A group of researchers at the University of Cologne in Germany has developed an “entirely novel” approach to treating some eating disorders associated with periods of binge eating.
According to the group’s findings, the cause of binge eating lies with a group of nerve cells situated in the brain’s hypothalamus. These cells control the release of endogenous lysophospholipids, which in turn control the excitability of nerve cells in the cerebral cortex, thus stimulating food intake.
In this process, the crucial step of the signalling pathway is dictated by an enzyme called autotaxin, which is itself responsible for the production of the lysophosphatidic acid (LPA) which impacts hunger levels.
Therefore, the scientists claim, the administration of autotaxin inhibitors can significantly reduce excessive food intake, and thus hinder the development of obesity, or help cure it.
Eating disorders and obesity are rife in developed countries around the world, and come with the risk of developing further health complications like cardiovascular diseases and diabetes.
According to the University of Cologne team, attempts to influence eating behaviour and reduce the incidence of obesity and eating disorders in the population with medication has so far been ineffective.
However, the team says the use of autotaxin inhibitors to control binge eating episodes could be a “decisive step” forward. So far, studies in mice have shown that correct and continuous administration of the inhibitors in overweight animals resulted in weight loss.
Professor Dr Johannes Vogt, a co-leader of the study and member of the university’s Faculty of Medicine, explained: “We saw a significant reduction in excessive food intake and obesity through gene mutation and pharmacological inhibition of autotaxin.
“Our fundamental findings on the LPA-controlled excitability of the brain, which we have worked on for years, therefore also play a central role for eating behaviour.”
It is hoped that the findings, which have been published in Nature, could be the first step towards developing a drug which could be used by those experiencing disordered eating and obesity.
Professor Dr Robert Nitsch, Director of the Institute for Translational Neurosciences at the University of Münster and co-leader of the study, added: “The data show that people with a disturbed synaptic LPA signalling pathway are more likely to be overweight and suffer from type II diabetes.
“This is a strong indication of a possible therapeutic success of ATX inhibitors, which we are currently developing together with the Hans Knöll Institute in Jena for use in humans.”
Additionally, the university team said: “These findings on the excitation control of neuronal networks in eating behaviour through lysophospholipids and the new therapeutic possibilities they suggest could in future contribute not only to treating eating disorders, but also neurological and psychiatric illnesses.”
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