Effects of acute sleep loss on leptin, ghrelin, and adiponectin in adults with healthy weight and obesity: A laboratory study.

Lieve T van Egmond, Elisa M S Meth, Joachim Engström, Maria Ilemosoglou, Jasmin Annica Keller, Heike Vogel, Christian Benedict

Journal: Obesity (Silver Spring, Md.) 2023;31(3):635-641

PMID: 36404495

Plain Language Summary

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A lack of sleep may be a risk factor for weight gain. Leptin is an adipocyte-derived hormone that activates satiety networks within the brain. Ghrelin, as opposed to leptin, is mainly produced by the stomach and it acts as a hunger hormone, signalling fuel status to the central nervous system. Some studies have found either no alterations or higher leptin and lower ghrelin blood levels following experimental sleep deprivation. The aim of this study was to investigate whether blood concentrations of leptin, ghrelin, and adiponectin are affected by acute total sleep deprivation in a sex- and weight-specific manner. This study is a laboratory study based on blood samples from 44 participants, mainly university students. Results show that: - acute total sleep deprivation is linked to lower serum levels of the adipokine leptin and higher blood levels of ghrelin. - following sleep deprivation, serum adiponectin levels were elevated. - the drop in serum leptin was larger in women after total sleep deprivation; however, there wasn’t a significant association between biological sex and experimental condition. - the increase in blood levels of adiponectin was slightly more pronounced among women, whereas there weren’t any differences in the effects of sleep loss on plasma ghrelin. Authors conclude that acute total sleep deprivation shifts the endocrine balance from the satiety hormone leptin toward the hunger-promoting hormone ghrelin. However, further investigation in larger samples focusing on their findings linked to sex- and weight-specific differences in leptin, ghrelin, and adiponectin are needed.

Expert Review

Reviewer: Gail Brady
20th Sep 2023
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Conflict of interest

None

Take home message

Sleep deprivation may shift the balance of appetite controlling hormones causing an increase in hunger and decreased satiety and therefore resulting in increased food intake. These changes may be more pronounced in biological females.

Evidence category

A: Meta-analyses, position-stands, randomized-controlled trials (RCTs)

Summary review

Introduction

Sleep deprivation may contribute to weight gain and obesity through its effect on the hormonal pathways promoting hunger and satiety. Research has also linked chronic sleep loss with an increase in the brain reward response to food, thus driving an increase in daily food intake. Leptin and ghrelin are hormones involved in the control of food intake. Some research has associated alterations in these hormones following sleep loss, whilst others have not.

This study aimed to investigate whether biological sex and weight status affect fasting serum levels of leptin, ghrelin and adiponectin following chronic sleep deprivation in a supervised laboratory setting.

Methods

This randomised crossover design study included n=44 mixed sex participants with a mean age of 24.9 years. A total of 19 of the participants were classed as obese, with the remaining n= 25 participants were considered normal weight. Participants completed 2 nights in experimental sessions under continuously supervised conditions in a laboratory. One night was spent awake and the other asleep. Fasting blood samples were taken the morning after each session to measure levels of leptin, ghrelin and adiponectin.

Results

Serum levels of leptin after one night’s sleep loss were around 7% lower than those measured after sleep (17.3 = +/-2.6 vs 18.6 +/- 2.8 ng/mL, p = 0.037). Adjustments using sex-stratified analysis showed significantly lower levels of serum leptin in women (25.8 +/_4.3 vs 28.1 +/_ 4.7 ng/mL, p = 0.030) but not for men (10.1 +/_ 2.4 vs 10.6 +/_ 2.3 ng/mL, p = 0.458). However, when comparing individual participant differences between sleep and wake sessions, the results were not significant. Additionally, no significant differences were found between normal weight and obese participants.

Higher levels of ghrelin were found following sleep deprivation in both sexes and weight sub-groups (839.4 +/-77.5 vs 741.4+/-63.2 pg/mL, p= 0.003). Adiponectin was also found to be elevated in all participants regardless of biological sex or weight status (7.5 +/- 0.6 vs 6.8 +/- 0.6ug/mL, p= 0.003). However, ghrelin was observed to increase slightly more in participants with obesity, whereas elevations in adiponectin were slightly greater in those of normal weight.

Conclusion

In this study, sleep loss was associated with lowered levels of leptin and higher levels of ghrelin. Analysis between biological sexes indicated that there may be a greater decrease in leptin in females. Serum levels of adiponectin were also found to be elevated after sleep deprivation for both sexes with a slightly larger increase in women. These changes may result in increased hunger and food intake and decreased satiety. No significant differences were found between normal weight and obese participants.

Notes: The authors reported no conflicts of interest.

Clinical practice applications

Sleep deprivation may lead to lower levels of leptin in both sexes with a greater decrease for females. Ghrelin and adiponectin levels may be increased in both men and women after sleep loss with a slightly larger increase in adiponectin for women. This could lead to an increase in appetite, food consumption and therefore weight gain, particularly in women.

Considerations for future research

  • Larger studies are needed to investigate sex and weight status related differences in serum levels of ghrelin, leptin and adiponectin.
  • It may be beneficial for blood samples to be taken at different points during the day to allow for fluctuations in hormone levels.
  • Food intake should be measured to monitor any increases in food intake.
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Abstract

OBJECTIVE

This study investigated whether blood concentrations of leptin, ghrelin, and adiponectin are affected by acute total sleep deprivation in a sex- and weight-specific manner.

METHODS

A total of 44 participants (mean age 24.9 years; 20 women; 19 with obesity) participated in a crossover design, including one night of sleep deprivation and one night of sleep in the laboratory. After each night, fasting blood was collected.

RESULTS

After sleep deprivation, fasting levels of leptin were lower (mean [SE], vs. sleep: 17.3 [2.6] vs. 18.6 [2.8] ng/mL), whereas those of ghrelin and adiponectin were higher (839.4 [77.5] vs. 741.4 [63.2] pg/mL and 7.5 [0.6] vs. 6.8 [0.6] μg/mL, respectively; all p < 0.05). The changes in leptin and adiponectin following sleep loss were more pronounced among women. Furthermore, the ghrelin increase was stronger among those with obesity after sleep loss. Finally, the sleep loss-induced increase in adiponectin was more marked among normal-weight participants.

CONCLUSIONS

Acute sleep deprivation reduces blood concentrations of the satiety hormone leptin. With increased blood concentrations of ghrelin and adiponectin, such endocrine changes may facilitate weight gain if persisting over extended periods of sleep loss. The observed sex- and weight-specific differences in leptin, ghrelin, and adiponectin call for further investigation.

© 2022 The Authors. Obesity published by Wiley Periodicals LLC on behalf of The Obesity Society.

Address: Department of Surgical Sciences, Sleep Science Laboratory, Uppsala University, Uppsala, Sweden.; Department of Pharmaceutical Biosciences, Molecular Neuropharmacology, Uppsala University, Uppsala, Sweden.; Department of Radiology, Leiden University Medical Center, Leiden, the Netherlands.; Department of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Nuthetal, Germany.; German Center for Diabetes Research (DZD), München-Neuherberg, Munich, Germany.; Research Group Genetics of Obesity, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Nuthetal, Germany.; Research Group Molecular and Clinical Life Science of Metabolic Diseases, Faculty of Health Sciences Brandenburg, University of Potsdam, Potsdam, Germany.

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