Sucrose-conditioned flavor preferences in sweet ageusic T1r3 and Calhm1 knockout mice

The present study compared the ability of sweet ageusic T1r3 knockout (KO) and Calhm1 KO mice to acquire preferences for a sucrose-paired flavor as well as for unflavored sucrose. The KO and wildtype (WT) mice were given 24-h one-bottle access to 8% sucrose containing one flavor CS+, e.g., grape) and to water containing a different flavor (CS-, e.g., cherry) over 4 training days. In subsequent two-bottle tests with the flavors in water only, the T1r3 KO and Calhm1 KO mice, like WT mice, preferred the CS+ to the CS-. After training with flavored solutions, both KO groups also preferred unflavored 8% sucrose to water although Calhm1 KO mice required more sugar experience to match the preference of the T1r3 KO mice. These findings demonstrate that Calhm1 KO mice, like T1r3 KO mice and WT mice, are sensitive to the post-oral preference conditioning actions of sucrose and can discriminate sugar from water. Yet, despite their acquired sucrose preferences, the Calhm1 KO and T1r3 KO mice consumed only half as much sugar per day as did WT mice. Thus, sweet taste signaling elements are not needed in the gut for sugar conditioning, but sweet taste signaling in the Mouth is essential for the full expression of sugar appetite. (C) 2013 Elsevier Inc. All rights reserved

Effects of hunger state on flavour pleasantness conditioning at home: flavour-nutrient learning vs. flavour-flavour learning

This study examined acquired liking of flavour preferences through flavour-flavour and flavour-nutrient learning under hungry or sated conditions in a naturalistic setting. Each participant consumed one of three versions of a test drink at home either before lunch or after lunch: minimally sweetened (CONTROL: 3% sucrose, 40kcal), artificially sweetened (3% sucrose 40kcal plus artificial sweeteners ASPARTAME) and sucrose-sweetened (SUCROSE: 9.9% sugar, 132kcal). The test drink was an uncarbonated peach-flavoured iced tea served in visually identical drink cans (330ml). Participants preselected as "sweet likers" evaluated the minimally sweetened flavoured drink (conditioned stimulus, CS) in the same state (hungry or sated) in which they consumed the test drink at home. Overall, liking for the CS flavour increased in participants who consumed the SUCROSE drink, however, this increase in liking was significantly larger when tested and trained hungry than sated, consistent with a flavour-nutrient model. Overall increases in pleasantness for the CS flavour in participants who consumed the SUCROSE drink when sated or the ASPARTAME drink independent of hunger state, suggest that flavour-flavour learning also occurred. These results are discussed in light of current learning models of flavour preference

Food after deprivation rewards the earlier eating

Food intake can be increased by learning to anticipate the omission of subsequent meals. We present here a new theory that such anticipatory eating depends on an associative process of instrumental reinforcement by the nutritional repletion that occurs when access to food is restored. Our evidence over the last decade from a smooth-brained omnivore has been that food after deprivation rewards intake even when those reinforced ingestive responses occur long before the physiological signals from renewed assimilation. Effects of food consumed after self-deprivation might therefore reward extra eating in human beings, through brain mechanisms that could operate outside awareness. That would have implications for efforts to reduce body weight. This food reward mechanism could be contributing to the failure of the dietary component of interventions on obesity within controlled trials of the management or prevention of disorders such as hypertension, atherosclerosis and type 2 diabetes

Learning of Food Preferences: Mechanisms and Implications for Obesity & Metabolic Diseases

Omnivores, including rodents and humans, compose their diets from a wide variety of potential foods. Beyond the guidance of a few basic orosensory biases such as attraction to sweet and avoidance of bitter, they have limited innate dietary knowledge and must learn to prefer foods based on their flavors and postoral effects. This review focuses on postoral nutrient sensing and signaling as an essential part of the reward system that shapes preferences for the associated flavors of foods. We discuss the extensive array of sensors in the gastrointestinal system and the vagal pathways conveying information about ingested nutrients to the brain. Earlier studies of vagal contributions were limited by nonselective methods that could not easily distinguish the contributions of subsets of vagal afferents. Recent advances in technique have generated substantial new details on sugar- and fat-responsive signaling pathways. We explain methods for conditioning flavor preferences and their use in evaluating gut–brain communication. The SGLT1 intestinal sugar sensor is important in sugar conditioning; the critical sensors for fat are less certain, though GPR40 and 120 fatty acid sensors have been implicated. Ongoing work points to particular vagal pathways to brain reward areas. An implication for obesity treatment is that bariatric surgery may alter vagal function

Flavour-nutrient learning in humans: an elusive phenomenon?

One widely cited model of how humans acquire liking for different foods is flavour-nutrient learning, where associations between the orosensory properties of the ingested food or drink (the flavour CS) and positive consequences of nutrient ingestion (the UCS) leads to acquired liking for the flavour (flavour-nutrient hedonic learning: FNL-H). Likewise, an association between the CS and the post-ingestive effects of ingested nutrients has been suggested to lead to learning about how satiating a particular food is (flavour-nutrient satiety learning: FNSH). However, whereas there is evidence for both FNL-H and FNL-S in experimental studies with non-human animals, evidence in humans is less convincing, with many failures to find the predicted changes in liking, preference or intake following repeated flavour-nutrient pairings. The present short review considers how subtle differences in experimental design might underlie this inconsistency, and identifies key design features which appear to increase the likelihood of success in human flavour-nutrient learning studies. Key factors include CS novelty, the level of nutrients ingested during training, the appetitive state of the consumer and individual consumer characteristics. A further complication is competition between FNL-H and FNL-S, and with other associations such as flavour-flavour learning. From this it is possible to make important inferences about the nature of human flavour-nutrient learning which firstly suggest that it has important similarities to that seen in other species, but secondly that the laboratory investigations of both FNL-H and FNL-S in humans can be compromised by subtle but important variations in experimental design

