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Faculty Advisor

Phillip E. Funk (DePaul), and D. Eric Walters (RFU)

Abstract

Rising rates of obesity and type 2 diabetes have prompted the usage and recommendation of nonnutritive sweeteners (NNS) as harmless sugar substitutes in attempts to decrease caloric intake. Contrary to the common belief that NNS remain physiologically inert post-consumption, evidence highlights their ability to alter metabolic processes via interactions in the gastrointestinal tract. An extensive review was conducted on the potential NNS-induced metabolic deviances by way of two non-mutually exclusive mechanisms. One possible mechanism involves their ability (or inability) to induce the secretion of GLP-1, a hormone produced in the gut that promotes satiety and accelerates glucose-dependent insulin secretion by interacting with sweet-taste receptors in the small intestine. Though NNS (sucralose, Ace K, and Rebaudioside A) show a high rate of GLP-1 secretion during in vitro studies, there are many discrepancies in results from human in vivo studies. A second mechanism proposes that NNS alter the composition of the gut microbiota, a vast community of microorganisms responsible for digesting food, releasing metabolites, and synthesizing vitamins. Differing forms of dysbiosis, alterations in bacterial composition, are observed, including an increased ratio of Firmicutes to Bacteroidetes and an increase in Lactobacilli spp. in exclusive studies, upon NNS exposure. Few experiments assessing NNS impact on the gut microbiota have been conducted with human subjects. Further investigations, specific to human subjects, should be explored in order to assess the true extent to which NNS impact incretin secretion and alterations in the gut microbiota.

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