The role of sweet taste in satiation and satiety

Increased energy consumption, especially increased consumption of sweet energy-dense food, is thought to be one of the main contributors to the escalating rates in overweight individuals and obesity globally. The individual's ability to detect or sense sweetness in the oral cavity is thought to be one of many factors influencing food acceptance, and therefore, taste may play an essential role in modulating food acceptance and/or energy intake. Emerging evidence now suggests that the sweet taste signaling mechanisms identified in the oral cavity also operate in the gastrointestinal system and may influence the development of satiety. Understanding the individual differences in detecting sweetness in both the oral and gastrointestinal system towards both caloric sugar and high intensity sweetener and the functional role of the sweet taste system may be important in understanding the reasons for excess energy intake. This review will summarize evidence of possible associations between the sweet taste mechanisms within the oral cavity, gastrointestinal tract and the brain systems towards both caloric sugar and high intensity sweetener and sweet taste function, which may influence satiation, satiety and, perhaps, predisposition to being overweight and obesity.

Oral zinc sulfate solutions inhibit sweet taste perception

We investigated the ability of zinc sulfate (5, 25, 50 mM) to inhibit the sweetness of 12 chemically diverse sweeteners, which were all intensity matched to 300 mM sucrose [800 mM glucose, 475 mM fructose, 3.25 mM aspartame, 3.5 mM saccharin, 12 mM sodium cyclamate, 14 mM acesulfame-K, 1.04 M sorbitol, 0.629 mM sucralose, 0.375 mM neohesperidin dihydrochalcone (NHDC), 1.5 mM stevioside and 0.0163 mM thaumatin]. Zinc sulfate inhibited the sweetness of most compounds in a concentration dependent manner, peaking with 80% inhibition by 50 mM. Curiously, zinc sulfate never inhibited the sweetness of Na-cyclamate. This suggests that Na-cyclamate may access a sweet taste mechanism that is different from the other sweeteners, which were inhibited uniformly (except thaumatin) at every concentration of zinc sulfate. We hypothesize that this set of compounds either accesses a single receptor or multiple receptors that are inhibited equally by zinc sulfate at each concentration.

Oral fatty acid sensitivity and dietary fat consumption

Lisa investigated the taste of fat and its influence on excess fat consumption and obesity. This research established that taste sensitivity to fat can be modulated by fat intake and may be used as an obesity prevention tool in the future.

Exploring the effects of genotypical and phenotypical variations in bitter taste sensitivity on perception, liking and intake of brassica vegetables in the UK

Brassicaceous vegetables (BV) have chemoprotective effects and yet consumption of BV in the UK is low. Previous studies suggest perception, liking and intake of BV are influenced by bitter taste sensitivity which this study further explores. Phenotypical taste sensitivity of 136 subjects was classified using propythiouracil (PROP) and sodium chloride and fungiform papillae density (FPD) was measured from tongue images. Polymorphisms of TAS2R38 and gustin (CA6) genes were analysed. Liking and bitterness of four raw vegetables (two BV (broccoli and white cabbage) and two non-BV (spinach and courgette)), as well as habitual consumption, were evaluated. There was a significant association between TAS2R38 genotype and PROP taster status (p<0.0001) and between FPD and PROP taster status (p=0.029). Individuals with greater sensitivity for PROP predominantly had TAS2R38 PAV/PAV genotype and greater FPD. BV were perceived as more bitter than non-BV (p<0.0001) with PAV/PAV subjects perceiving significantly stronger bitter intensity. There was a significant difference in liking for the four vegetables (p=0.002), and between consumers of different TAS2R38 genotype (p=0.0024). Individuals with TAS2R38 AVI/AVI genotype liked BV more. Regarding intake, both PAV/PAV and AVI/AVI individuals consumed more total vegetables and BV than PAV/AVI. Although PROP nontasters tended to consume more vegetables and BV than the other two phenotype groups, liking and vegetable intake were not significantly affected by taste phenotype. Although there was not a significant effect of CA6 genotype on bitterness ratings, there was a significant interaction between CA6 and TAS2R38, and in addition CA6 genotype was significantly associated with BV intake. However, these effects require validation as the proportions of the population with the CA6 G/G genotype was extremely small (7%). Our results confirmed that bitter taste perception in vegetables was influenced by both genotype and phenotype of bitter taste sensitivity. Moreover, our findings demonstrated that neither genotype nor phenotype of taste sensitivity alone accurately predict vegetable liking and intake as demographic factors were found to have a substantial influence.

