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Diurnal rhythm of circulating nicotinamide phosphoribosyltransferase (Nampt/Visfatin/PBEF): impact of sleep loss and relation to glucose metabolism.

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Shostak,  A.
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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Citation

Benedict, C., Shostak, A., Lange, T., Brooks, S. J., Schioth, H. B., Schultes, B., et al. (2012). Diurnal rhythm of circulating nicotinamide phosphoribosyltransferase (Nampt/Visfatin/PBEF): impact of sleep loss and relation to glucose metabolism. Journal of Clinical Endocrinology and Metabolism, 97(2), E218-E222. doi:10.1210/jc.2011-2241.


Cite as: http://hdl.handle.net/11858/00-001M-0000-000F-8888-3
Abstract
Context: Animal studies indicate that nicotinamide phosphoribosyltransferase [Nampt/visfatin/pre-B-cell colony-enhancing factor (PBEF)] contributes to the circadian fine-tuning of metabolic turnover. However, it is unknown whether circulating Nampt concentrations, which are elevated in type 2 diabetes and obesity, display a diurnal rhythm in humans. Objective: Our objective was to examine the 24-h profile of serum Nampt in humans under conditions of sleep and sleep deprivation and relate the Nampt pattern to morning postprandial glucose metabolism. Intervention: Fourteen healthy men participated in two 24-h sessions starting at 1800 h, including either regular 8-h-night sleep or continuous wakefulness. Serum Nampt and leptin were measured in 1.5- to 3-h intervals. In the morning, plasma glucose and serum insulin responses to standardized breakfast intake were determined. Main Outcome Measures: Under regular sleep-wake conditions, Nampt levels displayed a pronounced diurnal rhythm, peaking during early afternoon (P < 0.001) that was inverse to leptin profiles peaking in the early night. When subjects stayed awake, the Nampt rhythm was preserved but phase advanced by about 2 h (P < 0.05). Two-hour postprandial plasma glucose concentrations were elevated after sleep loss (P < 0.05), whereas serum insulin was not affected. The relative glucose increase due to sleep loss displayed a positive association with the magnitude of the Nampt phase shift (r = 0.54; P < 0.05). Conclusions: Serum Nampt concentrations follow a diurnal rhythm, peaking in the afternoon. Sleep loss induces a Nampt rhythm phase shift that is positively related to the impairment of postprandial glucose metabolism due to sleep deprivation, suggesting a regulatory impact of Nampt rhythmicity on glucose homeostasis.