Sucralose Increased Susceptibility to Colitis in Rats

Wang, Xiuhong; Guo, Junyu; Liu, Yuanli; Yu, Hengyuan; Qin, Xiaofa

doi:10.1093/ibd/izy196

Cited by 19 publications

(19 citation statements)

References 4 publications

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“…On the other hand, it has been shown that sucralose promotes inflammation in a mouse model of human Crohn's disease-like ileitis as well as dysbiosis of the gut microbiota [34]. Furthermore, sucralose causes a decrease in the number of Firmicutes species [35].…”

Section: Sucralosementioning

confidence: 99%

Plausible Biological Interactions of Low- and Non-Calorie Sweeteners with the Intestinal Microbiota: An Update of Recent Studies

et al. 2020

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Sweeteners that are a hundred thousand times sweeter than sucrose are being consumed as sugar substitutes. The effects of sweeteners on gut microbiota composition have not been completely elucidated yet, and numerous gaps related to the effects of nonnutritive sweeteners (NNS) on health still remain. The NNS aspartame and acesulfame-K do not interact with the colonic microbiota, and, as a result, potentially expected shifts in the gut microbiota are relatively limited, although acesulfame-K intake increases Firmicutes and depletes Akkermansia muciniphila populations. On the other hand, saccharin and sucralose provoke changes in the gut microbiota populations, while no health effects, either positive or negative, have been described; hence, further studies are needed to clarify these observations. Steviol glycosides might directly interact with the intestinal microbiota and need bacteria for their metabolization, thus they could potentially alter the bacterial population. Finally, the effects of polyols, which are sugar alcohols that can reach the colonic microbiota, are not completely understood; polyols have some prebiotics properties, with laxative effects, especially in patients with inflammatory bowel syndrome. In this review, we aimed to update the current evidence about sweeteners’ effects on and their plausible biological interactions with the gut microbiota.

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Section: Sucralosementioning

confidence: 99%

Plausible Biological Interactions of Low- and Non-Calorie Sweeteners with the Intestinal Microbiota: An Update of Recent Studies

et al. 2020

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“…Papers published in recent years in Nature showed that food additives such as artificial sweeteners and emulsifiers increased the risk of diabetes, obesity, and colitis through their adverse impact on gut bacteria (20,21). Studies by us and others revealed that sucralose, the widely used artificial sweetener, increased the risk of IBD in animal models for both ulcerative colitis and Crohn's disease (22,23). Our study showed that sucralose exacerbated dextran sulfate sodium (DSS)induced colitis along with dysbiosis of gut microbiota, decrease in bacterial β-glucuronidase, increase in fecal digestive protease, and aggravated damage of the gut barrier and gut tissue.…”

Section: Introductionmentioning

confidence: 99%

Sucralose Promotes Colitis-Associated Colorectal Cancer Risk in a Murine Model Along With Changes in Microbiota

Liu

et al. 2020

Front. Oncol.

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Sucralose is a calorie-free high-intensity artificial sweetener that is widely used in thousands of foods and beverages all over the world. Although it was initially regarded as a safe, inert food additive, its adverse effect on gut microbiota and health has drawn more and more attention as evidence accumulates. Studies by us and others revealed that sucralose exacerbated gut damage and inflammation in animal models for inflammatory bowel disease (IBD), including those for both ulcerative colitis, and Crohn's disease. Our study demonstrated that sucralose greatly aggravated dextran sulfate sodium (DSS)-induced colitis along with causing changes in gut microbiota, the gut barrier and impaired inactivation of digestive proteases mediated by deconjugated bilirubin. It is welldocumented that IBD greatly increases the risk of colorectal cancer (CRC), the globally third-most-common cancer, which, like IBD, has a high rate in the developed countries. Azoxymethane (AOM)/DSS has been the most commonly used animal model for CRC. In this study, we further explored the effect of sucralose on tumorigenesis and the possible mechanism involved using the AOM/DSS mouse model. First, 1.5 mg/ml sucralose was included in the drinking water for 6 weeks to reach a relatively stable phase of impact on gut microbiota. Then, 10 mg/kg AOM was administered through intraperitoneal injection. Seven days later, 2.5% DSS was put in the drinking water for 5 days, followed by 2 weeks without DSS. The 5 days of DSS was then repeated, and the mice were sacrificed 6 weeks after AOM injection. The results showed that sucralose caused significant increases in the number and size of AOM/DSS-induced colorectal tumors along with changes in other parameters such as body and spleen weight, pathological scores, mortality, fecal β-glucuronidase and digestive proteases, gut barrier molecules, gut microbiota, inflammatory cytokines and pathways (TNFα, IL-1β, IL-6, IL-10, and TLR4/Myd88/NF-κB signaling), and STAT3/VEGF tumor-associated signaling pathway molecules. These results suggest that sucralose may increase tumorigenesis along with dysbiosis of gut microbiota, impaired inactivation of digestive protease, damage to the gut barrier, and exacerbated inflammation.

