Food intake, appetite and satiety are mainly integrated at the level of hypothalamic neuronal circuits. Importantly, energy balance is also controlled by hedonic/reward brain systems encoded by the neuronal network of the mesolimbic dopaminergic system. Hedonic properties of food stimulate feeding and some food substances (e.g., sugars, sweeteners, salt, and lipids) are more prompt to be involved in these addictive processes. These effects are mediated by abrupt dopamine increases in the brain reward system. This mesocorticolimbic system encodes for the three psychological component of reward: liking, wanting and learning.
During obesity, this gut-to-brain axis is altered at the level of the hedonic responses to food intake, leading to an abnormal increase in energy consumption. Moreover, the concept of the implication of the gut microbiota in the gut-to-brain axis to control food intake emerged over these last years, however the mechanisms still remain incompletely known and the roles of the gut microbiota in the regulation of hedonic/reward aspects of food intake are completely unknown.
Therefore, it is of utmost importance to fill in this gap to better understand the alterations of the gut-to-brain axis to control food intake during obesity and the implication of the gut microbiota in that context.
The originality of this work is to investigate how gut microbes are able to control hedonic and reward system in healthy conditions as well as in the physiopathology of obesity.
In order to proof a causal link between gut microbiota and alterations of hedonic response to food intake associated with obesity, we use gut microbiota transplantation. Preliminary data suggest that transferring the gut microbiota from high-fat diet-induced obese mice into control diet fed mice is enough to alter the dopaminergic signalling in the striatum of the mice in a similar way to alterations observed during obesity such as reduction of D2 receptor. Moreover, these alterations of dopaminergic signalling are associated with alteration of psychological component of reward such as liking. Indeed mice transplanted with the gut microbiota from high-fat diet-induced obese mice present a reduction of the high-fat high-sugar diet consumption in comparison to mice transplanted with the gut microbiota from control fed mice. Altogether these data suggest for the first time the implication of the gut microbiota into the alteration of hedonic regulation of food intake during obesity. These preliminary data need to be confirmed and we will investigate the mechanisms involved in these interactions between the gut microbiota and the hedonic regulation of food intake during obesity.