For years, observational studies have linked short sleep patterns with obesity, and many scientists suspect it is the sleep irregularities causing metabolic dysfunction and appetite disruptions. New research from the University of Pennsylvania’s Perelman School of Medicine and the University of Nevada, Reno, investigating sleep in a laboratory worm model is suggesting the direction of this relationship should be reversed – it may be obesity causing the poor sleep, and not the other way around.
"We wanted to know, what is sleep actually doing?" says study co-author Alexander van der Linden. "Short sleep and other chronic conditions, like diabetes, are linked, but it's just an association. It's not clear if short sleep is causing the propensity for obesity, or that the obesity, perhaps, causes the propensity for short sleep.”
The primary goal of the research was to investigate the metabolic systems regulating sleep, outside of the brain and central nervous system. The hypothesis was that sleep serves a role to conserve energy in an organism, and it is disruptions to this mechanism in obese subjects that can result in poor sleep.
Exploring this hypothesis the researchers used the C. elegans worm as a model. This particular organism is often used in sleep science as researchers know exactly which of its neurons can be switched on or off to regulate sleep.
Across a number of experiments the study found the worms were unable to effectively sleep when signaling between fat stores and sleep neurons were disrupted. Co-author on the study, David Raizen, says the research suggests obese humans experiencing sleep irregularities may be suffering from a similar signaling problem between fat cells and the brain cells that control sleep. And it is the accumulation of excessive fat stores that precedes the development of sleep irregularities.
“There is a common, over-arching sentiment in the sleep field that sleep is all about the brain, or the nerve cells, and our work suggests that this isn’t necessarily true,” says Raizen. “There is some complex interaction between the brain and the rest of the body that connects to sleep regulation.”
The study concludes sleep is most likely regulated via a complex interaction between an organism’s energy needs, the way fat-storage cells respond to those energy needs, and the subsequent actions of sleep-inducing neurons.
“We think that sleep is a function of the body trying to conserve energy in a setting where energetic levels are going down,” says Raizen. “Our findings suggest that if you were to fast for a day, we would predict you might get sleepy because your energetic stores would be depleted.”
The new study was published in the journal PLOS Biology.
Source: Penn Medicine
