researcher at Department of Neuroscience, Functional Pharmacology
Keywords: diabetes sleep deprivation sleep obesity alzheimer memory lifestyle experiments cohort
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2013 State doctorate in neuroscience (Uppsala University, Sweden)
2008 Doctor in human biology, summa cum laude (University of Lübeck, Germany)
2003 Master in nutritional science, final grading: excellent (University of Kiel, Germany)
By utilizing functional magnetic resonance imaging, we were the first lab to demonstrate that acute sleep loss increases humans’ brain reward response to food. We further showed that acute sleep loss attenuates the cognitive ability to suppress salient brain responses to food. These effects on brain functions may account for increased food purchasing and selection of larger portions in sleep-deprived participants. Further tipping the energy balance in favour of weight gain, we found that short-term sleep loss reduces postprandial thermogenesis and physical activity energy expenditure. A shift in the endocrine balance from catabolic hormones, such as glucagon-like peptide 1 (GLP-1), toward anabolic hormones, such as ghrelin and endocannabinoids, potentially predisposing humans to gain weight, has also been observed. Work from my lab has also shown that recurrent partial sleep loss alters the balance of gut bacteria in humans, which has been widely implicated as key for maintaining a healthy metabolism. The same study also found reduced sensitivity to insulin after partial sleep loss. A recent study from my lab has further demonstrated that activity of circulating DPP-4 increased by about 14% in women, whereas it decreased by about 11% in men. DPP-4 is an enzyme that catalyzes a variety of important physiological processes in humans by cleavage of, e.g., the incretin hormones GLP-1 and gastric inhibitory polypeptide. These results highlight the importance of including both men and women in sleep deprivation studies. In a recent study from our lab, we investigated the genomic and physiological impact of acute sleep loss in peripheral tissues, by obtaining adipose tissue and skeletal muscle after one night of sleep loss and after one full night of sleep. We found that acute sleep loss alters genome-wide DNA methylation in adipose tissue, and unbiased transcriptomic-, protein- and metabolite-level analyses also revealed highly tissue-specific changes that are partially reflected by altered metabolite levels in blood. We observed transcriptomic signatures of inflammation in both tissues following acute sleep loss, but changes involving the circadian clock were evident only in skeletal muscle, and we uncovered molecular signatures suggestive of muscle breakdown that contrast with an anabolic adipose tissue signature. These findings provide insight into how disruption of sleep and circadian rhythms may promote weight gain and sarcopenia. Collectively, these studies show it is no surprise that metabolic disorders, such as obesity and type 2 diabetes, are on the rise since perturbed sleep is such a common feature of modern life.
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