Metabolic Phenotype Study of Sleep Deprivation

Lack of Sleep Can Lead to Obesity!

Abstract

When sleep is altered, the expression of clock genes also changes, indicating that these genes play a role in sleep regulation. For example, keeping animals awake during their normal sleep period affects clock gene expression in peripheral tissues such as the brain cortex, liver, and kidneys. Since clock gene expression responds to changes in feeding and sleep-wake behavior, some suggest that sleep deprivation (SD) might indirectly alter clock gene expression by increasing food intake. While this seems reasonable, the concept is not as straightforward as it appears.

Firstly, the effects of SD on clock gene expression are acute, observable just 3 hours after SD, which contrasts with the gradual re-entrainment observed over several days in food restriction experiments. Secondly, while humans indeed eat more and gain weight when sleep-deprived, it remains unclear how SD severely impacts food intake in mice. We found that during SD, mice consumed as much food as they did under baseline conditions, and changes in cortical clock gene expression after SD were not influenced by food deprivation.

Furthermore, despite normal food intake, mice lost weight during SD and ate more during the recovery period, suggesting that SD leads to metabolic imbalance. We believe this imbalance is due to the metabolic costs of staying awake, which we demonstrated by placing food intake within the sleep-wake context.

Purpose of the Study

Metabolic Phenotype Study of Sleep Deprivation

Materials and Methods

All mice used were male C57BL/6J mice aged 10–16 weeks, housed individually under 12-hour light/12-hour dark cycles at 23°C. Sleep deprivation (SD) was conducted between zeitgeber time (ZT) 0 (start of light) and ZT6 (midpoint of the 12-hour light phase), during which mice typically spend most of their time sleeping. Food intake was quantified using an energy metabolism monitoring system in a room that limited human interaction. The mice had ad libitum access to food (standard diet: 3436 Kliba Nafag, Switzerland, with 13.1 kJ/g of metabolic energy) and water.

Results Analysis 1

Sleep deprivation does not alter food intake, but animals eat more during recovery. The idea that changes in food intake contribute to SD-induced clock gene expression changes is based on the assumption that animals eat more during SD. To test this, we analyzed food intake during baseline (5 days pre-SD), during 6 hours of SD, and the recovery period (Days 2–5). There was no difference in food intake during SD compared to baseline.

Results Analysis 2

During SD, mice ate less than expected based on wake time. This energy imbalance may explain the increased food intake during recovery and the observed weight loss during SD. Despite having free access to food, SD resulted in a 4.8% weight loss.

Conclusion

Even though the mice ate as much during SD as they did during baseline, they still lost about 5% of their body weight. This suggests that food intake during SD is insufficient to cover the energy expenditure required to stay awake, leading to a metabolic deficit. Unlike humans, who tend to gain weight during SD, mice experience immediate weight loss, highlighting species differences in metabolic responses to SD. The findings suggest that sleep deprivation may have different effects on energy balance and weight regulation depending on the species studied.

Tow-Int Tech Animal Metabolism Monitoring System

The energy metabolism monitoring system consists mainly of an environmental cabinet, animal experimental cages, a data collection controller, gas supply and filtration components, a computer host, and software. The system uses a floor-standing environmental cabinet, capable of integrating up to 64 channels, allowing for continuous respiratory metabolism monitoring, food and water intake monitoring, spontaneous activity monitoring, and autonomous movement monitoring for small animals in the same batch. It records relevant data for phenotypic analysis.

This system has a wide range of applications, including cardiovascular diseases, insulin tolerance, metabolic syndrome, and the relationship between diabetes and aging. It is also applied in studies of metabolic diseases, nerve damage, epigenetic factors, antibiotic use, the effects of toxin exposure on brain function, evaluating metabolic demands, the relative thermic effects of various foods, beverages, activities, and drugs. Additionally, it is used in metabolic phenotyping analysis, behavioral research, nutrition studies, livestock research, and microbiome group research.

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Reference

Đukanović N, La Spada F, Emmenegger Y, Niederhäuser G, Preitner F, Franken P. Depriving Mice of Sleep also Deprives of Food. Clocks Sleep. 2022 Feb 11;4(1):37-51.