Orosensory perception of sweet stimulus is blunted in diet-induced obese (DIO) rodents. Although this alteration might contribute to unhealthy food choices, its origin remains to be understood. Cumulative evidence indicates that prebiotic manipulations of the gut microbiota are associated with changes in food intake by modulating hedonic and motivational drive for food reward. In the present study, we explore whether a prebiotic supplementation can also restore the taste sensation in DIO mice. The preference and licking behavior in response to various sucrose concentrations were determined using respectively two-bottle choice tests and gustometer analysis in lean and obese mice supplemented or not with 10% inulin-type fructans prebiotic (P) in a preventive manner. In DIO mice, P addition reduced the fat mass gain and energy intake, limited the gut dysbiosis and partially improved the sweet taste perception (rise both of sucrose preference and number of licks/10 s vs. non-supplemented DIO mice). No clear effect on orosensory perception of sucrose was found in the supplemented control mice. Therefore, a preventive P supplementation can partially correct the loss of sweet taste sensitivity found in DIO mice, with the efficiency of treatment being dependent from the nutritional status of mice (high fat diet vs. regular chow).
Diet-induced obesity (DIO) reduces the orosensory perception of lipids in rodents and in some humans. Although bariatric surgery partially corrects this alteration, underlying mechanisms remain poorly understood. To explore whether metabolic changes might explain this fat taste disturbance, plasma metabolome analyses, two-bottle choice tests and fungiform papillae (Fun) counting were performed in vertical sleeve gastrectomized (VSG) mice and sham-operated controls. An exploratory clinic study was also carried out in adult patients undergone a VSG. In mice, we found that (i) the VSG reduces both the plasma neurotoxic signature due to the tryptophan/kynurenine (Trp/Kyn) pathway overactivation and the failure of fat preference found in sham-operated DIO mice, (ii) the activity of Trp/Kyn pathway is negatively correlated to the density of Fun, and (iii) the pharmacological inhibition of the Kyn synthesis mimics in non-operated DIO mice the positive effects of VSG (i.e., decrease of Kyn synthesis, increase of Fun number, improvement of the fat taste perception). In humans, a reduction of the plasma Kyn level is only found in patients displaying a post-surgery improvement of their fat taste sensitivity. Altogether these data provide a plausible metabolic explanation to the degradation of the orosensory lipid perception observed in obesity.
A preferential consumption of healthier foods, low in fat and sugar, is often reported after bariatric surgery, suggesting a switch of taste-guided food choices. To further explore this hypothesis in well-standardized conditions, analysis of licking behavior in response to oily and sweet solutions has been realized in rats that have undergone a Roux-en-Y bypass (RYGB). Unfortunately, these studies have produced conflicting data mainly due to methodological differences. Paradoxically, whereas the vertical sleeve gastrectomy (VSG) becomes the most commonly performed bariatric surgery worldwide and is easier to perform and standardize in small animals, its putative impacts on the orosensory perception of energy-dense nutrients remains unknown. Using brief-access licking tests in VSG or RYGB mice, we found that (i) VSG induces a significant reduction in the fat mass in diet-induced obese (DIO) mice, (ii) VSG partially corrects the licking responses to lipid and sucrose stimuli which are degraded in sham-operated DIO mice, (iii) VSG improves the willingness to lick oily and sucrose solutions in DIO mice and (iv) RYGB leads to close outcomes. Altogether, these data strongly suggest that VSG, as RYGB, can counteract the deleterious effect of obesity on the orosensory perception of energy-dense nutrients in mice.