The simple sugars glucose and fructose share a common "sweet" taste quality mediated by the T1R2+T1R3 taste receptor. However, when given the opportunity to consume each sugar, rats learn to affectively discriminate between glucose and fructose on the basis of cephalic chemosensory cues. It has been proposed that glucose has a unique sensory property that becomes more hedonically positive through learning about the relatively more rewarding post-ingestive effects that are associated with glucose as compared to fructose. We tested this theory using intragastric (IG) infusions to manipulate the post-ingestive consequences of glucose and fructose consumption. Food-deprived rats with IG catheters repeatedly consumed multiple concentrations of glucose and fructose in separate sessions. For rats in the "Matched" group, each sugar was accompanied by IG infusion of the same sugar. For the "Mismatched" group, glucose consumption was accompanied by IG fructose, and vice versa. This condition gave rats orosensory experience with each sugar but precluded the differential post-ingestive consequences. Following training, avidity for each sugar was assessed in brief access and licking microstructure tests. The Matched group displayed more positive evaluation of glucose relative to fructose than the Mismatched group. A second experiment used a different concentration range and compared responses of the Matched and Mismatched groups to a control group kept naïve to the orosensory properties of sugar. Consistent with results from the first experiment, the Matched group, but not the Mismatched or Control group, displayed elevated licking responses to glucose. These experiments yield additional evidence that glucose and fructose have discriminable sensory properties and directly demonstrate that their different post-ingestive effects are responsible for the experience-dependent changes in the motivation for glucose versus fructose.

In studies of eating behavior that have been conducted in humans, the tendency to consume more when given larger portions of food, known as the portion size effect (PSE), is one of the most robust and widely replicated findings. Despite this, the mechanisms that underpin it are still unknown. In particular, it is unclear whether the PSE arises from higher-order social and cognitive processes that are unique to humans or, instead, reflects more fundamental processes that drive feeding, such as conditioned food-seeking. Importantly, studies in rodents and other animals have yet to show convincing evidence of a PSE. In this series of studies, we used several methods to test for a PSE in adult male Sprague Dawley rats. Our approaches included using visually identifiable portions of a palatable food; training on a plate cleaning procedure; providing portion sizes of food pellets that were signaled by auditory and visual food-predictive cues; providing food with amorphous shape properties;and providing standard chow diet portions in home cages. In none of these manipulations did larger portions increase food intake. In summary, our data provide no evidence that a PSE is present in male Sprague Dawley rats, and if it is, it is more nuanced, dependent on experimental procedure, and/or smaller in size than it is in humans. In turn, these findings suggest that the widely-replicated PSE in humans may be more likely to reflect higher-order cognitive and social processes than fundamental conditioned behaviors. Highlights:• Portion size effect (PSE) refers to increased food intake induced by large portions.• Although widely replicated in human feeding studies, it may not exist animals.• Presence of a PSE in animals would shed light on mechanisms, which are not known.• Here, we find no evidence of PSE in male Sprague Dawley rats under a number of experimental conditions.• This suggests that the human PSE is more likely due to socio-cognitive processes.

In studies of eating behavior that have been conducted in humans, the tendency to consume more when given larger portions of food, known as the portion size effect (PSE), is one of the most robust and widely replicated findings. Despite this, the mechanisms that underpin it are still unknown. In particular, it is unclear whether the PSE arises from higher-order social and cognitive processes that are unique to humans or, instead, reflects more fundamental processes that drive feeding, such as conditioned food-seeking. Importantly, studies in rodents and other animals have yet to show convincing evidence of a PSE. In this series of studies, we used several methods to test for a PSE in adult male Sprague Dawley rats. Our approaches included using visually identifiable portions of a palatable food; training on a plate cleaning procedure; providing portion sizes of food pellets that were signaled by auditory and visual food-predictive cues; providing food with amorphous shape properties; and providing standard chow diet portions in home cages. In none of these manipulations did larger portions increase food intake. In summary, our data provide no evidence that a PSE is present in male Sprague Dawley rats, and if it is, it is more nuanced, dependent on experimental procedure, and/or smaller in size than it is in humans. In turn, these findings suggest that the widely-replicated PSE in humans may be more likely to reflect higher-order cognitive and social processes than fundamental conditioned behaviors. Highlights:• Portion size effect (PSE) refers to increased food intake induced by large portions.• Although widely replicated in human feeding studies, it may not exist animals.