Leptin and obesity in mother-child pairs

Defects in the leptin gene or the leptin receptor may be a genetic cause of obesity, but little is known about the familial associations of leptin and obesity. This study compared plasma leptin and measures of obesity in a sample of 248 subjects (124 mother-offspring pairs); 34% were African American and 66% were white. Youth were aged 12 to 16 years. Plasma leptin and body mass index (BMI) were higher in mothers than in their offspring and, among the offspring, higher in girls than boys, even after correcting for BMI or body fat. Racial differences in leptin were present in both mothers and youth when adjusting for percentage body fat but disappeared when adjusting for BMI. In univariate analyses of the associations between mothers and offspring, BMI was associated with leptin in all groups but was most strongly associated in white pairs and in mother-son pairs. In multiple regression analyses, when adjusting for BMI, significant predictors of leptin levelfor the boys and girls together were gender, BMI, and pubertal status of the offspring; in girls only BMI was significant (R2 = 0.72), and in boys the significant predictors were their BMI (R2 = 0.66) followed by their pubertal status (R2 = 0.06) and the leptin level of their mothers (R2 = 0.02). When adjusting for body fat, the predictors were the offspring's percentage bodyfat (R2 = 0. 67) and mother's leptin (R2 = 0.03), with similar results in gender-specific analyses. The authors conclude that leptin levels of youth are most closely associated with their degree of obesity or body fat; mother's leptin and, for boys only, pubertal status also play a small role. Although the small association between maternal leptin on leptin in their offspring could be due to either heredity or shared environment, the results of this study suggest that individual obesity and environmental factors are important predictors of leptin levels in children.