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“…Other sucralose-containing commercial products, such as Sweetal (sucralose + sorbitol), significantly elevated liver enzyme levels (ALT, AST) and kidney function enzymes (urea, creatinine) in Balb/c albino mice after 18 weeks (administered 5 h/day in drinking water; 5.2 mg/ml sucralose) (2). Similar in vivo pro-inflammatory effects [hepatic mediators (5), severity of chemically-induced colitis (6, 57)] following pure sucralose supplementation have also been reported (5,6,57).…”

Section: Artificial Sweeteners On Digestive Inflammation Outcomesmentioning

confidence: 62%

“…In another study, 6-week sucralose supplementation at the same dosage in C57BL/6 mice prior to colitis induction reduced the deactivation of digestive proteases mediated by deconjugated bilirubin (6). Other studies on rats have shown that sucralose or saccharin (6 weeks) significantly increased fecal chymotrypsin and trypsin, and decreased β-glucuronidase, an enzyme required for the deconjugation of conjugated bilirubin (57,126).…”

Section: Bile Acid Metabolismmentioning

confidence: 94%

“…Intriguingly, increases in body weight, not attributed to food intake, have been reported in mice administered with Splenda in "low" doses (100 mg/kg bw/day) but not "high" doses (300, 500, and 1,000 mg/kg) (56). Human, animal, and in vitro studies suggest that sucralose reduces bacterial growth (1,56,57), may selectively inhibit or promote bacterial growth (29), and promote intestinal dysbiosis (33,49), consistent with the observation that bacteria in a culture do not utilize sucralose as a carbon source (58,59). Sucralose may increase Escherichia coli antimicrobial resistance and mutation frequency to antimicrobials (60) and inhibit the bacterial physiology of differentiating filamentous cyanobacteria and polysaccharide sheath induction (61).…”

Section: Metabolism and Bacterial Utilization Of Artificial Sweetenersmentioning

confidence: 99%

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Artificial Sweeteners: History and New Concepts on Inflammation

2021

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Since the introduction of artificial sweeteners (AS) to the North American market in the 1950s, a growing number of epidemiological and animal studies have suggested that AS may induce changes in gut bacteria and gut wall immune reactivity, which could negatively affect individuals with or susceptible to chronic inflammatory conditions such as inflammatory bowel disease (IBD), a disorder that has been growing exponentially in westernized countries. This review summarizes the history of current FDA-approved AS and their chemical composition, metabolism, and bacterial utilization, and provides a scoping overview of the disease mechanisms associated with the induction or prevention of inflammation in IBD. We provide a general outlook on areas that have been both largely and scarcely studied, emerging concepts using silica, and describe the effects of AS on acute and chronic forms of intestinal inflammation.

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Sucralose Increased Susceptibility to Colitis in Rats

Cited by 19 publications

References 4 publications

Plausible Biological Interactions of Low- and Non-Calorie Sweeteners with the Intestinal Microbiota: An Update of Recent Studies

Plausible Biological Interactions of Low- and Non-Calorie Sweeteners with the Intestinal Microbiota: An Update of Recent Studies

Sucralose Promotes Colitis-Associated Colorectal Cancer Risk in a Murine Model Along With Changes in Microbiota

Artificial Sweeteners: History and New Concepts on Inflammation

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