Circulating soluble leptin receptor, leptin, and insulin resistance before and after weight loss in obese children

OBJECTIVE: To study the relationships between leptin, soluble leptin receptor (sOB-R), and insulin resistance in obese children before and after weight reduction. METHODS: We determined fasting serum leptin, sOB-R, and insulin resistance index ( Homeostasis model assessment (HOMA) in 36 obese children at baseline and 1y later and compared them to 72 lean children matched for age, gender, and pubertal stage. The changes of leptin (Dleptin) and sOB-R (DsOB-R) over the 1y period were correlated to the changes of HOMA (DHOMA), the changes of weight status, and the changes of percentage body fat (Delta%BF) based on skinfold measurements. Multiple linear regression analyses were conducted for the dependent variables Dleptin and Delta sOB-R, including Delta BMI and DHOMA as independent variables adjusted for age, gender, and pubertal stage. Changes of leptin and sOB-R levels were analyzed in 11 obese children after they had lost weight substantially (decrease SDS-BMI > 0.5) and compared to 11 obese children without substantial weight loss matched for age, gender, and pubertal stage. RESULTS: Obese children showed significantly (P < 0.001) higher leptin and lower sOB-R levels. Dleptin correlated significantly to DSDS-BMI (r=0.28, P < 0.05), Delta%BF (r=0.44, P < 0.05), and DHOMA (r=0.42, P < 0.01), while Delta sOB-R correlated significantly to DSDS-BMI (r= -0.42, P < 0.01) and Delta%BF (r= -0.47, P < 0.01), but not to DHOMA. In contrast to DsOB-R, Dleptin correlated significantly to DHOMA (P=0.02) in multiple linear regression analysis. Substantial weight loss led to a significant increase in sOB-R (P=0.02) and to a decrease in HOMA (P=0.02). In children without substantial weight loss, there were no changes in sOB-R, while HOMA (P=0.04) and leptin (P=0.02) increased significantly. CONCLUSIONS: The decrease of sOB- R and the increase of leptin levels in obese children normalized after weight loss. Therefore, these changes are consequences rather than the cause of overweight. In contrast to sOB-R, leptin levels are associated with insulin resistance.