Losing just one night of sleep can have a negative impact on human metabolism at the tissue level, according to a study published last week. The findings may explain how long-term shift work and chronic sleep loss can impair metabolism and adversely affect human body composition.
Previous studies have shown that the risk for obesity and type 2 diabetes is greater in those who suffer from chronic sleep loss or who carry out shift work.
The study is the first to link how sleep loss, at the cellular level, affects metabolism in two tissues that are key for regulating metabolism. It found that even one night of sleep loss – similar to the lack of sleep someone working an overnight shift might experience – can alter how genes and proteins are expressed in a tissue-specific manner in adipose tissue (fat) and skeletal muscle.
The study was published in the journal Science Advances.
“Until now, we’ve never known whether sleep loss can cause molecular changes at the tissue level, but now that we do, it may explain how disrupted or mistimed sleep in the long run can increase the risk of adverse weight gain in humans,” saidfirst author Dr. Jonathan Cedernaes, research associate in the department of endocrinology at Northwestern University Feinberg School of Medicine, who conducted the research at Uppsala University in Sweden.
While one night of sleep loss negatively impacted the tissue, Cedernaes said the sleep loss would need to become chronic before leading to actual weight gain.
In the study,15 healthy, normal-weight individuals had a normal night of sleep (more than eight hours) during one session and were kept awake the entire night during another session. The morning after each nighttime intervention, small tissue samples were taken from the participants’ fat and skeletal muscle, which often exhibit disrupted metabolism in conditions such as obesity and diabetes. At the same time in the morning, blood samples also were 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.
By taking biopsies of the tissues that are responsible for carrying out metabolic functions, such as blood glucose regulation after a meal, the scientists were able to see that sleep loss altered the levels of genes and proteins that are involved in regulating the tissues’ circadian rhythms, as well as their metabolic functions.
The researchers observed a change in how genes were regulated through what’s known as an epigenetic modification. This modification was only altered in adipose tissue – fat – and in genes that also have been found to have altered gene regulation in, for example, type-2 diabetic or obese individuals. The researchers believe these changes may help explain how disrupted or mistimed sleep can lead to an increased risk of metabolic disease.
“We were surprised that these types of changes occurred so rapidly, but further studies with more frequent tissue sampling will be needed to investigate how dynamic these changes are across the 24-hour sleep/wake cycle, for understanding what mechanisms that may cause them and how they develop or disappear over time,” Cedernaes said.
The scientists only studied the impact of one night of sleep loss and therefore do not know how other forms of sleep disruption or circadian misalignment would have affected the participants’ metabolism across the investigated tissues.
“It will be interesting to investigate to what extent one or more nights of recovery sleep can normalize the metabolic changes that we observed at the tissue level as a result of sleep loss,” Cedernaes said.
While physical activity and meal intake were standardized as part of the study, the group did not investigate the role that diet and exercise play to combat weight gain associated with sleep loss. However, Cedernaes said based on previous research, lifestyle choices such as eating healthier and exercising may be able to modulate the negative impact sleep loss has on a person’s metabolism at the tissue level.
“Because of the complexity of doing these types of studies and analyses, we were limited to investigating a fairly smaller set of individuals who were all healthy, young and normal weight,” Cedernaes said. “It will therefore also be of interest and important to investigate how these types of molecular and genomic changes differ in people already suffering from metabolic disease, such as diabetes or obesity, and whether they are further modulated by, for example, sex, age and fitness level.”
Much of the study’s funding was provided by AFA Försäkring (140006), the Novo Nordisk Foundation, the Swedish Research Council (2015-03100 and 2014-6888) and the Åke Wiberg Foundation (M15-0218 and M160248), administered by Uppsala University, Sweden. The study was further supported by the Knut and Alice Wallenberg Foundation as part of the National Bioinformatics Infrastructure Sweden at SciLifeLab, Sweden.