Abstract

Adipokine dysregulation is an early biomarker of adipose tissue dysfunction, which has been shown to relate to metabolic health. We aimed to investigate whether the profiles of certain adipokines in childhood might predict the incidence of obesity and contribute to BMI trajectory from childhood to young adulthood. A total of 3211 children aged 6-18ys from the Beijing Child and Adolescent Metabolic Syndrome (BCAMS) study were evaluated at baseline, and 989 of these participants were assessed at 10-year follow-up. Physical activity, dietary and sleep information were collected by questionnaires. Baseline plasma adiponectin, leptin, resistin, retinol binding protein 4, osteonectin and fibroblast growth factor 21 (FGF-21) were measured by ELISA. The sex-adjusted z scores for adipokine levels were examined for their association with adiposity measures (BMI and waist circumference). Only 10.4% of the children who were non-obese at baseline developed obesity at 10-year follow-up, while over 65% of children presenting with obesity remained obese at follow-up, suggesting a well-established obesity trajectory over time. After adjusting for age, tanner stage, diet, exercise and sleep, decreased adiponectin and FGF-21 levels, as well as increased leptin, were associated with obesity risk both at baseline and 10-year follow-up (all P < 0.05). Multivariate analysis showed that after adjusting for confounding factors, each 1-SD increment in the leptin : adiponectin ratio was associated with a 3.26-fold (95% CI:2.08 - 5.10) higher risk for obesity at 10-year follow-up, while each 1-SD increment in FGF-21 level reduced the risk of obesity by 30% (95% CI: 0.48 - 0.96). Finally, among children with obesity at baseline, each 1-SD of elevation in resistin increased the risk of persistent obesity by 1.41-fold (95% CI: 1.13 - 1.77). These findings suggest that certain aberrant patterns of adipokine regulation during childhood may serve as biomarkers for the subsequent development of obesity. Disclosure S. Gao: None. M. Li: None. S.M. Willi: Advisory Panel; Self; Boehringer Ingelheim International GmbH. Research Support; Self; Eli Lilly and Company, Janssen Pharmaceuticals, Inc., Tolerion, Inc. Other Relationship; Self; Caladrius Biosciences, Inc. Funding National Natural Science Foundation of China (81970732); National Key Research Program of China (2016YFC1304801); Key Program of Beijing Municipal Science and Technology Commission (D111100000611001, D111100000611002); Beijing Natural Science Foundation (7172169); Beijing Science and Technology Star Program (2004A027), Novo Nordisk Union Diabetes Research Talent Fund (2011A002); National Key Program of Clinical Science (WBYZ2011-873); Central Research Institute Fund of Chinese Academy of Medical Sciences (2017PT32020, 2018PT32001); Beijing Chaoyang Hospital (JXPY201606)

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