Abstract
Background/objectivesShort sleep is an obesity risk factor, however, little is known about its interplay with genetic predisposition and pathways involved in obesity pathogenesis, especially in the longitudinal setting. We aimed to investigate a possible sleep-gene interaction for childhood obesity risk, and whether the interaction in childhood longitudinally contributes to obesity risk at a 10-year follow-up and further to test if there is any mediation through the leptin pathway.Subjects/methodsA total of 3211 children from China (6–18 years) at baseline and 848 participants at 10-year follow-up from the Beijing Child and Adolescent Metabolic Syndrome (BCAMS) cohort study were analyzed. Baseline leptin concentrations and 12 established adult body mass index (BMI) loci were examined for the associations with habitual sleep duration.ResultsAfter adjusting for covariates, including pubertal stages and behavioral factors, short sleep duration at baseline was significantly associated with increased overweight/obesity risk at both baseline and follow-up. Genetic predisposition scores (GPS), particularly consisting of leptin-related SNPs (GPSleptin), were robustly associated with baseline overweight/obesity in children who slept ≤8 h/day (P < 0.001), whereas the association was ablated in those who slept ≥10 h/day (P > 0.05). Comparable observations were made at follow-up. Mediation analysis revealed a modest direct effect of the GPSleptin-sleep interaction on BMI at baseline, while a significant indirect effect of this interaction was found to be mediated principally through elevated leptin (proportion: 52.6%); moreover, the mediation effect via leptin remained stable over 10 years.ConclusionsThis study suggests that shorter sleep duration in children from China (< 8h/day), compared to longer sleep duration (≥10 h/day), has a long-term impact on the association of polygenic risk for obesity from childhood to young adulthood and leptin pathway explains a key mechanism via a modification effect. Therefore, adequate sleep duration during childhood is important for the early prevention of obesity, especially if there is a genetic predisposition to this trait.
Highlights
Obesity rates have increased sharply over the past 20–30 years, in childhood
In our recent cohort study of children from China with risk for metabolic syndrome (MS) [13], we found that short sleep duration was associated with both increased obesity risk and leptin concentrations
The study was conducted in 3211 baseline and 848 followup unrelated individuals recruited through the Beijing Child and Adolescent Metabolic Syndrome (BCAMS) study
Summary
Obesity rates have increased sharply over the past 20–30 years, in childhood. Among the changeable environmental factors that can influence risk, the obesogenic diet, and low physical activity are considered two major adult risk factors; other potentially plausible environmental factors, like short sleep duration, have been gaining increasing attention in recent years [2, 3]. A hormone secreted by white adipocytes, acts on specific receptors in the hypothalamus, a key tissue in satiety regulation and day-night circadian, and has been recently proposed as one possible mechanistic link between decreased habitual sleep duration and increased risk of obesity in both adults [7] and children [8,9,10,11,12]. In our recent cohort study of children from China with risk for metabolic syndrome (MS) [13], we found that short sleep duration was associated with both increased obesity risk and leptin concentrations. The studies concerning the association between leptin levels and sleep duration are still inconsistent [14] and the underlying mechanisms still need to be elucidated
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