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Sweetness is an important driver for food intake and one of the most popular taste sensations. At present, there is a preliminary understanding of the signaling pathways of sweetness and the mechanisms that affect sweetness sensation. Human sweetness sensation is expressed through at least two types of signaling pathways, one of which is mediated by heterodimers formed by the taste receptor family 1 member 2 (T1R2) and the taste receptor family 1 member 3 (T1R3), whereas the other by sodium glucose co-transporters (SGLT) and glucose transporters (GLUT). This article reviews the structure of T1R2/T1R3 heterodimer and the mechanism of sweet signal transduction, and discusses the effects of internal and external factors such as bitterness, sourness, umami, anti-sweetness substances, aroma compounds, saliva, obesity and age on sweetness sensation. The shortcomings of the current research are presented, such as little effect of the current available noncaloric sweeteners (NCSs) in attenuating obesity and diabetes, few studies on the interactions of sweet taste with the other four taste sensations, unclear understanding of the molecular basis of the regulation mechanisms of anti-sweetness substances at the receptor level, and limitations of using rodents as an experimental substitute for humans in sweet taste research. This article aims to understand how sweet substances exert their functions in complex food matrices, hoping to provide theoretical support and ideas for future development and application of NCS-containing foods.

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Sweet taste, a proxy for sugar-derived calories, is an important driver of food intake, and animals have evolved robust molecular and cellular machinery for sweet taste signaling. The overconsumption of sugar-derived calories is a major driver of obesity and other metabolic diseases. A fine-grained appreciation of the dynamic regulation of sweet taste signaling mechanisms will be required for designing novel noncaloric sweeteners with better hedonic and metabolic profiles and improved consumer acceptance. Sweet taste receptor cells express at least two signaling pathways, one mediated by a heterodimeric G-protein coupled receptor encoded by taste 1 receptor members 2 and 3 (TAS1R2 + TAS1R3) genes and another by glucose transporters and the ATP-gated potassium (KATP) channel. Despite these important discoveries, we do not fully understand the mechanisms regulating sweet taste signaling. We will introduce the core components of the above sweet taste signaling pathways and the rationale for having multiple pathways for detecting sweet tastants. We will then highlight the roles of key regulators of the sweet taste signaling pathways, including downstream signal transduction pathway components expressed in sweet taste receptor cells and hormones and other signaling molecules such as leptin and endocannabinoids. [ABSTRACT FROM AUTHOR]

Background It has been suggested that low-energy sweeteners (LES) may be associated with an increased risk of metabolic diseases, possibly due to stimulation of glucose-responsive mechanisms. Objective We conducted a systematic review and meta-analysis of human intervention studies examining the acute effect of LES intake on postprandial glucose (PPG) and postprandial insulin (PPI) responses, in order to comprehensively and objectively quantify these relations. Methods We systematically searched the Medline, OVID FSTA, and SCOPUS databases until January 2020. Randomized controlled trials comparing acute postprandial effects on PPG and/or PPI after exposure to LES, either alone, with a meal, or with other nutrient-containing preloads to the same intervention without LES were eligible for inclusion. PPG and PPI responses were calculated as mean incremental area under the curve divided by time. Meta-analyses were performed using random effects models with inverse variance weighing. Results Twenty-six papers (34 PPG trials and 29 PPI trials) were included. There were no reports of statistically significant differences in the effects of LES on PPG and PPI responses compared with control interventions. Pooled effects of LES intake on the mean change difference in PPG and PPI were −0.02 mmol/L (95% CI: −0.09, 0.05) and −2.39 pmol/L (95% CI: −11.83, 7.05), respectively. The results did not appreciably differ by the type or dose of LES consumed, cointervention type, or fasting glucose and insulin levels. Among patients with type 2 diabetes, the mean change difference indicated a smaller PPG response after exposure to LES compared with the control (−0.3 mmol/L; 95% CI: −0.53, −0.07). Conclusions Ingestion of LES, administered alone or in combination with a nutrient-containing preload, has no acute effects on the mean change in postprandial glycemic or insulinemic responses compared with a control intervention. Apart from a small beneficial effect on PPG (−0.3 mmol/L) in studies enrolling patients with type 2 diabetes, the effects did not differ by type or dose of LES, or fasting glucose or insulin levels. This review and meta-analysis was registered at PROSPERO as CRD42018099608. [ABSTRACT FROM AUTHOR]

