The impact of sleep disturbances on adipocyte function and lipid metabolism.
Classically, sleep has been considered to serve an essential restorative function for the brain. However, there are an increasing number of studies linking decreased sleep quantity and/or quality in humans to an increased obesity and diabetes risk. Reductions in sleep quantity or quality lead to an increase in hunger and appetite, which chronically could predispose an individual to obesity. Carefully controlled studies have shown that two nights of insufficient sleep is causally linked to a decrease in disposition index, the most commonly used predictor of an individual's diabetes risk, and impairments in glucose tolerance and insulin sensitivity. Thus, sleep appears to play a critical role in modulating energy metabolism in peripheral tissues. Here we will discuss recent work implicating adipose tissue as a potential direct target of disruption of sleep quality, and explore the potential mechanistic links between sleep, adipose tissue and the global control of energy metabolism in humans.
Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, 1333 San Pablo Street, MMR 626, Los Angeles, CA 90089, USA. josiane.broussard@usc.edu
Josiane
J
Broussard
Matthew J
MJ
Brady
D017667:Adipocytes / Q000378:metabolism / Q000502:physiology*; D000818:Animals; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D020738:Leptin / Q000378:metabolism; D050356:Lipid Metabolism / Q000502:physiology*; D012890:Sleep / Q000502:physiology; D012893:Sleep Wake Disorders / Q000150:complications / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000502:physiology / Q000503:physiopathology
D020738:Leptin