These results are published in the journal Nature Communications, on 25 October 2013.
Obesity affects more than 15% of adults in France, and its constitutive mechanisms are still not completely explained. Normally, fine control of weight and food intake is coordinated by a specialised part of the brain (the hypothalamus). It adjusts food intake depending on reserves and needs. In this way, after a period of excessive food intake and weight gain, a healthy subject will tend spontaneously to reduce their food intake for a while to return to their previous weight.
In many of the morbidly obese, this mechanism is faulty: despite their efforts, they continue to consume too much food (hyperphagia), contributing to maintaining a higher weight or even increasing it further.
Even so, their brain should take in the information about over-eating and reduce food intake to encourage weight loss. This observation is all the more surprising given that the hunger hormone ghrelin, produced by the stomach and acting on the hypothalamus, is most frequently found at a normal, or even a reduced level in obese patients.
The study conducted by Sergue Fetissov and the team from joint research unit 1073 "Nutrition, inflammation and dysfunction of the gut-brain axis" (Inserm/University of Rouen), directed by Pierre Dchelotte, collaborating with Prof Akio Inui's team at the University of Kagoshima (Japan), reveals the molecular mechanism of this paradoxical hyperphagia.
The researchers have highlighted the presence of specific antibodies, or immunoglobulins, in the blood of obese patients, antibodies that recognise ghrelin and regulate appetite.
By binding to ghrelin, the immunoglobulins protect the hunger hormone from being broken down rapidly in the bloodstream. The ghrelin can then act on the brain for longer and stimulate appetite.
"The immunoglobulins have different properties in obese patients", explains Sergue Fetissov,
|Contact: Sergueï Fetissov|
INSERM (Institut national de la sant et de la recherche mdicale)