|Why we need a siesta after dinner
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|Author:||Francis [ Tue Jun 06, 2006 3:55 pm ]|
|Post subject:||Why we need a siesta after dinner|
Why we need a siesta after dinner
* 15:42 05 June 2006
* NewScientist.com news service
* Linda Geddes
The mystery of why we often feel sleepy after eating a big meal may finally have been resolved. Researchers have discovered that high blood glucose levels, similar to those after eating a big meal, can switch off the brain cells that normally keep us awake and alert.
The findings make evolutionary sense since sleepiness could be the body’s way of telling us to relax and conserve energy once we have found and eaten our food, says Denis Burdakov of the University of Manchester, UK, who led the research.
“It has been known for a while that people and animals can become sleepy and less active after a meal, but the brain signals responsible for this were poorly understood,” he says.
Burdakov’s team studied a group of brain cells called orexin neurons, which are found in the hypothalamus and produce proteins called orexins that are essential for maintaining normal wakefulness in humans. These neurons are less active at night and when they malfunction this can lead to narcolepsy, where sufferers cannot stay awake.
Previously, researchers have shown that orexin neurons can be inhibited by glucose, but it was not known how sensitive they were. Burdakov’s team exposed orexin neurons to subtle changes in glucose levels similar to those that occur in the blood during daily cycles of eating and hunger, then measured their firing rate.
“What we discovered is the activity of the neurons can be turned off by minute elevations in glucose associated with normal meals,” says Burdakov. The glucose is thought to act on potassium ion channels in the neurons’ membrane.
He believes this could explain why we naturally feel sleepy after a meal and also why it can be difficult to sleep when we are hungry, since the activity of the neurons would be higher when there is less glucose in the blood.
“We think orexin neurons make sure that we are awake and alert when hungry, in order to ensure optimal food-seeking,” Burdakov says. He adds that it makes evolutionary sense for animals to turn off their wakefulness and conserve energy once they have eaten their food, since it could be risky or wasteful to expend too much energy looking for more food.
Changes in the sensitivity of orexin neurons to glucose could lead to obesity, Burdakov speculates.
Orexin neurons are known to help regulate appetite and metabolic rate, and when they become faulty this can trigger late-onset obesity. Researchers are currently trying to understand exactly how orexin neurons interact with other brain circuits involved in appetite regulation.
“The role of orexin neurons in the control of numerous central nervous system processes makes the discovery of their ability to sense small changes in glucose potentially quite important,” says Joel Elmquist at the University of Texas Southwestern Medical Center in Dallas, US, writing in a commentary accompanying the paper in Neuron.
This is because it means a whole range of physiological processes can be regulated by the amount of fuel that is available. “Dysfunction of glucosensing may have profound effects on wakefulness and coordinated autonomic responses,” he says.
Journal reference: Neuron (vol 50, p 711)
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