Food after deprivation rewards the earlier eating

Food intake can be increased by learning to anticipate the omission of subsequent meals. We present here a new theory that such anticipatory eating depends on an associative process of instrumental reinforcement by the nutritional repletion that occurs when access to food is restored. Our evidence over the last decade from a smooth-brained omnivore has been that food after deprivation rewards intake even when those reinforced ingestive responses occur long before the physiological signals from renewed assimilation. Effects of food consumed after self deprivation might therefore reward extra eating in human beings, through brain mechanisms that could operate outside awareness. That would have implications for efforts to reduce body weight. This food reward mechanism could be contributing to the failure of the dietary component of interventions on obesity within controlled trials of the management or prevention of disorders such as hypertension, atherosclerosis and type 2 diabetes

On a theorem of Y. Miyashita

Background: Portion size is an important driver of larger meals. However, effects on food choice remain unclear. Objective: Our aim was to identify how portion size influences the effect of palatability and expected satiety on choice. Methods: In Study 1, adult participants (n = 24, 87.5% women) evaluated the palatability and expected satiety of 5 lunchtime meals and ranked them in order of preference. Separate ranks were elicited for equicaloric portions from 100 to 800 kcal (100-kcal steps). In Study 2, adult participants (n = 24, 75% women) evaluated 9 meals and ranked 100–600 kcal portions in 3 contexts (scenarios), believing that 1) the next meal would be at 1900, 2) they would receive only a bite of one food, and 3) a favorite dish would be offered immediately afterwards. Regression analysis was used to quantify predictors of choice. Results: In Study 1, the extent to which expected satiety and palatability predicted choice was highly dependent on portion size (P < 0.001). With smaller portions, expected satiety was a positive predictor, playing a role equal to palatability (100-kcal portions: expected satiety, β: 0.42; palatability, β: 0.46). With larger portions, palatability was a strong predictor (600-kcal portions: β: 0.53), and expected satiety was a poor or negative predictor (600-kcal portions: β: −0.42). In Study 2, this pattern was moderated by context (P = 0.024). Results from scenario 1 replicated Study 1. However, expected satiety was a poor predictor in both scenario 2 (expected satiety was irrelevant) and scenario 3 (satiety was guaranteed), and palatability was the primary driver of choice across all portions. Conclusions: In adults, expected satiety influences food choice, but only when small equicaloric portions are compared. Larger portions not only promote the consumption of larger meals, but they encourage the adoption of food choice strategies motivated solely by palatability

Increased Oral Detection, but Decreased Intestinal Signaling for Fats in Mice Lacking Gut Microbiota

Germ-free (GF) mice lacking intestinal microbiota are significantly leaner than normal (NORM) control mice despite consuming more calories. The contribution of microbiota on the recognition and intake of fats is not known. Thus, we investigated the preference for, and acceptance of, fat emulsions in GF and NORM mice, and associated changes in lingual and intestinal fatty acid receptors, intestinal peptide content, and plasma levels of gut peptides. GF and NORM C57Bl/6J mice were given 48-h two-bottle access to water and increasing concentrations of intralipid emulsions. Gene expression of the lingual fatty acid translocase CD36 and protein expression of intestinal satiety peptides and fatty-acid receptors from isolated intestinal epithelial cells were determined. Differences in intestinal enteroendocrine cells along the length of the GI tract were quantified. Circulating plasma satiety peptides reflecting adiposity and biochemical parameters of fat metabolism were also examined. GF mice had an increased preference and intake of intralipid relative to NORM mice. This was associated with increased lingual CD36 (P<0.05) and decreased intestinal expression of fatty acid receptors GPR40 (P<0.0001), GPR41 (P<0.0001), GPR43 (P<0.05), and GPR120 (P<0.0001) and satiety peptides CCK (P<0.0001), PYY (P<0.001), and GLP-1 (P<0.001). GF mice had fewer enteroendocrine cells in the ileum (P<0.05), and more in the colon (P<0.05), relative to NORM controls. Finally, GF mice had lower levels of circulating leptin and ghrelin (P<0.001), and altered plasma lipid metabolic markers indicative of energy deficits. Increased preference and caloric intake from fats in GF mice are associated with increased oral receptors for fats coupled with broad and marked decreases in expression of intestinal satiety peptides and fatty-acid receptors

Intravascular Food Reward

Consumption of calorie-containing sugars elicits appetitive behavioral responses and dopamine release in the ventral striatum, even in the absence of sweet-taste transduction machinery. However, it is unclear if such reward-related postingestive effects reflect preabsorptive or postabsorptive events. In support of the importance of postabsorptive glucose detection, we found that, in rat behavioral tests, high concentration glucose solutions administered in the jugular vein were sufficient to condition a side-bias. Additionally, a lower concentration glucose solution conditioned robust behavioral responses when administered in the hepatic-portal, but not the jugular vein. Furthermore, enteric administration of glucose at a concentration that is sufficient to elicit behavioral conditioning resulted in a glycemic profile similar to that observed after administration of the low concentration glucose solution in the hepatic-portal, but not jugular vein. Finally using fast-scan cyclic voltammetry we found that, in accordance with behavioral findings, a low concentration glucose solution caused an increase in spontaneous dopamine release events in the nucleus accumbens shell when administered in the hepatic-portal, but not the jugular vein. These findings demonstrate that the postabsorptive effects of glucose are sufficient for the postingestive behavioral and dopaminergic reward-related responses that result from sugar consumption. Furthermore, glycemia levels in the hepatic-portal venous system contribute more significantly for this effect than systemic glycemia, arguing for the participation of an intra-abdominal visceral sensor for glucose