Introduction: Introduction: consumption of non-caloric sweeteners (NCS) has increased worldwide in the last 35 years. Objective: to determine the consumption of NCS among pregnant Chilean women and measure if consumption exceeded the acceptable daily intake. Methods: we conducted a cross-sectional study of pregnant women from the two main cities in Chile. Women were interviewed to determine the consumption of NCS and socioeconomic level; anthropometry was measured. Results: six hundred and one pregnant women were interviewed; 98% of pregnant women surveyed consumed NCS. The most consumed sweetener was sucralose (95.6%), followed by acesulfame k (80.6%), stevia (78.3%), aspartame (75.1%), saccharin (14.8%), and cyclamate (10%). We observed that consumption closest to the acceptable daily intake was reported for stevia (82.5%), followed by acesulfame k (44%). However, except stevia, which reached 12%, average values were under 5% of the acceptable daily intake. No pregnant woman in the sample exceeded the acceptable daily intake and there were no differences in sweetener consumption by trimester of pregnancy or by socioeconomic level. Conclusions: a high prevalence of NCS consumption was observed, however, none of the pregnant women exceeded the acceptable daily intake. [ABSTRACT FROM AUTHOR]

Background: Activation of gastrointestinal (GI) sweet taste receptors by caloric sweeteners triggers secretion of anorexigenic and inhibition of orexigenic GI hormones to regulate food intake. The effect of noncaloric sweeteners on these mechanisms is controversial. We have recently shown that motilin-induced gastric phase III contractions signal hunger feelings, thereby identifying GI motility, and its regulatory hormone motilin, as novel players in food intake regulation. Objective: The objective of the present study was to determine the effect of caloric and noncaloric sweeteners on GI motility, GI hormone secretion, and hunger in humans. Design: The study was a randomized, double-blind, crossover trial. Twelve healthy volunteers underwent 4 gastroduodenal manometry recordings in which the occurrence of phase III contractions was followed by the intragastric (i.g.) administration of 250 mL tap water or equisweet caloric (1) 50 g glucose and 2) 25 g fructose) and noncaloric sweeteners [220 mg acesulfame-K (ace-K)] dissolved in 250 mL tap water. Measurement continued until ≥1 subsequent phase III. Blood samples were collected for the measurement of GI hormones. Visual analog scales were used to rate hunger and satiety feelings. Response curves were analyzed using (generalized) linear mixed models. Results: We found: 1) an inhibitory effect of the 2 caloric sweeteners on antral motility (P < 0.01), but no effect after ace-K, 2) an inhibitory effect of the 2 caloric sweeteners on motilin secretion (P < 0.01), but no effect after ace-K, 3) an early increase in chole-cystokinin (CCK) secretion after the 2 caloric sweeteners (P < 0.01), but no effect after ace-K, and 4) an initial stronger decrease in hunger feelings and stronger increase in satiety after ace-K (P < 0.05), followed by a steeper return of hunger and decrease of satiety after ace-K (P < 0.05). Conclusions: Our results demonstrate, for the first time to our knowledge, that the caloric sweeteners glucose and fructose, but not the noncaloric sweetener ace-K, inhibit motilin secretion and antral motility while increasing CCK secretion. This trial was registered at clinicaltrials.gov as NCT02891525. Am J ClinNutr 2018;107:707-716. [ABSTRACT FROM AUTHOR]

Noncaloric sweeteners have enabled a reduction of carbohydrate sweeteners in the diet for many years, thus combating obesity, diabetes, and other health disorders. However, many consumers reject noncaloric sweeteners, as they exhibit delays in sweetness onset, objectionable lingering sweet aftertaste, and the absence of sugar-like mouthfeel. We propose that the temporal taste differences between carbohydrate and noncaloric sweeteners result from slowed diffusion of the latter to and from sweetener receptors through the amphipathic mucous hydrogel covering the tongue. Also, we demonstrate that formulation of noncaloric sweeteners with K + /Mg 2+ /Ca 2+ mineral salt blends markedly attenuates lingering sweetness, an effect believed to be due to a composite of osmotic and chelate-mediated compaction of the mucous hydrogel covering the tongue. For example, sweetness linger values (intensity units in % sucrose eq) for rebaudioside A and aspartame are reduced from 5.0 (0.5 SD) to 1.6 (0.4 SD) and from 4.0 (0.7 SD) to 1.2 (0.4 SD), respectively, by formulation with 10 mM KCl/3 mM MgCl 2 /3 mM CaCl 2 . Finally, we propose that sugar-like mouthfeel is a consequence of K + /Mg 2+ /Ca 2+ activation of the calcium-sensing receptor present in a subset of taste bud cells. For example, the mouthfeel intensity of a sucrose solution increased from 1.8 (0.6 SD) to 5.1 (0.4 SD).

