Stating that sleep is an essential biological process seems as obvious as saying that the sun rises every morning. Yet, researchers’ understanding of the molecular mechanisms underlying the effects of sleep loss is still in its earliest stages. The risk for a host of metabolic disorders, including weight gain, diabetes, obesity, and cardiovascular disease, associated with reduced sleep is driving basic investigations on the topic.

In a?study published this week in the?Proceedings of the National Academy of Sciences,?Amita Sehgal, PhD, a professor of Neuroscience at the?Perelman School of Medicine?at the University of Pennsylvania?and a Howard Hughes Medical Institute investigator, along with co-first authors?Aalim M. Weljie, PhD, a research assistant professor of Systems Pharmacology and Translational Therapeutics, and Peter Meerlo, PhD, from the University of Groningen, The Netherlands, found common molecules signifying perturbed metabolism in response to sleep restriction in a comprehensive metabolic profiling of blood from both rats and humans. Their findings point to an overall shift in how lipids are metabolized and evidence of systemic oxidative stress due to decreased sleep in both species.

Oxidative stress and lipid metabolism are important factors in metabolic diseases, although further work needs to be done to establish a mechanistic link between the markers found and specific diseases, stress the researchers.

“One possibility is that sleep drives metabolite clearance and so acts as a reparative process at the metabolic level,” says Sehgal. “The impact of sleep restriction on circadian biology is particularly relevant given what we now know about how metabolites also oscillate in humans on a daily basis.” Metabolites are chemical intermediates or end products of metabolism, so while they are generated through the breakdown of fats, carbohydrates, and proteins, their function is not restricted to these processes.

They also have roles in signaling, regulating enzymatic activity, growth, and development.