Abstract
Intense sweeteners (IS) are often marketed as a healthier alternative to sugars, with the potential to aid in combating the worldwide rise of diabetes and obesity. However, their use has been counterintuitively associated with impaired glucose homeostasis, weight gain and altered gut microbiota. The nature of these associations, and the mechanisms responsible, are yet to be fully elucidated. Differences in their interaction with taste receptors may be a potential explanatory factor. Like sugars, IS stimulate sweet taste receptors, but due to their diverse structures, some are also able to stimulate bitter taste receptors. These receptors are expressed in the oral cavity and extra-orally, including throughout the gastrointestinal tract. They are involved in the modulation of appetite, glucose homeostasis and gut motility. Therefore, taste genotypes resulting in functional receptor changes and altered receptor expression levels may be associated with metabolic conditions. IS and taste receptors may both interact with the gastrointestinal microbiome, and their interactions may potentially explain the relationship between IS use, obesity and metabolic outcomes. While these elements are often studied in isolation, the potential interactions remain unexplored. Here, the current evidence of the relationship between IS use, obesity and metabolic outcomes is presented, and the potential roles for interactions with taste receptors and the gastrointestinal microbiota in modulating these relationships are explored.
Highlights
Intense sweeteners (IS) are many times sweeter than sugar, and can be used in drastically smaller amounts, resulting in little to no energy contribution [1]
This study found that artificial sweetener use was associated with increased body weight over a 1-year period
This study demonstrates the ability of IS exposure to affect weight, food intake, blood glucose and glucagon-like peptide-1 (GLP-1) secretion in an animal model
Summary
Intense sweeteners (IS) are many times sweeter than sugar, and can be used in drastically smaller amounts, resulting in little to no energy contribution [1]. Bitter receptors are involved in protection from the ingestion of bacteria and potential toxins, which relates to their relatively large numbers These receptors are expressed throughout the gastrointestinal (GI) tract, where they are involved in the modulation of multiple metabolic processes, including glucose homeostasis, satiation and gut motility [16,17,18]. There is evidence to suggest that health issues like cardiovascular disease, metabolic syndrome and non-alcoholic fatty liver disease may be associated with IS use [8,25], potentially via the activation of gastrointestinal taste receptors and subsequent altered hormone secretion, and/or perturbations to the intestinal microflora. The current evidence of the relationship between IS use, obesity and metabolic outcomes is presented here, and the potential roles for interactions with taste receptors and the gastrointestinal microbiota in modulating these relationships are explored
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