Lack of association between apelin, insulin resistance, cardiovascular risk factors, and obesity in children: a longitudinal analysis

Apelin has been proposed as a novel beneficial adipokine that is related to insulin resistance, cardiovascular risk factors, and obesity. However, findings in humans are controversial; and longitudinal analyses in childhood are still missing. We compared apelin levels between 80 obese and 40 lean children of the same age, sex, and pubertal stage. In addition, we analyzed the relationships between apelin levels and weight status (as standard deviation of body mass index [SDS-BMI]), body fat, insulin resistance (homeostasis model assessment [HOMA]), leptin, and cardiovascular risk factors associated with obesity (waist circumference, blood pressure, lipids, and adiponectin) in 80 obese children before and after participating in a 1-year lifestyle intervention. Apelin levels did not differ significantly (P = .061) between obese (1.50 +/- 0.47 ng/mL, mean +/- SD) and lean children (1.67 +/- 0.49 ng/mL). Apelin concentrations were not significantly related to age, pubertal stage, SDS-BMI, body fat, leptin, or any cardiovascular risk factor. In longitudinal analyses, no significant correlations were found between changes of apelin and changes of SDS-BMI, body fat, leptin, HOMA, or any cardiovascular risk factor. Adiponectin, HOMA, blood pressure, waist circumference, and triglycerides improved significantly in 39 obese children with SDS-BMI reduction, whereas leptin decreased significantly and apelin did not change significantly in these children. In 41 children with increase of SDS-BMI, no significant changes were observed in 1-year follow-up period. This is the first study demonstrating that weight loss in obese children was not associated with a change of apelin concentrations. Our data do not support a significant relationship in childhood between apelin on one hand and leptin, HOMA, cardiovascular risk factors, or weight status on the other. (C) 2011 Elsevier Inc. All rights reserved.