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Brain histamine participates in the hypophagic and cognitive effects of gut chemical OEA.

The interaction of the two compounds to influence food intake and memory consolidation.

A team of researchers lead by Dr Beatrice Passani of the University of Florence found a relationship between two brain systems known to influence eating behaviour, regulate food intake, and control appetite. Speaking to delegates on 3 July at the FENS Forum of Neuroscience in Copenhagen, Dr Passani described how a series of signals activate brain centres regulating appetite, inducing us to eat less. This presentation follows a study published on PNAS in 2014. ("Satiety factor oleoylethanolamide recruits the brain histaminergic system to inhibit food intake" doi:10.1073/pnas.1322016111)

Scientists know that consuming certain dietary fats induces release of oleoylethanolamide (OEA), a chemical in the small intestine, in turn stimulating production of oxytocin, inhibiting food intake. They also know that histamine in the brain, which regulates functions including wakefulness and memory consolidation, is also known to influence appetite, eating behaviour, and to regulate food intake. High histaminergic activity seems to suppress food intake, and low activity increases intake. Dr Passani and colleagues investigated whether OEA also involves the brain's histamine neurotransmitter system to induce satiety.  

Her team measured food intake and behavioural indicators of satiety in mice with extremely low histamine levels. After 12 hours of food deprivation, followed by OEA injections, and re-exposure to food, a striking difference occurred: normal mice ate much less, as expected, but the low histamine mice ate eagerly. When researchers induced histamine release in normal mice, they observed increased appetite suppression stimulated by OEA. The researchers also found that in the brain's cortex, OEA indirectly increased the amount of histamine released.

“We found that these two systems do talk to each other,” said Dr Passani. The complex gut brain axis seems mediated by the histaminergic system. OEA induces histamine release to exert an appetite-suppressing effect. This indicates that the brain’s histamine system controls several behaviours, including OEA as trigger and affecting appetite. 

These findings suggest that normal appetite suppression depends on interactions between OAE secreted from the intestines and the brain's histamine system that seems to serve as a relay station, controlling eating behaviour.

Because histamine regulates functions such as wakefulness, appetite and memory consolidation, disruption of histamine may be associated with various brain disorders. Anti-histamines, including over-the-counter medications for allergies, are based on blocking histamine responses on histamine H1 receptors. Antipsychotic drugs for disorders such as schizophrenia, bind strongly to histamine H1 receptors in the brain, which seems to be the cause of unintended side effects such as obesity and sedation associated with antipsychotic treatment.

“These findings have implications in prevention of obesity, and in various disorders associated with antipsychotic treatments,” she added. “We should take into account that these drugs may induce obesity and other unintended effects." She hopes that a better understanding these drugs’ effects might contribute to the development of better medications to manage both cognitive and eating disorders.

04 July 2016