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Research at Manchester University has shown why humans and animals become dozy after a hearty meal. Brain cells which keep the body and mind active are switched off after eating, making us drowsy and in need of a good nap.
The discovery focuses upon the effects of glucose on neurons, which release orexins, tiny proteins central to the regulation of states of consciousness -
Glucose interferes with the mechanism through which the neurons release orexins, thus affecting the body's wakefulness.
These neurons are extremely sensitive to variations in glucose levels, and even a slight change can have a large impact. This is why a normal lunch can make us feel tired.
The lead researcher, Dr Denis Burdakov said "Considering these crucial roles of orexin neurons, their recently described inhibition by glucose is likely to have considerable implications for the regulation of states of consciousness and energy balance."
It is the malfunction of the orexin neurons, which can result in the chronic neurological disorder narcolepsy, which can cause sufferers to fall asleep involuntarily.
Problems in the functioning of the cells have also been linked to obesity and there is further evidence to demonstrate that they play a role in learning, reward seeking, and addiction.
Overall, according to Dr Burdakov "Modulation of orexin cells by glucose has a much wider behavioural role, contributing to the daily readjustments in the level of arousal and alertness."
During their experiments', scientists managed to isolate the neurons in brain slices from mice and explore how they reacted to changes in glucose levels.
In particular, they exposed the neurons to the subtle changes in glucose levels which occur in daily cycles of hunger and eating.
Until now, little was understood about how the basic energy molecule, glucose, regulated wakefulness and other energy-related behaviours.
The experiments conducted by Burdakov and his colleagues have shed light on one of the most elusive operations of the brain.

Copyright Associated Press of Pakistan, 2006

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