If we already know the consequences of a diet that is too rich in bad fats on health, Belgian and French researchers think they have discovered where our irrepressible desire to get back into the pack after the first crisps comes from. In their research, published in the journal NatureCommunications this Monday, January 28, they describe the role of an enzyme in the intestine essential in the regulation of appetite, which malfunctions in the event of a diet that is too fatty.
NAPE-PDL, an essential enzyme
When we eat, the messages of satiety are carried by this famous enzyme, called “n-acyl phosphatidylethanolamine phospholipase D” or more simply “NAPE-PDL”. Produced by the intestine, this substance is responsible for transmitting saturation signals to the brain. The anorectic neurons are thus activated in the hypothalamus, and stop food intake. But in the case of a continuously high-fat diet, the activity of NAPE-PDL drops. The gut-brain axis is altered, and appetite control is deregulated.
To reach these conclusions, the researchers carried out work on mice lacking this enzyme. They realized that by exposing these rodents to a high-fat diet, they couldn’t stop eating, and therefore ate more than normal rodents exposed to the same diet. They thus became obese and developed a foie gras.
Towards new therapeutic treatments
Thus, scientists believe that overweight or obese people could suffer from a dysfunction of this NAPE-PDL enzyme. ” We have […] put his finger on a key mechanism in the regulation of metabolism. It won’t stop overweight or obese people from eating, but it helps explain why they’re always hungry, and look for solutions.”Explain to BFM TV Patrice Cani, professor at the Catholic University of Louvain (UCL) who participated in the study.
This discovery could indeed open the way to new therapeutic treatments to combat obesity. Molecules produced by the enzyme could be administered to patients to reduce their appetite. Solutions could also be developed to prevent the degradation of the substance or to reactivate it.
“As part of our study, we injected the bacterium Akkermansia, which restores the dialogue between the intestine and the brain. A start-up is trying to develop this track. She hopes to offer a food supplement within 3 years”, announces Patrice Cani. This bacterium would in fact be able to modulate the production of bioactive fatty acids, without going through the enzyme.
Read also :
- Junk food in France: a report for the future
- Fat and sugar, the enemies of your liver
