The gene responsible for sleep deprivation and diabetes has been identified – offering hope for people who suffer from insomnia.
The study is the first to identify that a conserved gene – translin – works as a modulator of sleep in response to metabolic changes.
Researchers made the vital breakthrough after studying the sleep habits of fruit flies as they are “remarkably similar” to humans.
Fruit flies get most of their sleep at night, while certain drugs and stimulants such as caffeine can negatively affect their sleep. And if they get a lousy night’s sleep it can even affect their memory.
And the researchers said fruit flies can tell us a lot about the connection between sleep deprivation and metabolic disorders such as diabetes, obesity, and blood glucose levels.
The study, published in the journal Current Biology, establishes that translin is an essential integrator of sleep and metabolic state.
Acute sleep loss in humans is associated with increased appetite and insulin insensitivity, while chronically sleep-deprived people are more likely to develop obesity, metabolic syndrome, type 2 diabetes, and cardiovascular disease.
But metabolic state has a potent impact on modulating sleep and our body clocks.
Study corresponding author Doctor Alex Keene, of Florida Atlantic University in the US, said: “In humans, sleep and feeding are tightly interconnected, and pathological disturbances of either process are associated with metabolism-related disorders.
“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.”
When fruit flies are hungry, they sleep less because they will sacrifice sleep for their quest to search for food.
Dr Keene and his collaborators used fruit flies in their study and created various scenarios between sleeping and foraging to test each gene one at a time to determine which gene didn’t affect their sleep.
They discovered that translin, when knocked down in neurons, causes starving flies to sleep as soundly as they would on a full stomach.
They also observed the same inability to suppress sleep while in starvation mode in the flies that carried a null mutation in translin.
Co-first author Kazuma Murakami said: “While many genes have been identified as genetic regulators of sleep or metabolic state, mounting evidence from our study indicates that translin functions as a unique integrator of these processes.
“We also have been able to show that this gene is not required for general modulation of sleep. Furthermore, we now know that the energy stores in mutant flies are normal and that the starvation-induced sleep suppression phenotype is not due to increased nutrient storage.”
Dr Keene said results of the study provide important evidence that translin is not required for the perception of starvation or to stimulate hunger-related behaviors, but is required to stimulate wakefulness in the absence of food.
He added: “The identification of genes regulating sleep-feeding interactions will provide important insight into how the brain integrates and controls the expression of complex behaviors.”
By Stephen Beech