Relationship between changes in plasma leptin concentrations and plasminogen activator inhibitor-1 in obese prepubertal children after nine months of treatment.

BACKGROUND/AIMS: The metabolic syndrome (MS) is associated with insulin resistance (IR), inappropriate fibrinolysis and high plasma leptin concentrations. The aim of this study was to quantify fibrinolysis and MS-related variables in obese prepubertal children and to evaluate changes in these variables as a result of improved body mass index (BMI), IR and leptin levels following 9 months of treatment. METHODS: The homeostasis model assessment for insulin resistance (HOMA-IR), leptin, plasminogen activator inhibitor-1 (PAI-1) and lipid profile were studied at baseline in obese (n = 50) and nonobese children (n = 50), and after 9 months of treatment in obese children. RESULTS: In the cross-sectional study the mean values for insulin, HOMA-IR, triglycerides, leptin and PAI-1 were significantly higher in obese children than in controls. High-density lipoprotein cholesterol (HDLc) and apolipoprotein A-1 were significantly lower. In the longitudinal study, after 9 months, children with lowered BMI standard deviation score displayed a significant decrease in insulin, HOMA-IR, PAI-1, leptin and triglyceride levels, and an increase in HDLc. Only leptin proved to be an independent predictive factor for changes in PAI-1 (p = 0.010). CONCLUSION: Obesity-linked disorders appear in obese children prior to puberty; these disorders can be improved by decreasing BMI. Changes in leptin levels were found to independently predict changes in PAI-1 in obese children and can help to diagnose complications associated with the obesity.

Changes in body mass index are associated with changes in inflammatory and endothelial dysfunction biomarkers in obese prepubertal children after 9 months of body mass index SD score loss.

The metabolic syndrome is associated with insulin resistance, a systemic low-grade inflammatory state, and endothelial dysfunction. These disorders may arise at a very early age in obese children. The aim of this study was to confirm changes in endothelial dysfunction and inflammatory biomarkers in obese prepubertal children and to evaluate the effect of body mass index (BMI) modification on these biomarkers. Biomarkers for inflammation, endothelial dysfunction, and insulin resistance were measured in obese children (47) and healthy controls (47). Baseline pretreatment levels of insulin (P = .019), homeostasis model assessment of insulin resistance (P = .004), soluble intercellular adhesion molecule (sICAM) (P = .003), and C-reactive protein (CRP) (P < .001) were significantly higher in obese children than in controls. After 9 months of treatment, obese children with lowered BMI SD score (SDS-BMI) displayed a significant decrease in insulin (P = .011), homeostasis model assessment of insulin resistance (P = .012), CRP (P = .006), and interleukin-6 (IL-6) (P = .045) levels compared with obese children with stable SDS-BMI; they also displayed a nonsignificant drop in sICAM levels. Similarly, obese children with lowered SDS-BMI displayed a decrease in CRP (P = .005) and IL-6 (P = .065) compared with baseline levels before treatment. In the total obese group, changes in SDS-BMI correlated positively with changes in CRP (P = .035), IL-6 (P = .027), and sICAM-1 (P = .038) levels. Only SDS-BMI was an independent predictive factor for CRP (P = .031), IL-6 (P = .027), and sICAM-1 (P = .033). Prepubertal obese children displayed alterations indicative of endothelial dysfunction, insulin resistance, and inflammatory state. Lowering of the SDS-BMI after 9 months of treatment was associated with an improvement in these variables compared with those in obese children with stable SDS-BMI status.