期刊
SLEEP
卷 37, 期 3, 页码 613-620出版社
OXFORD UNIV PRESS INC
DOI: 10.5665/sleep.3510
关键词
Sleep; leptin; obesity; youth
资金
- NIH [NIH HL07567, HL60957, UL1-RR024989, 1U54CA116867]
- ResMed Foundation
- ResMed Inc
- [T32 CA 09001]
Study Objectives: Poor sleep in childhood is associated with increased obesity risk, possibly by affecting appetite-regulating hormones such as leptin. We examined short-and long-term sleep duration and quality in relation to leptin in two US pediatric cohorts. Design: Analysis of data from two prospective cohort studies. Setting: Population-based. Adolescent polysomnography assessments performed in a clinical research unit. Patients or Participants: Children in Project Viva (n = 655) and adolescents in the Cleveland Children's Sleep & Health Study (n = 502). Interventions: N/A. Measurements and Results: In Project Viva, mothers reported average child sleep duration annually from infancy through age 7, and we measured leptin at ages 3 and 7. In the Cleveland Children's Sleep & Health Study, we collected self-reported sleep duration, polysomnography-derived measures of sleep quality, and fasting leptin at ages 16-19. In sex-stratified linear regression analyses adjusted for sociodemographic characteristics and adiposity, chronic curtailed sleep was associated with lower leptin at age 7 in girls; a one-unit decrease in sleep score was associated with a 0.08 decrease in log leptin (95%CI: 0.01,0.15). The association was stronger in girls with greater adiposity (P = 0.01). Among adolescents, shorter sleep was associated with lower leptin in males; each one-hour decrease in sleep duration was associated with a 0.06 decrease in log leptin (95%CI: 0.00, 0.11). Sleep duration was not associated with leptin at other ages. Sleep quality indices were not associated with leptin. Conclusions: Our results suggest possible age-specific sexual dimorphism in the influence of sleep on leptin, which may partly explain inconsistencies in the literature.
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