The influence of sweet taste sensitivity on food intake is not well understood. We investigated the involvement of salivary leptin and SNP of the sweet taste receptor genes (TAS1R2/TAS1R3) on sweet taste sensitivity, sensory-specific satiety (SSS) and macronutrient intake in healthy human adults. In all, nineteen high sweet sensitivity (HS) and eleven low sweet sensitivity (LS) subjects were classified based on the sweetness perception of one solution (9 mm sucrose) forced-choice triangle test. All participants completed a randomised crossover design experiment where they consumed one of three iso-energetic soup preloads differing in primary taste quality (sweet, non-sweet taste-control or no-taste energy-control). A period of 1 h after the preload, participants were offered a buffet meal consisting of foods varying in taste (sweet or non-sweet) and fat content. Subjective measures included hunger/fullness and SSS for sweetness. Saliva and buccal cells were collected to measure leptin level and to study the TAS1R2/TAS1R3 specific SNP, respectively. Salivary leptin concentrations were significantly higher in LS than HS participants (P<0·05). In addition, HS showed stronger sweet SSS compared with LH participants (P<0·05), and consumed less carbohydrate (% energy) and more non-sweet foods than LS (P<0·01 and P<0·05, respectively). Alleles from each TAS1R2 locus (GG compared with AA alleles of rs12033832, and CT/CC compared with TT alleles of rs35874116) were related to higher consumption of carbohydrates (% energy) and higher amount of sweet foods, respectively (P<0·05). In contrast, no associations were found for the TAS1R3 alleles. These results contribute to understand the links between taste sensitivity, macronutrient appetite and food consumption.

Complementary neuronal recordings and functional neuroimaging in human subjects show that the primary taste cortex in the anterior insula provides separate and combined representations of the taste, temperature and texture (including fat texture) of food in the mouth independently of hunger and thus of reward value and pleasantness. One synapse on, in the orbitofrontal cortex (OFC), these sensory inputs are for some neurons combined by learning with olfactory and visual inputs, and these neurons encode food reward in that they only respond to food when hungry, and in that activations correlate with subjective pleasantness. Cognitive factors, including word-level descriptions, and attention modulate the representation of the reward value of food in the OFC and a region to which it projects, the anterior cingulate cortex. Further, there are individual differences in the representation of the reward value of food in the OFC. It is argued that over-eating and obesity are related in many cases to an increased reward value of the sensory inputs produced by foods, and their modulation by cognition and attention that over-ride existing satiety signals. It is proposed that control of all rather than one or several of these factors that influence food reward and eating may be important in the prevention and treatment of overeating and obesity.

Complementary neurophysiological recordings in rhesus macaques (Macaca mulatta) and functional neuroimaging in human subjects show that the primary taste cortex in the rostral insula and adjoining frontal operculum provides separate and combined representations of the taste, temperature and texture (including viscosity and fat texture) of food in the mouth independently of hunger and thus of reward value and pleasantness. One synapse on, in the orbitofrontal cortex, these sensory inputs are for some neurons combined by learning with olfactory and visual inputs. Different neurons respond to different combinations, providing a rich representation of the sensory properties of food. In the orbitofrontal cortex feeding to satiety with one food decreases the responses of these neurons to that food, but not to other foods, showing that sensory-specific satiety is computed in the primate (including the human) orbitofrontal cortex. Consistently, activation of parts of the human orbitofrontal cortex correlates with subjective ratings of the pleasantness of the taste and smell of food. Cognitive factors, such as a word label presented with an odour, influence the pleasantness of the odour, and the activation produced by the odour in the orbitofrontal cortex. Food intake is thus controlled by building a multimodal representation of the sensory properties of food in the orbitofrontal cortex and gating this representation by satiety signals to produce a representation of the pleasantness or reward value of food that drives food intake. Factors that lead this system to become unbalanced and contribute to overeating and obesity are described.

Two experiments explored the hypothesis that distraction causes a reduced sensitivity to the physiological and sensory cues that signal when to terminate a meal. In Experiment 1, eighty-eight females ate five ‘Jaffa Cakes’ either while distracted by a computer game or while sitting in silence. Analysis of the difference in rated hunger, fullness and desire to eat (pre- to post-intake) revealed that distracted participants experienced smaller changes in their desire to eat and fullness than did non-distracted participants. Experiment 2 assessed whether changes in ratings are attenuated because sensory-specific satiety (or a related process) fails to develop. Using a similar procedure, eighty-four females provided desire to eat, pleasantness and intensity ratings for Jaffa Cakes and for two ‘uneaten’ foods, both before and at three time-points after consuming five Jaffa Cakes. Non-distracted participants reported a reduction in their desire to eat the eaten food relative to the uneaten food (food-specific satiety), whereas distracted participants maintained a desire to eat all foods. Moreover, this difference between distracted and non-distracted participants was evident 5 and 10 min after the eating episode had terminated. The present findings invite speculation that distraction attenuates the development of sensory-specific satiety, and that this effect persists (at least for a brief period) after the distractor has terminated. More generally, this kind of phenomenon warrants further scrutiny because it holds the potential to contribute towards overeating, either by prolonging an eating episode or by reducing the interval between meals.