The role of the brain in obesity
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Researchers from the French Inserm institute have tested young mice with a diet rich in sugar and fat… And guess what? This diet completely modified their enteric nervous system (ENS).
In addition to our “principal” brain, protected by the skull, our organism is helped by a “second” brain: a group of nearly 100 million neurons lodged in the digestive tube – the enteric nervous system (ENS). And its main job? To regulate digestive function, such as gastric drainage, colonic transit, absorption of nutrients and the regulation of food intake.
So many important functions, but which have rarely been studied in the case of obesity. This has now been in part corrected through the joint Franco-German research project, coordinated by Inserm’s research director Michel Neunlist, and Raphaël Moriez. The research team compared gastric functions of young mice fed “normally” or with a diet qualified as “Western”, meaning rich in fat and sugar.
The result was that the mice that received the richer “Western” diet had faster gastric drainage. Normally this drainage, which consists of emptying the stomach of its contents, usually takes around 2-3 hours. But if this drainage happens too rapidly, the ENS doesn’t have time to send the satiety signals, telling the “primary” brain that enough has been eaten. Without these satiety signals, the stomach demands more food and as such, dietary intake increases. And that’s exactly what happened to those young mice that were fed a rich diet…
The Inserm researchers noted that this same phenomena of accelerated gastric drainage also occurred with obese human patients. According to them, the high sugar, high fat diet is thus directly implicated in obesity, whether it is mice or humans. This diet modifies the ENS and blocks normal neuronal activity that takes place with a “normal” diet.
This neuroplastic change caused by a diet rich in sugar and fat prevents the digestive tube from "ageing" and adapting to an adult diet, when dietary requirements are less than for children.
“We believe that by preventing the natural evolution of the ENS over time, the fat and sugar rich diet will prevent the digestive tube from adapting to a diet corresponding to the adult age, thus maintaining its young phenotype, corresponding to a time of life when dietary intake is at its highest,” summarises Raphaël Moriez.
Another neuroplastic change is, "An increase in gastric production by a neuroprotective factor, GDNF, itself caused by leptin, a hormone now well known to regulate satiety in humans,” says Inserm.
This discovery confirms that while genetic disposition is important in the development of obesity, environmental influence counts too! An unbalanced diet from childhood will probably encourage the development of obesity at an adult age.
The confirmation of the influence of these acquired neuronal digestive modifications should, in the long-term, be useful for researchers to try to modify the “second” brain’s functioning in the case of adult obesity.
Sources:
"Obésité : notre second cerveau serait-il trop efficace ?" Inserm press release, January 2012
"Diet-induced obesity has neuroprotective effects in murine gastric enteric nervous system: involvement of leptin and GDNF," C. Baudry and al, The Journal of Physiology
Yamina Saïdj
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