Abstract
BackgroundPlasminogen activator inhibitor-1 (PAI-1) is mainly produced in the liver and in the adipose tissue. Normal fibrin clearance mechanisms were found to be affected by high plasma PAI-1 levels and thus increases risk of thrombosis. The aim of the current study was to expound the childhood obesity effect on circulating PAI-1 and interpret the relation of PAI-1 to metabolic syndrome. This cross-sectional study was conducted on 43 obese children following in the Children Hospital and compared to 44 healthy sex- and age-matched controls. All recruited cohort are subjected to anthropometric measurements: weight, height, BMI, waist circumference, hip circumference, and skin fold thickness (biceps, triceps, and subscapular), and laboratory investigations in the form of lipid profile, fasting blood sugar, fasting insulin, insulin resistance estimated by HOMA-IR, and plasminogen activator inhibitor-1.ResultsThe level of plasminogen activator inhibitor-1 in the obese group was significantly higher than that in the control group (47.98 ± 17.42 vs. 28.00 ± 11.35 respectively). PAI-1 showed positive significant correlation to anthropometric measurements: BMI (p = 0.000), weight (p = 0.000), biceps skin fold thickness (p = 0.04), triceps skin fold thickness (p = 0.4), and subscapular skin fold thickness (p = 0.04). Also, a significant positive correlation was found between PAI-1 and systolic (p = 0.000) and diastolic blood pressure (p = 0.04). Positive correlations were found between PAI-1 and cholesterol (p = 0.000), triglycerides (p = 0.02), LDL-c (p = 0.000), insulin (p = 0.000), and HOMA-IR (r = 0.5, p = 0.02).ConclusionFat mass accumulation is related to high PAI-1 levels, which might in turn contribute to cardiovascular risk. Plasminogen Activator Inhibitor-1 is a good predictive test for metabolic syndrome in obese children.
Highlights
Plasminogen activator inhibitor-1 (PAI-1) is mainly produced in the liver and in the adipose tissue
Cases were compared to 44 healthy children, age and sex matched; they had normal Body mass index (BMI) according to the Egyptian growth charts (2002) [12], with no clinical evidence or family history of obesity or metabolic syndrome
Patients excluded from the study were those with identified syndromes and chromosomal defects or endocrinal disorders causing obesity, those who were on medications like glucocorticoids or any affecting clotting profile, any diseases affecting fibrinolytic states, and children with type 1diabetes
Summary
Plasminogen activator inhibitor-1 (PAI-1) is mainly produced in the liver and in the adipose tissue. The aim of the current study was to expound the childhood obesity effect on circulating PAI-1 and interpret the relation of PAI-1 to metabolic syndrome. Plasminogen activator inhibitor-1 (PAI-1) is the main regulator of fibrinolysis It is a serine protease inhibitor which is secreted by the liver, adipose tissue, and vascular endothelium [2]. PAI-1 is responsible for the inhibition of the fibrin degradation process endogenously. It works through blockage of the PAI-1 has been shown to be elevated in metabolic syndrome and generally is correlated with the number of components of metabolic syndrome present, such that the more severe the metabolic syndrome, the higher the PAI-1 levels [10, 11]
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