Hunger and histamine

September 22, 2014

Hunger and histamine

A research has conducted by University of Florence and the Institute of Cell Biology and Neurobiology of the National Research Council (IBCN-CNR) in Rome, in collaboration with the Department of Physiology and Pharmacology, Sapienza University of Rome, which identified a key mechanism through which the brain translates some peripheral signals of satiety. The title of the work, published in PNAS (Proceedings of the National Academy of Sciences), is “Satiety factor oleoylethanolamide recruits the brain histaminergic system to inhibit food intake.”

It turned out that the satiety signal produced by the intestine during a meal by a lipid, the oleoiletanolamide (OAS), activates specific areas of the brain that use histamine as a neurotransmitter, thus promoting the cessation of ‘feeding activity.

It is demonstrated for the first time, through experimental researches, that the anorexic effect of OEA is drastically attenuated in both animals deprived of the possibility to synthesize histamine, both in animals whose reserves neuronal histamine were temporally inactivated through the direct administration in brain of an inhibitor agent. With this research we were able to identify the nature of the neurotransmitters involved and to understand the mechanisms by which neurons in the brain at the level of the hypothalamus translate the information mediated by OAS on the nutritional status of the organism and the corresponding level of satiety.

In the system neurotransmitter histamine has identified one of the key components to transfer the message of satiety generated by OEA in the intestine.

The knowledge of these neural mechanisms, which play an essential role in feeding behaviour, as they contribute to the reduction of appetite, offers new perspectives to develop safer and more effective drugs for the treatment of obesity, which aim to increase the release of histamine in the brain.