Taste sensitivity to NaCl is associated with liking of salty foods and BMI

Background – It is widely acknowledged that sodium is consumed in excess in most developed countries. Sodium (Na) consumption has been a target of public health interventions in recent years due to its link to numerous adverse health affects such as hypertension and cardiovascular disease. While much of the current research is directed at strategies to reduce sodium in foods and the diet, little is known about the factors which determine salt consumption and preference. Currently, there is no research relating NaCl taste sensitivity and liking of food, or if NaCl taste sensitivity may manifest in changes in BMI.
Objective – Establish whether a relationship exists between NaCl taste sensitivity, preference for salty foods and BMI.
Design – Taste sensitivity to NaCl was determined for 119 subjects (104 female) according to the procedure laid out by “ISO 3972:1991 – Method of investigating sensitivity of taste”. In a separate session subjects rated their liking of generic biscuit with 2 levels of added NaCl [low (2.9g/100g) & high (19.1g/100g)] using the 9-point hedonic scale. BMI was calculated from self reported height and weight data collected. Spearman’s rank order correlation was used to determine whether an association existed between NaCl taste sensitivity, preference for salty foods and BMI.
Outcomes – A significant positive correlation was found between BMI and NaCl taste sensitivity (r=0.204, p<0.05). In addition there was a significant positive correlation between BMI and liking of low NaCl biscuits (r=0.267, p<0.01). No significant associations were identified between the high NaCl cracker and NaCl taste sensitivity or BMI. A paired t-test showed there was no significant difference in liking of the low and commercial NaCl crackers (p=0.078).
Conclusion – This study revealed that individuals with a higher BMI have a greater liking of low NaCl biscuits, and this may be due to their increased NaCl taste sensitivity. The results suggest that NaCl taste sensitivity may be a factor in foods consumed by an individual which in turn may influence weight status.

Fat taste sensitivity

Hyposensitivity to fatty acid taste is associated with greater intake of fat, higher BMI and attenuated gastrointestinal (GI) function. These observations are consistent amongst healthy and overweight/obese subjects, who display attenuated taste and GI function, and consume excess fat.

Leptin as a modulator of sweet taste sensitivities in mice

Leptin acts as a potent inhibitory factor against obesity by regulating energy expenditure, food intake, and adiposity. The obese diabetic db/db mouse, which has defects in leptin receptor, displays enhanced neural responses and elevated behavioral preference to sweet stimuli. Here, we show the effects of leptin on the peripheral taste system. An administration of leptin into lean mice suppressed responses of peripheral taste nerves (chorda tympani and glossopharyngeal) to sweet substances (sucrose and saccharin) without affecting responses to sour, salty, and bitter substances. Whole-cell patch-clamp recordings of activities of taste receptor cells isolated from circumvallate papillae (innervated by the glossopharyngeal nerve) demonstrated that leptin activated outward K+ currents, which resulted in hyperpolarization of taste cells. The db/db mouse with impaired leptin receptors showed no such leptin suppression. Taste tissue (circumvallate papilla) of lean mice expressed leptin-receptor mRNA and some of the taste cells exhibited immunoreactivities to antibodies of the leptin receptor. Taken together, these observations suggest that the taste organ is a peripheral target for leptin, and that leptin may be a sweet-sensing modulator (suppressor) that may take part in regulation of food intake. Defects in this leptin suppression system in db/db mice may lead to their enhanced peripheral neural responses and enhanced behavioral preferences for sweet substances.

The role of environmental and genetic influences on fatty acid taste sensitivity

 The studies conducted in this thesis add to the growing body of literature supporting the existence of fatty acid taste. Data contributes to the novel, yet mounting research for a functional role of fat taste in food intake regulation, which may have important implications for overweight and obesity.

Sensory and consumer research update : Sweet taste and diet

There is much attention on sugar in the food supply given the recent sugar tax in Britain. Sugar remains a controversial, yet much loved ingredient. A new comprehensive study from Deakin University Centre for Advanced Sensory Science (CASS) looked at the relationship between sweet taste function, diet and anthropometry among 60 adults. Low et al used six different sweeteners (glucose, fructose, sucrose, sucralose, erythritol, and Rebaudioside A) and measured detection, recognition threshold and perceived intensity of all the sweeteners in all subjects. They assessed diet in all subjects as well as height, weight and waist circumference.

