097:blood; D014280:Triglycerides / Q000097:blood; D015431:Weight Loss
chemical_list: D001786:Blood Glucose; D007328:Insulin; D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides; D010959:Tissue Plasminogen Activator