Obesity and bad sleep habits among teenagers are two rising health concerns that seems intertwined. Indeed, many studies trace obesity to poor sleep hygiene. This is especially concerning because (i) adolescents get less and less sleep as screens invade their bedroom and (ii) obese children have a very strong risk to later develop cardiometabolic diseases such as hypertension and diabetes. Yet, we still do not know why sleep is so important for metabolic health. To understand how the brain and the fat tissue communicate while we sleep, we propose SmartSense, an ambitious and innovative project, resulting from the convergence of four research groups with expertise in sleep, fat tissue biology, epigenetics and sensor technology, all located at the University of Oslo. We will develop mouse models and new “smart” sensors, using the latest advances in molecular biology and cell phone technology to wirelessly monitor brain-fat tissue communication in real-time. With such breakthrough techniques, we will study how sleep deprivation during adolescence affects fat tissue development and the emergence of metabolic disorders later in life. One of our core hypotheses is that this long-term effect is written on top of our DNA during adolescence and remains for the rest of our life, as an epigenetic memory. Our ambition is to understand whether sleep could be a new therapeutic target for the prevention and treatment of obesity and other metabolic disorders.
Obesity and poor sleep heath are concurrent epidemics in teenagers. Childhood obesity is one of the most serious current public health challenges because adults who are obese during childhood inevitably acquire cardiometabolic risks. Many studies trace obesity to bad sleep habits. This is concerning because adolescents get less and less sleep as technology invades their bedroom. Innovative preventive measures could be targeted towards sleep regulation, but first we need to unveil physiological and molecular processes linking adolescence sleep deprivation (SD) to metabolic diseases. We aim to understand how adolescence sleep deprivation elicits long-term metabolic imbalance by deciphering the mechanisms of brain-adipose tissue crosstalk.
We propose SmartSense, an ambitious, innovative and transdisciplinary project, only possible from the integration of state-of-the-art expertise in neurophysiology, adipose tissue biology, epigenetics and sensor technology at the University of Oslo. Using innovative mouse models of SD, we will 1) determine the effects of adolescence SD on adipose tissue maturation and metabolic homeostasis in the young, 2) characterize impacts on metabolic fitness in adulthood, thereby testing an epigenetic memory hypothesis, while 3) we will develop ‘smart’ probes sensing multiple components in vivo, monitoring brain-adipose tissue communication in real time. SmartSense is built on 3 work packages and 4 teams led by 2 rising female investigators and 2 established investigators. Critical challenges are 1) design and construction of biosensors small enough not to cause discomfort to young mice, 2) disentangle effects of SD from altered feeding behavior, 3) cell numbers available for the full extent of epigenetic mapping. Our preliminary data and fall-back strategies however argue for the feasibility and success of the project. We foresee several scientific breakthroughs and significant impacts on society.