Elevated ghrelin predicts food intake during experimental sleep restriction
Objective Sleep curtailment has been linked to obesity, but underlying mechanisms remain to be elucidated. This study assessed whether sleep restriction alters 24‐h profiles of appetite‐regulating hormones ghrelin, leptin, and pancreatic polypeptide during a standardized diet and whether these hormo...
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Published in: | Obesity (Silver Spring, Md.) Vol. 24; no. 1; pp. 132 - 138 |
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Main Authors: | , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
United States
Blackwell Publishing Ltd
01-01-2016
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Subjects: | |
Online Access: | Get full text |
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Summary: | Objective
Sleep curtailment has been linked to obesity, but underlying mechanisms remain to be elucidated. This study assessed whether sleep restriction alters 24‐h profiles of appetite‐regulating hormones ghrelin, leptin, and pancreatic polypeptide during a standardized diet and whether these hormonal alterations predict food intake during ad libitum feeding.
Methods
Nineteen healthy, lean men were studied under normal sleep and sleep restriction in a randomized crossover design. Blood samples were collected for 24 h during standardized meals. Subsequently, participants had an ad libitum feeding opportunity (buffet meals and snacks) and caloric intake was measured.
Results
Ghrelin levels were increased after sleep restriction as compared with normal sleep (P < 0.01). Overall, sleep restriction did not alter leptin or pancreatic polypeptide profiles. Sleep restriction was associated with an increase in total calories from snacks by 328 ± 140 kcal (P = 0.03), primarily from carbohydrates (P = 0.02). The increase in evening ghrelin during sleep restriction was correlated with higher consumption of calories from sweets (r = 0.48, P = 0.04).
Conclusions
Sleep restriction as compared with normal sleep significantly increases ghrelin levels. The increase in ghrelin is associated with higher consumption of calories. Elevated ghrelin may be a mechanism by which sleep loss leads to increased food intake and the development of obesity. |
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Bibliography: | This work was supported by NIH grants R01‐HL‐075079, P01‐AG11412, CTSA‐UL1 TR000430, P50‐HD057796, P60‐DK20595, Department of Defense award W81XWH‐07‐2‐0071, and Society in Science, The Branco Weiss Fellowship, administered by the ETH Zürich (to J.L.B.) The authors declared no conflict of interest. Disclosure Funding agencies ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-News-1 ObjectType-Feature-3 content type line 23 |
ISSN: | 1930-7381 1930-739X |
DOI: | 10.1002/oby.21321 |