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Acute sleep deprivation delays the glucagon-like peptide 1 peak response to breakfast in healthy men.

MPG-Autoren
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Barclay,  J. L.
Research Group of Circadian Rhythms, MPI for biophysical chemistry, Max Planck Society;

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Oster,  H.
Research Group of Circadian Rhythms, MPI for biophysical chemistry, Max Planck Society;

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Benedict, C., Barclay, J. L., Ott, V., Oster, H., & Hallschmid, M. (2013). Acute sleep deprivation delays the glucagon-like peptide 1 peak response to breakfast in healthy men. Nutrition and Diabetes, 3: e78. doi:10.1038/nutd.2013.20.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-0014-16FF-4
Zusammenfassung
OBJECTIVE: Previous experiments have demonstrated that acute sleep loss impairs glucose homeostasis and increases food intake in humans. The incretin hormone glucagon-like peptide 1 (GLP-1) enhances postprandial insulin secretion and promotes satiety. Hypothesizing that the detrimental metabolic effects of sleep curtailment imply alterations in GLP-1 signaling, we investigated 24-h serum total GLP-1 concentrations during total sleep deprivation (TSD) and a normal sleep/wake cycle (comprising similar to 8h of sleep) in 12 healthy young men. METHODS: Sessions started at 1800 h, and subjects were provided with standardized meals. Assessments of serum GLP-1 took place in 1.5- to 3-h intervals, focusing on the response to breakfast intake (3.8 MJ). RESULTS: Across conditions, 24-h concentration profiles of GLP-1 were characterized by the expected postprandial increases (P<0.001). Although there were no differences in magnitude between conditions (P>0.11), the postprandial GLP-1 peak response to breakfast intake was delayed by similar to 90 min following sleep loss in comparison with regular sleep (P<0.02). CONCLUSIONS: Results indicate that acute TSD exerts a mild, but discernible effect on the postprandial dynamics of circulating GLP-1 concentrations in healthy men.