Genetic Cost of Lost Sleep

Previous studies report that metabolism is negatively affected by sleep loss, with sleep loss linked to an increased risk of obesity and type-2 diabetes.  Jonathan Cedernaes, from Uppsala University (Sweden), and colleagues  studied 15 healthy normal-weight men who on two separate occasions came to the lab for almost 2-night long stays. During the second night the participants slept as usual (over 8 hours) in one of the two sessions, while they were kept awake in the other of these sessions, but in random order. To minimize the influence of various environmental factors, light conditions, food intake and activity levels in the lab were strictly controlled and the participants were bed-restricted when they were kept awake. Following the second night on both occasions that the men were studied, small tissue samples were taken from the superficial fat on the stomach, and from the muscle on the thigh – two kinds of tissues that are important for regulating metabolism and controlling blood sugar levels. Blood samples were also taken before and after the participants had consumed a sugar solution to test their insulin sensitivity, a practice commonly done to exclude the presence of diabetes or a metabolic state called impaired insulin sensitivity, which can precede type-2 diabetes.  Molecular analyses of the collected tissue samples showed that the regulation and activity of clock genes was altered after one night of sleep loss. The activity of genes is regulated by a mechanism called epigenetics. This involves chemical alterations to the DNA molecule such as methyl groups – a process called methylation – which regulates how the genes are switched on or off. The researchers found that clock genes had increased numbers of such DNA marks after sleep loss. They also found that the expression of the genes, which is indicative of how much of the genes’ product is made, was altered.  The study authors report that: “Our findings demonstrate that a single night of wakefulness can alter the epigenetic and transcriptional profile of core circadian clock genes in key metabolic tissues.”