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Review
. 2023 Dec 20;14(1):10.
doi: 10.3390/life14010010.

The Effects of Artificial Sweeteners on Intestinal Nutrient-Sensing Receptors: Dr. Jekyll or Mr. Hyde?

Affiliations
Review

The Effects of Artificial Sweeteners on Intestinal Nutrient-Sensing Receptors: Dr. Jekyll or Mr. Hyde?

Edit Posta et al. Life (Basel). .

Abstract

The consumption of artificial and low-calorie sweeteners (ASs, LCSs) is an important component of the Western diet. ASs play a role in the pathogenesis of metabolic syndrome, dysbiosis, inflammatory bowel diseases (IBDs), and various inflammatory conditions. Intestinal nutrient-sensing receptors act as a crosstalk between dietary components, the gut microbiota, and the regulation of immune, endocrinological, and neurological responses. This narrative review aimed to summarize the possible effects of ASs and LCSs on intestinal nutrient-sensing receptors and their related functions. Based on the findings of various studies, long-term AS consumption has effects on the gut microbiota and intestinal nutrient-sensing receptors in modulating incretin hormones, antimicrobial peptides, and cytokine secretion. These effects contribute to the regulation of glucose metabolism, ion transport, gut permeability, and inflammation and modulate the gut-brain, and gut-kidney axes. Based on the conflicting findings of several in vitro, in vivo, and randomized and controlled studies, artificial sweeteners may have a role in the pathogenesis of IBDs, functional bowel diseases, metabolic syndrome, and cancers via the modulation of nutrient-sensing receptors. Further studies are needed to explore the exact mechanisms underlying their effects to decide the risk/benefit ratio of sugar intake reduction via AS and LCS consumption.

Keywords: IBD; artificial sweeteners; gastrointestinal; incretin; microbiome; nutrient-sensing receptor.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic signaling pathway of nutrient sensing, G−protein coupled receptors. Ligands (grey triangle) bind to nutrient−sensing receptors and coupled G−proteins to activate PLCβ2. IP3 is activated by PLCβ2 and binds to IP3 receptors to cause intracellular Ca2+ release (red arrow), which drives the opening of the TRPM5 cation channel and Na+ influx (dark yellow arrow). These changes lead to increased incretin and cytokine secretion by enteroendocrine cells. These molecules could have an influence on the gene and protein expressions, various cytokine and hormone secretion, and modified cell proliferation of target cells.
Figure 2
Figure 2
Schematic figure about our review stages.

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