Leptin and insulin levels in prepubertal obese children before and after an intensive educational program: preliminary data

The present study evaluated fasting levels of glucose, insulin and leptin in a group of prepubertal obese children before and after weight loss. We enrolled 64 prepubescent obese children and 20 normal-weight prepubescent children as controls. Fasting plasma concentration of glucose, insulin, Homeostasis Model assessment for insulin resistance (HOMA-IR), and leptin levels were measured at baseline and after a 6- month an intensive educational program (i.e. improved nutrition and increased physical activity). At baseline, obese children showed significantly (p<0.001) higher leptin levels than control subjects. Weight loss significantly (p<0.001) diminished plasma leptin and insulin concentrations. Weight loss in prepubescent children is associated with a significant change in leptin and insulin levels. These results confirm the hypothesis that these hormones are closely associated with obesity in childhood and might take part in glucose, fat and energy metabolism. Fasting plasma insulin levels were 7.9±4.5 "U/ml (range 2.0- 15.0 "U/ml) and significantly higher (p<0.001) than control group (2.8 . ± 1.1 "U/ml; range 1.3-5.3 "U/ml). 3/35 showed fasting hyperinsulinism (8.6%), without clinical signs (i.e. acanthosis, skin tags). HOMA-IR was 1.8± 1.0 (range 0.3- 3.6). Nine patients had impaired insulin sensitivity HOMA- IR (25.7%). Leptin levels were 44.6 ± 6.7 ng/ml (range 34.2 - 59.3 ng/ml) and they were significantly (p<0.001) higher with respect to control group (9.1±3.4 ng/ml; range 4.2 -15.3 ng/ml). After diet weight, BMI, BMI z-score significantly decreased (p<0.05). HOMA IR, insulin and leptin concentrations decreased significantly (p<0.001) (Table 1). Discussion Pediatric obesity is a worldwide growing public health problem. Obesity and abdominal adiposity may be related to serious complications. Insulin resistance or hyperinsulinemia, in obese subjects, are associated with an increased risk for type 2 diabetes and metabolic syndrome. It has been reported that obese children have a twofold risk to have diabetes than children with normal weight (7). Leptin and insulin regulate energy homeostasis and body weight at the hypothalamic level.It has been reported that obese subjects generally show hyperleptinemia and hyperinsulinemia, and are often resistant to the effects of both hormones. Leptin reduction in obese children during weight loss is associated to improved insulin sensitivity (8). Our study included a population of prepubescent obese children who were compared with normal-weight children at baseline and after a weight reduction program. Attention was focused in prepubescent children to avoid the influence of puberty on insulin-resistance. This study design also provided the opportunity to evaluate the role played by a short-term (6 months) nutritional and physical activity intensive program on clinical characteristics and their association with fasting levels of glucose, insulin and leptin. At baseline obese group showed higher insulin and leptin levels than in the controls. Educational intervention, prescribed in the present study, led to a significant drop in the BMI-SDS, leptin, and insulin concentrations, confirming previous reports (9). It has been reported that a group of obese adolescents showed higher basal concentrations of leptin compared to the lean controls; after a 3-month randomized controlled physical activity based life intervention leptin levels dropped (10). In conclusion, the present study confirms the positive effects of a short-term educational program, related to dietary and physical activity recommendations, on metabolic and clinical parameters in prepubescent obese children, though there was a significant dropout rate. These preliminary results confirmed the hypothesis that insulin and leptin levels are closely associated with obesity in childhood. Further longitudinal studies are required to improve our understanding of other hormones on weight gain and loss in prepubescent children. Table 1. Main auxological and metabolic data of control group and obese children