Scientists have identified a new neural signaling pathway influencing binge eating. Such a discovery opens the way to treatments that can significantly reduce food intake and thus promote weight loss.
An enzyme inhibitor to prevent binge eating
Published in the journal Naturethis work, carried out by an international team of researchers, focused on the agouti-related peptide neurons (AgRP)which reside in the hypothalamus and which promote feelings of hunger when activated. When tracking mice subjected to periods of fasting, the team found that the rodents had higher blood levels of a biomolecule called lysophosphatidylcholine (LPC), which was found to be controlled by AgRP.
When they reach the brain, these lipid molecules are converted into lysophosphatidic acid (LPA) by an enzyme called autotaxin (ATX). This process excites neurons in the cerebral cortex, which in mice resulted in typical foraging behaviors. Scientists have discovered that administration of an ATX enzyme inhibitor allowed to regulate these behaviors, involving significant weight loss in treated obese rodents.
« We observed a significant reduction in excessive food intake and obesity through genetic mutation and pharmacological inhibition of ATX “, explains Johannes Vogt, researcher at the University of Cologne and lead author of the study. ” These fundamental findings on LPA-controlled brain excitability confirm that such a pathway plays a central role in eating behavior. »
Similar mechanisms in humans
Although these effects were seen in mice, scientists found evidence of similar mechanisms in humans. In subjects with impaired APL signaling function, the team reports higher rates of obesity and type 2 diabetes, and states that work is underway on drugs targeting this particular pathway.
« Data shows people with disrupted synaptic LPA signaling pathway are more likely to be overweight and have type 2 diabetes “, highlighted Robert Nitsch, co-author of the study. ” This is a strong indication of a possible therapeutic success of ATX inhibitors, which we are currently developing with the Hans Knöll Institute in Jena for clinical use.. »