Baseline leptin and leptin reduction predict improvements in metabolic variables and long-term fat loss in obese children and adolescents: a prospective study of an inpatient weight-loss program

Abstract

Background: It is unclear whether high plasma leptin in obese individuals represents leptin resistance or whether individuals with marked reductions in leptin concentrations in response to weight loss may be at greater risk of regaining weight. Moreover, whether changes in leptin predict metabolic improvements during weight loss is uncertain. Objective: The objective was to prospectively examine associations between plasma leptin, body fat, and weight and metabolic risk factors in obese children during weight loss. Design: In obese children and adolescents [n = 203; mean age: 14.1 y, .98th body mass index (BMI) percentile for age and sex] participating in a 2-mo inpatient weight-loss program, we measured changes in body composition (by dual-energy X-ray absorptiometry), plasma leptin, insulin, and lipids. After discharge, anthropometric measures and plasma leptin were remeasured at 6 (n = 139) and 12 (n = 100) mo. Results: During the 2-mo program, mean (6SD) weight and fat loss were 13.9 6 4.0 kg and 9.2 6 2.5 kg, respectively; and mean plasma leptin decreased by 76%. Weight and fat loss were sustained, and no significant differences in BMI-SD score (SDS) or body composition were found between 12 and 2 mo. Baseline leptin was a negative predictor for percentage fat loss at 2, 6, and 12 mo (P , 0.05). The percentage change in leptin during the 2-mo intervention positively correlated with the relative change in fasting insulin, the relative change in LDL cholesterol at 2 mo, percentage fat loss, and change in BMI-SDS at 2 and 6 mo (P , 0.02). Conclusions: Even in obese children with strongly elevated baseline leptin, large leptin reductions that predict short-and long-term loss of body fat and improvements in lipids and insulin sensitivity can be achieved. Thus, increased plasma leptin in obese children may not necessarily reflect leptin resistance; many children appear to remain leptin sensitive at this age.Am J Clin Nutr 2011;93:695-702.

Hyperleptinemia and Hypoadiponectinemia in Extreme Pediatric Obesity

“…This particular finding is important because leptin is an independent predictor of increasing BMI, 21,22 and is associated with reduced weight loss efficacy, in youth. 26,27 Our finding of exceedingly high levels of leptin in EO children is congruent with a previous report by Freedman et al 5 demonstrating very strong tracking of adiposity from childhood to adulthood in EO youth. Therefore, in addition to the immediate metabolic and vascular consequences of hyperleptinemia in extreme pediatric obesity, the exceedingly high leptin levels in this group portend an increased risk of weight gain over time and potentially reduced efficacy of weight loss interventions in this subset of obese youth and suggest that standard approaches to weight management may be less effective in these children.…”

Decreased cardiotrophin-1 levels are associated with a lower risk of developing the metabolic syndrome in overweight/obese children after a weight loss program

“…Likely, Murer et al [50] did show that changes in leptin levels were predictors for cholesterol and LDL-cholesterol after a WL program in obese children and adolescents [50]. Our results indicate that the greater the reduction in CT-1 levels, the greater the reduction in cholesterol levels, confirming the potential role of CT-1 in ameliorating unfavorable metabolic features.…”

Size and phospholipid coating of lipid droplets in the diet of young mice modify body fat accumulation in adulthood

“…Evidence from clinical studies showed that 5% reduction in body fat percentage improved cardiometabolic risk profile in obese children (21) and adults (22). Very few experimental studies have focused on prevention of obesity and metabolic Few studies have shown that exposure to n3 long-chain polyunsaturated fatty acids throughout life protects against the detrimental effects of an adverse fetal environment on blood pressure, inflammation, leptin sensitivity, and glucose homeostasis in adult rats (26,27).…”