Sleep deprivation: Single gene explains why lack of sleep leads to increased appetite
Scientists have identified a gene linked to sleep deprivation, which appears to regulate the interactions between sleep and metabolic state.
Published in Current Biology, this research looks at the association that is often made between sleep loss in humans, increased appetite and potential metabolic disorders, like obesity or metabolic syndrome. It shows that, in fruit flies, a protein called translin drives the complex relationship between hunger and lack of sleep. This protein is encoded by a specific gene, TSN.
While extensive scientific literature has previously emphasized the correlation between disrupted sleep patterns and risks of metabolic disorders, none really pinpointed the gene involved in this process.
"In humans, sleep and feeding are tightly interconnected, and pathological disturbances of either process are associated with metabolism-related disorders," explains study author Alex C Keene, "Despite the widespread evidence for interactions between sleep loss and metabolic dysfunction, little is known about the molecular basis of this interaction and how these processes integrate within the brain."
Translin in fruit flies
According to the study's authors, the insects display much of the same habits as humans when it comes to sleeping. Indeed, they get most of their rest at night-time, have a harder time sleeping with caffeine, and can face memory problems when they don't sleep enough. "We use fruit flies which are similar to humans to look at more complex biological models", Keene told IBTimes UK.
Scientists know from their behaviours that when fruit-flies are hungry, they sacrifice sleep to spend more time looking for food. The team carried out a screening of 12,000 genes to identify which of their genes kept the flies awake when they searched for food. They discovered that the one encoding the translin protein influenced the relationship between lack of sleep and hunger.
When translin was active starving flies fell asleep, even though they were on the lookout for food. When the gene coding the protein was suppressed however, normal sleep patterns and behaviours towards food were respected, suggesting that the gene only affected how metabolic state and sleep interacted with each other.
"Our study is important, because we think that if we are able to find genes that are integrate both sleep deprivation and metabolic state, we will be able, on the long term, to find clues to treat metabolic problems", Keene concludes.
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