Dietary fat restriction increases fat taste sensitivity in people with obesity

OBJECTIVE: Individuals with obesity may be less sensitive to the taste of fat, and it is hypothesized that this is due to excess dietary fat intake. This study assessed the effect of a 6-week low-fat (LF) or portion control (PC) diet matched for weight loss on fat taste thresholds, fat perception, and preference in people with overweight/obesity.

METHODS: Participants (n = 53) completed a randomized dietary intervention and consumed either a LF diet (25% fat) or PC diet (33% fat) for 6 weeks. Fat taste thresholds (lowest detectable fat concentration), fat perception (discrimination ability), preference, and anthropometry were assessed at baseline and week 6.

RESULTS: Consumption of a LF diet (n = 26) and PC diet (n = 27) reduced participants' weight (P < 0.001), with no significant differences between groups (LF, -2.9%, PC, -2.7%). Both diets resulted in a decrease in fat taste thresholds (P = 0.014), and the effect tended to be stronger in the LF diet vs. the PC diet (P = 0.060). The ability to perceive different fat concentrations in foods was increased after the LF diet only (P = 0.017); however, food preference did not change on either diet.

CONCLUSIONS: A PC and LF diet both increase fat taste sensitivity in people with overweight/obesity, with the strongest effect after the LF diet.

The association between sweet taste function, anthropometry, and dietary intake in adults

Variation in ability to detect, recognize, and perceive sweetness may influence food consumption, and eventually chronic nutrition-related conditions such as overweight and obesity. The aim of this study was to investigate the associations between sweet taste function, anthropometry, and dietary intake in adults. Participants' (n = 60; mean age in years = 26, SD = ±7.8) sweet taste function for a range of sweeteners (glucose, fructose, sucrose, sucralose, erythritol, and Rebaudioside A) was assessed by measuring detection and recognition thresholds and sweetness intensity. Height, weight, and waist circumference were also measured, and participants also completed a Food Frequency Questionnaire. There was large inter-individual variation in detection, recognition and sweetness intensity measures. Pearson's correlation coefficient revealed no robust correlations between measures of sweet taste function, anthropometry, and dietary intake, with the exception of suprathreshold intensity, which was moderately correlated with total energy intake (r = 0.23-0.40). One-way analysis of variance revealed no significant differences between the most and least sensitive participants in terms of BMI, waist circumference, and dietary intake for all measures of sweet taste function and sweeteners (all p > 0.01). When stratified into BMI categories, there were no significant differences in any measure of sweet taste function between the normal weight and overweight/obese participants (all p > 0.01). Results show that that sweet taste function is not associated with anthropometry and sweetness intensity measures are the most appropriate measure when assessing links between sweet taste and food consumption.

Oral sensitivity to fatty acids, food consumption and BMI in human subjects

Fatty acids are the chemical moieties that are thought to stimulate oral nutrient sensors, which detect the fat content of foods. In animals, oral hypersensitivity to fatty acids is associated with decreased fat intake and body weight. The aims of the present study were to investigate oral fatty acid sensitivity, food selection and BMI in human subjects. The study included two parts; study 1 established in thirty-one subjects (29 (sem 1·4) years, 22·8 (sem 0·5) kg/m²) taste thresholds using 3-AFC (3-Alternate Forced Choice Methodology) for oleic, linoleic and lauric acids, and quantified oral lipase activity. During study 2, fifty-four subjects (20 (sem 0·3) years, 21·5 (sem 0·4) kg/m2) were screened for oral fatty acid sensitivity using oleic acid (1·4 mm), and they were defined as hypo- or hypersensitive via triplicate triangle tests. Habitual energy and macronutrient intakes were quantified from 2 d diet records, and BMI was calculated from height and weight. Subjects also completed a fat ranking task using custard containing varying amounts (0, 2, 6 and 10 %) of fat. Study 1 reported median lipase activity as 2 μmol fatty acids/min per l, and detection thresholds for oleic, linoleic and lauric acids were 2·2 (sem 0·1), 1·5 (sem 0·1) and 2·6 (sem 0·3) mm. Study 2 identified twelve hypersensitive subjects, and hypersensitivity was associated with lower energy and fat intakes, lower BMI (P < 0·05) and an increased ability to rank custards based on fat content (P < 0·05). Sensitivity to oleic acid was correlated to performance in the fat ranking task (r 0·4, P < 0·05). These data suggest that oral fatty acid hypersensitivity is associated with lower energy and fat intakes and BMI, and it may serve as a factor that influences fat consumption in human subjects.