Diet soda consumption has not been associated with tangible weight loss. Aspartame (ASP) commonly substitutes sugar and one of its breakdown products is phenylalanine (PHE), a known inhibitor of intestinal alkaline phosphatase (IAP), a gut enzyme shown to prevent metabolic syndrome in mice. We hypothesized that ASP consumption might contribute to the development of metabolic syndrome based on PHE's inhibition of endogenous IAP. The design of the study was such that for the in vitro model, IAP was added to diet and regular soda, and IAP activity was measured. For the acute model, a closed bowel loop was created in mice. ASP or water was instilled into it and IAP activity was measured. For the chronic model, mice were fed chow or high-fat diet (HFD) with/without ASP in the drinking water for 18 weeks. The results were that for the in vitro study, IAP activity was lower ( p < 0.05) in solutions containing ASP compared with controls. For the acute model, endogenous IAP activity was reduced by 50% in the ASP group compared with controls (0.2 ± 0.03 vs 0.4 ± 0.24) ( p = 0.02). For the chronic model, mice in the HFD + ASP group gained more weight compared with the HFD + water group (48.1 ± 1.6 vs 42.4 ± 3.1, p = 0.0001). Significant difference in glucose intolerance between the HFD ± ASP groups (53 913 ± 4000.58 (mg·min)/dL vs 42 003.75 ± 5331.61 (mg·min)/dL, respectively, p = 0.02). Fasting glucose and serum tumor necrosis factor-alpha levels were significantly higher in the HFD + ASP group (1.23- and 0.87-fold increases, respectively, p = 0.006 and p = 0.01). In conclusion, endogenous IAP's protective effects in regard to the metabolic syndrome may be inhibited by PHE, a metabolite of ASP, perhaps explaining the lack of expected weight loss and metabolic improvements associated with diet drinks. [ABSTRACT FROM AUTHOR]

With the high demand for a healthy diet, it is necessary and important to explore natural sweeteners used in food that enhance palatability but minimize calories. Citrus is considered a good potential source of noncaloric sweeteners, but to date, only one sweetness modulator has been found in this most common fruit crop. Herein, an efficient strategy based on an in-house database and the untargeted and targeted metabolomics analyses was proposed to screen sweeteners or sweet-enhancing compounds from citrus. Eight sweeteners or sweetness-enhancing compounds were screened out, seven of which were newly identified from the genus Citrus . Surprisingly, we identified naturally occurring oxime V, which previously was only known as a synthetic compound. The contents of five compounds, in 11 citrus cultivars or unreleased selections across two production years, were compared. Successful identification of these natural sweeteners and sweetness-enhancing compounds in citrus fruit indicated the potential to identify the relevant biosynthetic pathways and to breed new citrus cultivars containing these compounds that provided both palatability and lower sugar consumption. This study also demonstrated that the proposed metabolomics-based screening strategy could greatly boost the identification of taste modulators with low contents in natural resources.

Over the past decades, Mexico has become one of the main sweetener-consuming countries in the world. Large amounts of these sweeteners are in dairy products aimed at the children's market in various presentations such as yogurt, flavored milk, flan, and cheeses. Although numerous studies have shown the impact of sweeteners in adults, the current evidence for children is insufficient and discordant to determine if these substances have any risk or benefit on their well-being. Therefore, this study aimed to describe the sweeteners present in 15 dairy products belonging to the school-age children's market in Mexico and their impact on health. These dairy products were selected through a couple of surveys directed at parents of school-age children. After that, the list of ingredients of each product was analyzed to identify their sweetener content. From there, exhaustive bibliographic research on sweeteners and their possible health effects was carried out, which included 109 articles and 18 studies. The results showed that at a neurological, endocrinological, cardiovascular, metabolic, osseous, renal, hepatic, dental, reticular, carcinogenic, and gut microbiota level; sucrose, fructose, high-fructose corn syrup, maltodextrins, sucralose, and acesulfame K, have a negative effect. While maltodextrins, stevia, polydextrose, and modified starch have a positive one. For these reasons, it is necessary to evaluate the advantages and disadvantages that the consumption of each sweetener entails, as well as a determination of the appropriate acceptable daily intake (ADI). [ABSTRACT FROM AUTHOR]

The present review of noncaloric sweeteners (NCSs) by the Asociación Mexicana de Gastroenterología was carried out to analyze and answer some of the most frequent questions and concerns about NCS consumption in patients with gastrointestinal disorders, through a thorough review of the medical literature. A group of gastroenterologists and experts on nutrition, toxicology, microbiology, and endocrinology reviewed and analyzed the published literature on the topic. The working group formulated conclusions, based on the scientific evidence published, to give an opinion with respect to NCS ingestion. Current evidence does not confirm the carcinogenic potential of NCSs. However, the studies analyzed showed that saccharin could have a proinflammatory effect and that polyols can cause gastrointestinal symptoms and manifestations, depending on the dose and type of compound. The ingestion of xylitol, erythritol, sucralose, aspartame, acesulfame K, and saccharin could increase the secretion of the gastrointestinal hormones that regulate intestinal motility, and stevia and its derivatives could have a favorable effect on the percentage of liver fat. Caution should be taken in recommending aspartame consumption in patients with chronic liver disease because it reduces the ratio of branched-chain amino acids to aromatic amino acids. In addition, NCS ingestion could modify the composition of the intestinal microbiota, having an effect on gastrointestinal symptoms and manifestations. It is important to continue conducting causality studies on humans to be able to establish recommendations on NSC consumption., (Copyright © 2019 Asociación Mexicana de Gastroenterología. Publicado por Masson Doyma México S.A. All rights reserved.)