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Researchers at Uppsala University demonstrate that one night of sleep loss has a tissue-specific impact on the regulation of gene expression and metabolism in humans. This may explain how shift work and chronic sleep loss impairs metabolism and adversely affects our body composition.
Epidemiological studies have shown that the risk for obesity and type 2 diabetes is elevated in those who suffer from chronic sleep loss or carry out shift work. Other studies have shown an association between disrupted sleep and adverse weight gain, in which fat accumulation is increased at the same time as the muscle mass is reduced.
Skeletal muscle and adipose tissue are adversely affected by disrupted sleep and circadian rhythms. In the new study, the researchers studied 15 healthy normal-weight individuals who participated in two in-lab sessions in which activity and meal patterns were highly standardised. In randomised order, the participants slept a normal night of sleep (over eight hours) during one session, and were instead kept awake the entire night during the other session.
After each night-time intervention, small tissue samples (biopsies) were taken from the participants’ subcutaneous fat and skeletal muscle. These two tissues often exhibit disrupted metabolism in conditions such as obesity and diabetes. At the same time in the morning, blood samples were also taken to enable a comparison across tissue compartments of a number of metabolites. These metabolites comprise sugar molecules, as well as different fatty and amino acids.
The tissue samples were used for multiple molecular analyses, which revealed that the sleep loss condition resulted in a tissue-specific change in DNA methylation, one form of mechanism that regulates gene expression. DNA methylation is a so-called epigenetic modification that is involved in regulating how the genes of each cell in the body are turned on or off, and is impacted by both hereditary as well as environmental factors, such as physical exercise.
Sleep loss causes tissue-specific changes to the degree of DNA methylation in genes spread throughout the human genome. DNA methylation is not regulated similarly in these tissues in response to acute sleep loss.The period of wakefulness simulates the overnight wakefulness period of many shift workers assigned to nightwork.
A possible explanation for why the two tissues respond in the observed manner could be that overnight wakefulness periods exert a tissue-specific effect on tissues’ circadian rhythm, resulting in misalignment between these rhythms. Researchers observed molecular signatures of increased inflammation across tissues in response to sleep loss, they also saw specific molecular signatures that indicate that the adipose tissue is attempting to increase its capacity to store fat following sleep loss. Changes in skeletal muscle levels of proteins involved handling blood glucose.