Does oral experience terminate ingestion?

Using data from studies of ingestive behavior in developing rat pups we demonstrate how oral experience can contribute to the termination of ingestion. In rat pups, repeated oral stimulation with sweet solutions causes a decline in oral responsiveness. The diminished responsiveness is specific to the flavor of the stimulus experienced orally and can persist for several hours. We suggest that this experience-based decrement in responsiveness is best considered "oral habituation" and that oral habituation largely accounts for the onset of satiety. Post-ingestive feedback signals may have their influence through the oral habituation process or act in the context of oral habituation. Oral habituation is also shown to depend on the pattern of stimulus presentation, a phenomenon that adds considerable complexity to assessing the contributions of oral experience to satiety. The concept of oral habituation may be useful in understanding the immediate control of ingestion and the moment-to-moment expression of ingestive behavior in adult animals.     

Habituation of oral responding in adult rats.

The effects of repeated oral stimulation on ingestive responding were investigated in adult rats. A series of brief intraoral infusions of flavored diet was delivered to female rats once every minute through an oral cannula. When the flavor of the infused diet remained constant, significant decreases in mouthing behavior were observed by the end of testing, whereas switching the flavor of the diet during testing resulted in enhanced responding and infusions delivered through gastric cannulas produced minimal effects. Patterns of oral responding were also similar in food-restricted rats. These patterns of responding suggest that adult rats habituate to oral stimulation. Finally, oral habituation led to decreased ingestion, whereas gastric infusions had minimal effects. Thus, oral habituation may represent a mechanism influencing intake in rats at all ages. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Fat substitutes promote weight gain in rats consuming high-fat diets.

The use of food products designed to mimic the sensory properties of sweet and fat while providing fewer calories has been promoted as a method for reducing food intake and body weight. However, such products may interfere with a learned relationship between the sensory properties of food and the caloric consequences of consuming those foods. In the present experiment, we examined whether use of the fat substitute, olestra, affect energy balance by comparing the effects of consuming high-fat, high-calorie potato chips to the effects of consuming potato chips that sometimes signaled high calories (using high-fat potato chips) and that sometimes signaled lower calories (using nonfat potato chips manufactured with the fat substitute olestra). Food intake, body weight gain and adiposity were greater for rats that consumed both the high-calorie chips and the low-calorie chips with olestra compared to rats that consumed consuming only the high-calorie chips, but only if animals were also consuming a chow diet that was high in fat and calories. However, rats previously exposed to both the high- and low-calorie chips exhibited increased body weight gain, food intake and adiposity when they were subsequently provided with a high fat, high calorie chow diet suggesting that experience with the chips containing olestra affected the ability to predict high calories based on the sensory properties of fat. These results extend the generality of previous findings that interfering with a predictive relationship between sensory properties of foods and calories may contribute to dysregulation of energy balance, overweight and obesity. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

General and persistent effects of high-intensity sweeteners on body weight gain and caloric compensation in rats.

In an earlier work (S. E. Swithers & T. L. Davidson, 2008), rats provided with a fixed amount of a yogurt diet mixed with saccharin gained more weight and showed impaired caloric compensation relative to rats given the same amount of yogurt mixed with glucose. The present 4 experiments examined the generality of these findings and demonstrated that increased body weight gain was also demonstrated when animals consumed a yogurt diet sweetened with an alternative high-intensity sweetener (acesulfame potassium; AceK) as well as in animals given a saccharin-sweetened base diet (refried beans) that was calorically similar but nutritionally distinct from low-fat yogurt. These studies also extended earlier findings by showing that body weight differences persist after saccharin-sweetened diets are discontinued and following a shift to a diet sweetened with glucose. In addition, rats first exposed to a diet sweetened with glucose still gain additional weight when subsequently exposed to a saccharin-sweetened diet. The results of these experiments add support to the hypothesis that exposure to weak or nonpredictive relationships between sweet tastes and caloric consequences may lead to positive energy balance. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A role for sweet taste: Calorie predictive relations in energy regulation by rats.

Animals may use sweet taste to predict the caloric contents of food. Eating sweet noncaloric substances may degrade this predictive relationship, leading to positive energy balance through increased food intake and/or diminished energy expenditure. These experiments were designed to test the hypothesis that experiences that reduce the validity of sweet taste as a predictor of the caloric or nutritive consequences of eating may contribute to deficits in the regulation of energy by reducing the ability of sweet-tasting foods that contain calories to evoke physiological responses that underlie tight regulation. Adult male Sprague-Dawley rats were given differential experience with a sweet taste that either predicted increased caloric content (glucose) or did not predict increased calories (saccharin). We found that reducing the correlation between sweet taste and the caloric content of foods using artificial sweeteners in rats resulted in increased caloric intake, increased body weight, and increased adiposity, as well as diminished caloric compensation and blunted thermic responses to sweet-tasting diets. These results suggest that consumption of products containing artificial sweeteners may lead to increased body weight and obesity by interfering with fundamental homeostatic, physiological processes. (PsycINFO Database Record (c) 2010 APA, all rights reserved)