0966 Youth with Delayed Sleep Phase Have Higher Leptin Levels: The Charisma Study

Abstract Introduction Adolescents have short and delayed sleep, which may have metabolic consequences. Leptin, an adipocytokine linked with adverse cardiometabolic outcomes when dysregulated, has been associated with shorter sleep in some adolescent studies. We hypothesized that shorter sleep duration and later sleep timing are associated with increased leptin in overweight youth. Methods We enrolled healthy youth 12-21y with BMI>=80%ile (or >=23kg/m2 if >=18y) from three ancestry groups: South Asian (SA), African American (AA), and White (W). Participants wore actigraphy for 14d and underwent a fasting blood draw to measure leptin. We derived average sleep duration, mid-sleep time, and sleep onset. We examined the association between the outcome leptin (log-transformed due to non-normality) and main independent variables of sleep duration and timing using multi-variable linear while adjusting for confounders. Results Participants (n=74, 38F) had median(IQR) age 19.1y(17.5, 20.9), BMIZ 1.1(0.6, 1.6), leptin 24.6ng/mL(12.1, 54.4), sleep duration 7.5h(6.8, 8.0), sleep onset 12:58am(11:56pm, 1:48am) and mid-sleep time 4:34am(3:44am, 5:35am). In univariable models, BMIZ, age, sex, and ancestry were associated with leptin or sleep, and therefore these variables were included in multivariable models. Later mid-sleep time was associated with higher leptin, adjusting for BMIZ, sex, age, and ancestry[p=0.01]. Sleep duration and sleep onset were not associated with leptin. Ancestral groups were similar except for older age [11 SA of median age: 20.7y, 30 AA: 18.4y, 33 W: 19.1y, p=0.02] and later sleep in SA [sleep onset median: SA 1:48am, AA 12:58am, W 12:43am, p=0.02 vs W; mid-sleep time: SA 5:50am, AA 4:29am, W 4:34am, p=0.04 vs W]. We found that (1) in SA, longer sleep durations[p=0.04], later sleep onset[p=0.02], and later mid-sleep time[p=0.02] were associated with higher leptin; (2) in W, later mid-sleep time[p=0.02] was associated with higher leptin. The AA group did not have relationships between sleep and leptin. There was no effect modification by ancestry. Conclusion Later mid-sleep time was associated with higher leptin in overweight youth. These relationships differed across ancestral groups. Further studies are needed to examine if delayed sleep is a modifiable risk factor to help prevent cardiometabolic outcomes, and which factors may heighten ancestry-specific susceptibility. Support (if any) NIH R01DK115648; CTSA: CHOP: UL1TR001878, Hopkins: UL1TR001079

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SLEEP
Published
2026-05-01
DOI
https://doi.org/10.1093/sleep/zsag091.0965
Primary Topic
Regulation of Appetite and Obesity
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article
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article

0966 Youth with Delayed Sleep Phase Have Higher Leptin Levels: The Charisma Study

Cynthia Wang, SARA MALINA, Andrea Kelly, Jonathan Jun et al.
SLEEP
Regulation of Appetite and Obesity
article

0966 Youth with Delayed Sleep Phase Have Higher Leptin Levels: The Charisma Study

Cynthia Wang, SARA MALINA, Andrea Kelly, Jonathan Jun, Talia Hitt, Francis Sgambati, Sheela Magge
article en

Abstract

Abstract Introduction Adolescents have short and delayed sleep, which may have metabolic consequences. Leptin, an adipocytokine linked with adverse cardiometabolic outcomes when dysregulated, has been associated with shorter sleep in some adolescent studies. We hypothesized that shorter sleep duration and later sleep timing are associated with increased leptin in overweight youth. Methods We enrolled healthy youth 12-21y with BMI>=80%ile (or >=23kg/m2 if >=18y) from three ancestry groups: South Asian (SA), African American (AA), and White (W). Participants wore actigraphy for 14d and underwent a fasting blood draw to measure leptin. We derived average sleep duration, mid-sleep time, and sleep onset. We examined the association between the outcome leptin (log-transformed due to non-normality) and main independent variables of sleep duration and timing using multi-variable linear while adjusting for confounders. Results Participants (n=74, 38F) had median(IQR) age 19.1y(17.5, 20.9), BMIZ 1.1(0.6, 1.6), leptin 24.6ng/mL(12.1, 54.4), sleep duration 7.5h(6.8, 8.0), sleep onset 12:58am(11:56pm, 1:48am) and mid-sleep time 4:34am(3:44am, 5:35am). In univariable models, BMIZ, age, sex, and ancestry were associated with leptin or sleep, and therefore these variables were included in multivariable models. Later mid-sleep time was associated with higher leptin, adjusting for BMIZ, sex, age, and ancestry[p=0.01]. Sleep duration and sleep onset were not associated with leptin. Ancestral groups were similar except for older age [11 SA of median age: 20.7y, 30 AA: 18.4y, 33 W: 19.1y, p=0.02] and later sleep in SA [sleep onset median: SA 1:48am, AA 12:58am, W 12:43am, p=0.02 vs W; mid-sleep time: SA 5:50am, AA 4:29am, W 4:34am, p=0.04 vs W]. We found that (1) in SA, longer sleep durations[p=0.04], later sleep onset[p=0.02], and later mid-sleep time[p=0.02] were associated with higher leptin; (2) in W, later mid-sleep time[p=0.02] was associated with higher leptin. The AA group did not have relationships between sleep and leptin. There was no effect modification by ancestry. Conclusion Later mid-sleep time was associated with higher leptin in overweight youth. These relationships differed across ancestral groups. Further studies are needed to examine if delayed sleep is a modifiable risk factor to help prevent cardiometabolic outcomes, and which factors may heighten ancestry-specific susceptibility. Support (if any) NIH R01DK115648; CTSA: CHOP: UL1TR001878, Hopkins: UL1TR001079

SLEEPVol. 49(Supplement_1)
University of Maryland, Baltimore (US), Children's Hospital of Philadelphia (US), Johns Hopkins University (US), Johns Hopkins Medicine (US)
Openalex Percentile: Top 6%
Regulation of Appetite and Obesity
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