Williams Cancer Institute



Intense sweeteners (IS) are significantly sweeter than sugar, allowing their use in minimal amounts with little to no energy contribution. IS, both artificial and natural, over 30 times sweeter than sucrose, are promoted as a healthier sugar alternative within acceptable daily intake (ADI) levels. Despite their reduced energy content, evidence suggests a link between regular IS consumption and obesity-related issues.

IS exhibit higher sweetness intensity due to their strong affinity for sweet taste receptors. While there are numerous sweet compounds, commonly used IS are limited.

IS, like sugars, interact with sweet taste receptors (T1Rs) on the tongue and may activate bitter taste receptors (T2Rs), both G-protein coupled. These receptors extend throughout the gastrointestinal tract, impacting metabolic processes like glucose homeostasis and gut motility. Recent interest revolves around taste receptors’ role in obesity development and the gut microbiome’s association with metabolic conditions.

Multiple factors influence the relationship between IS consumption and obesity. Epidemiological evidence suggests a link, and while reverse causality bias may contribute, biological mechanisms such as interactions with taste receptors and the gut microbiota need consideration. In a review article by Turner et al., 2020, the following article was published. explores the current evidence on the IS, obesity, and metabolic outcomes relationship.

Weight gain and obesity have been associated with IS consumption, primarily in artificially sweetened beverages. Studies report conflicting results, suggesting varied metabolic effects among different sweeteners. Alterations in GLP-1 secretion, insulin function, and appetite regulation contribute to metabolic dysfunction linked to IS use. Despite inconsistent findings, IS consumption is associated with increased risks of weight gain and type 2 diabetes.

On the other hand, taste receptor genetics, specifically TAS2R38, play a role in determining dietary preferences. IS activation of both sweet (T1Rs) and bitter (T2Rs) taste receptors may influence food intake. IS consumers tend to have higher sugar intake, possibly due to altered taste receptor expression. Genetic variations in taste receptors may impact IS preferences and intake, subsequently influencing diet and metabolic health.

Taste receptors are not confined to the oral cavity but are found throughout the body. Human taste receptors have been identified in various organs, including the brain, heart, and lungs. Particularly in the respiratory tract, certain taste receptors (T2Rs) detect bacteria and signaling molecules, initiating immune responses. Similarly, the gastrointestinal tract in humans expresses at least 3 different T2Rs. Upon activation, these extra-oral taste receptors regulate the secretion of metabolic hormones involved in appetite, energy intake, gut motility, and glucose homeostasis.

Stimulation of extra-oral taste receptors by intense sweeteners (IS) can have metabolic consequences. For instance, studies suggest that IS may impact the secretion of hormones such as GLP-1, a crucial player in appetite regulation and glucose homeostasis. The hormonal response to IS may differ from that elicited by caloric sweeteners.

Furthermore, IS have been observed to influence the gut microbiota, potentially linking them to metabolic conditions. The interplay between IS and the microbiota may contribute to obesity, insulin resistance, and other metabolic disorders. Studies indicate that IS consumption can induce dysbiosis in mice, negatively affecting the bacterial composition in the intestines. This alteration in the microbiota has been associated with glucose intolerance, especially when transferring the gut bacteria from IS-consuming mice to germ-free mice.

The gut microbiome may play a role in influencing taste preferences and the consumption of intense sweeteners (IS) by manipulating taste receptor expression. Interestingly, bariatric surgery, which alters satiety, food preferences, and gastrointestinal microbiota, also leads to changes in taste receptor expression. This suggests a connection between intestinal dysbiosis and modified taste preferences. Additionally, germ-free mice exhibit a higher number of gastrointestinal sweet receptors and a greater preference for sweet-tasting foods compared to control mice. Overall, the gut microbiota might impact taste preferences by regulating taste receptor expression, subsequently influencing microbial composition and altering the risk of metabolic disorders.

Metabolic conditions such as insulin resistance and obesity, linked to IS consumption and gut dysbiosis, are also associated with specific TASR genotypes and altered taste receptor expression levels. Notably, taste receptors can be activated by bacteria and bacterial compounds, and they can stimulate the secretion of antimicrobial agents. Moreover, changes in receptor expression levels may occur in response to shifts in bacterial compositions, leading to modified metabolic functions. Given the pivotal roles of taste receptors and the gut microbiome in metabolic health, a bidirectional interaction between these receptors and gastrointestinal microbes is proposed, altered in response to IS consumption. However, further investigations are necessary to establish the mechanisms of this seemingly counterintuitive relationship.

In conclusion, taste receptors may serve as a link between IS consumption, intestinal dysbiosis, weight gain, and metabolic outcomes. While the metabolic effects of IS consumption on T1Rs have been studied in humans, the potential activation of bitter taste receptors and the subsequent metabolic effects of that activation have been largely overlooked. In general, IS consumption could alter the risk of metabolic disorders through interactions with taste receptors and the intestinal microbiota. If this is the case, certain dietary or microbial interventions may be employed for the prevention or treatment of metabolic conditions related to gastrointestinal dysbiosis and IS consumption. However, more studies are needed to confirm this association in humans and define the involved mechanisms.

Reference: Turner, A., Veysey, M., Keely, S., Scarlett, C. J., Lucock, M., & Beckett, E. L. 28 April 2020. Intense Sweeteners, Taste Receptors and the Gut Microbiome: A Metabolic Health Perspective. International journal of environmental research and public health, 17(11), 4094. https://doi.org/10.3390/ijerph17114094

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