Intriguing new evidence points to a molecular and cellular basis for the previously poorly understood meal-induced drowsiness. Burdakov et al. (2006) , at the University of Cambridge (UK), have revealed that the rise in blood glucose that occurs after a large meal is sensed by glucose-inhibited neurones in the lateral hypothalamus, a region of brain important for maintained wakefulness (remarkably, narcoleptic patients are found to lack 85-95% of these neurones ). These orexin expressing neurones are reportedly hyperpolarised by a glucose activated potassium current mediated by TASK family potassium channels. This glucose mediated inhibition is believed to reduce the output from orexin neurones to amineregic, cholinergic, and glutamatergic arousal pathways of the brain. This molecular pathway for the action of glucose on this critical orexin-expressing arousal centre in brain was previously entirely unknown.
While postprandial dip is usually physiological after a generous meal, a very sharp or sustained drop in blood glucose may be associated with a disorder of glucose metabolism.