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OBJECTIVE: To evaluate the relationship between serum leptin levels and metabolic syndrome, fasting insulin level and anthropometric index in obese pre-pubertal children. DESIGN: A cross-sectional study was carried out on obese children. SUBJECTS: A study was made of 41 obese children (aged 6 -9 y) and the same number of non-obese children (control group), matched by age and sex. METHODS: Body mass index (BMI), waist=hip ratio (WHR) and blood pressure were determined in each child. Serum leptin, glucose, insulin, lipid profile, sex hormone binding globulin (SHBG), plasminogen activator inhibitor-1 (PAI-1), tissueplasminogen activator (t-PA) and fibrinogen were all measured. RESULTS: The serum leptin level was significantly higher in obese children (15.47 vs 4.73 ng=ml). In the obese group, leptin showed a positive correlation with BMI (P < 0.001), insulin (P < 0.001), triglycerides (P < 0.05), PAI-1 (P < 0.05) and t-PA (P < 0.05), and correlated negatively with SHBG (P < 0.01), apolipoprotein A-I (P < 0.05) and high-density lipoproteins cholesterol (HDL-C) (P < 0.05). Corrected for BMI and WHR, leptin (P partial ¼ 0.002) is only an independent predictive factor for basal insulin. Using multivariant regression analysis, only insulin (P partial ¼ 0.003) and BMI (P partial ¼ 0.018) were independent predictive factors for leptin. CONCLUSION: For this age group, high leptin resistance may be another component of metabolic syndrome, and may be involved in its etiopathogenesis. The involvement of leptin in this syndrome may be indirect, modulating the insulin's action.

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Objective: A relationship between hyperinsulinemia and decreased serum sex hormone-binding globulin (SHBG) has been described in adults. We evaluated the usefulness of SHBG as an index of hyperinsulinemia and/or insulin resistance in obese children (aged 6±9 years) of both sexes and its possible in¯uence on the androgenic status. Design: We carried out a cross-sectional study of cases and controls. We studied 61 obese children (22 males, 39 females) with body mass index (BMI) superior to the 90 th percentile and a control group of age-and sex-matched non-obese children. We measured serum glucose, insulin, TSH, free thyroxine, 17b-estradiol, testosterone and SHBG. Also, we correlated these parameters with anthropometric measures. Results: The obese group presented signi®cantly elevated levels of insulin (P 0:001) and insulin/ glucose ratio (P 0:0012) compared with the control group. SHBG (P 0:0001) and testosterone (P 0:0169) levels were signi®cantly lower than those in the non-obese group. We did not ®nd any difference in the free androgen index (FAI). Fasting insulin (r À0.4512; P < 0:001), BMI (r À0.3185; P < 0:05) and testosterone (r À0.3705; P < 0:01) were inversely correlated with SHBG concentration. According to multivariate analyses, insulin was the only independent predictor factor for serum SHBG concentration in the obese group (r partial=0.1280; P 0:0171). Conclusions: In summary, at this age there is a strong relationship between insulin and SHBG. The changes in SHBG levels of the obese group did not affect FAI and, therefore, they did not cause changes in the androgenic status. Our data support the role of insulin in the regulation of serum SHBG levels.

We have studied the effects of melatonin and retinol palmitate (RP) on the nephropathy and oxidative stress induced by a single and high dose of adriamycin (AD) in Wistar male rats. A dose of melatonin (75 microg/kg/day) and a dose of RP (0.25 g oily solution/kg/day, s.c.) were injected 3 and 9 days before and after the administration of AD (25 mg/kg, i.p.), respectively. After the decapitation, samples were taken from the neck vascular trunk in order to determine the triglycerides, total cholesterol, phospholipids, HDL-cholesterol, total proteins, urea, lipoperoxides, and reduced glutathione (GSH). We estimated the lipoperoxide and glutathione (GSH) contents in renal homogenates, and the excretion of proteins in urine over a 24 hr period. The administration of AD caused significant increases in proteinuria and in the other parameters studied [lipids (triglycerides, total cholesterol, phospholipids, and HDL-cholesterol), non-protein nitrogen compounds, and lipoperoxides]. AD increased the lipoperoxide content, but it decreased the GSH content in the kidney. Both melatonin and RP, although melatonin more significantly, decreased the intensity of the changes produced by the administration of AD alone. In fact, melatonin was quite efficient in reducing the formation of lipoperoxides, restoring renal GSH content and decreasing remarkably the severity of proteinuria. These results support the powerful antioxidant action of melatonin at renal level and a lower antioxidant action of retinol. Likewise, these data reinforce the hypothesis which supports the pathogenetic role and the close relation between the oxidative stress and the expression of the nephropathy induced by AD. However, in spite of this obvious antioxidant effect of melatonin in the kidney, additional studies are required to establish accurately the role of this pineal indole in the regulation and dynamics of the antioxidative defense enzyme system, which neutralizes the damaging effect of free radicals, both endogenous and exogenous, in this organ.

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