Obesity results from a temporary or prolonged positive energy balance due to an alteration in the homeostatic feedback of energy balance. Food, with its discriminative and hedonic qualities, is a key element of reward-based energy intake. An alteration in the brain reward system for highly palatable energy-rich foods, comprised of fat and carbohydrates, could be one of the main factors involved in the development of obesity by increasing the attractiveness and consumption of fat-rich foods. This would induce, in turn, a decrease in the taste of fat. A better understanding of the altered reward system in obesity may open the door to a new era for the diagnosis, management and treatment of this disease.
Aspartame and Stevia are widely substituted for sugar. Little is known about cerebral activation in response to low-caloric sweeteners in comparison with high-caloric sugar, whereas these molecules lead to different metabolic effects. We aimed to compare gustatory evoked potentials (GEPs) obtained in response to sucrose solution in young, healthy subjects, with GEPs obtained in response to aspartame and Stevia. Twenty healthy volunteers were randomly stimulated with three solutions of similar intensities of sweetness: Sucrose 10 g/100 mL of water, aspartame 0.05 g/100 mL, and Stevia 0.03 g/100 mL. GEPs were recorded with EEG (Electroencephalogram) electrodes. Hedonic values of each solution were evaluated using the visual analog scale (VAS). The main result was that P1 latencies of GEPs were significantly shorter when subjects were stimulated by the sucrose solution than when they were stimulated by either the aspartame or the Stevia one. P1 latencies were also significantly shorter when subjects were stimulated by the aspartame solution than the Stevia one. No significant correlation was noted between GEP parameters and hedonic values marked by VAS. Although sucrose, aspartame, and Stevia lead to the same taste perception, cerebral activation by these three sweet solutions are different according to GEPs recording. Besides differences of taste receptors and cerebral areas activated by these substances, neural plasticity, and change in synaptic connections related to sweet innate preference and sweet conditioning, could be the best hypothesis to explain the differences in cerebral gustatory processing after sucrose and sweeteners activation.
Background: Several carbohydrate-based models of feeding have been described. The influence of the substrate oxidation rate on liking, wanting, and macronutrient selection, however, is not known in humans.