Nutrients (Apr 2023)

Late, but Not Early, Night Sleep Loss Compromises Neuroendocrine Appetite Regulation and the Desire for Food

  • Svenja Meyhöfer,
  • Rodrigo Chamorro,
  • Manfred Hallschmid,
  • Denisa Spyra,
  • Nelli Klinsmann,
  • Bernd Schultes,
  • Hendrik Lehnert,
  • Sebastian M. Meyhöfer,
  • Britta Wilms

DOI
https://doi.org/10.3390/nu15092035
Journal volume & issue
Vol. 15, no. 9
p. 2035

Abstract

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Objective: There is evidence that reduced sleep duration increases hunger, appetite, and food intake, leading to metabolic diseases, such as type 2 diabetes and obesity. However, the impact of sleep timing, irrespective of its duration and on the regulation of hunger and appetite, is less clear. We aimed to evaluate the impact of sleep loss during the late vs. early part of the night on the regulation of hunger, appetite, and desire for food. Methods: Fifteen normal-weight ([mean ± SEM] body-mass index: 23.3 ± 0.4 kg/m2) healthy men were studied in a randomized, balanced, crossover design, including two conditions of sleep loss, i.e., 4 h sleep during the first night-half (‘late-night sleep loss’), 4 h sleep during the second night-half (‘early-night sleep loss’), and a control condition with 8h sleep (‘regular sleep’), respectively. Feelings of hunger and appetite were assessed through visual analogue scales, and plasma ghrelin and leptin were measured from blood samples taken before, during, and after night-time sleep. Results: Ghrelin and feelings of hunger and appetite, as well as the desire for food, were increased after ‘late-night sleep loss’, but not ‘early-night sleep loss’, whereas leptin remained unaffected by the timing of sleep loss. Conclusions: Our data indicate that timing of sleep restriction modulates the effects of acute sleep loss on ghrelin and appetite regulation in healthy men. ‘Late-night sleep loss’ might be a risk factor for metabolic diseases, such as obesity and type 2 diabetes. Thereby, our findings highlight the metabolic relevance of chronobiological sleep timing.

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