Non-caloric artificial sweeteners (NASs) provide sweet tastes to food without adding calories or glucose. NASs can be used as alternative sweeteners for controlling blood glucose levels and weight gain. Although the consumption of NASs has increased over the past decade in Japan and other countries, whether these sweeteners affect the composition of the gut microbiome is unclear. In the present study, we examined the effects of sucralose or acesulfame-K ingestion (at most the maximum acceptable daily intake (ADI) levels, 15 mg/kg body weight) on the gut microbiome in mice. Consumption of sucralose, but not acesulfame-K, for 8 weeks reduced the relative amount of Clostridium cluster XIVa in feces. Meanwhile, sucralose and acesulfame-K did not increase food intake, body weight gain or liver weight, or fat in the epididymis or cecum. Only sucralose intake increased the concentration of hepatic cholesterol and cholic acid. Moreover, the relative concentration of butyrate and the ratio of secondary/primary bile acids in luminal metabolites increased with sucralose consumption in a dose-dependent manner. These results suggest that daily intake of maximum ADI levels of sucralose, but not acesulfame-K, affected the relative amount of the Clostridium cluster XIVa in fecal microbiome and cholesterol bile acid metabolism in mice.

The gut microbiota produce hundreds of bioactive compounds, including B‐vitamins, which play significant physiological roles in hosts by supporting the fitness of symbiotic species and suppressing the growth of competitive species. B‐vitamins are also essential to the host and certain gut bacterium. Although dietary B‐vitamins are mainly absorbed from the small intestine, excess B‐vitamins unable to be absorbed in the small intestine are supplied to the distal gut. In addition, B‐vitamins are supplied from biosynthesis by distal gut microbiota. B‐vitamins in the distal colon may perform many important functions in the body. They act as 1) nutrients for a host and their microbiota, 2) regulators of immune cell activity, 3) mediators of drug efficacy, 4) supporters of survival, or the fitness of certain bacterium, 5) suppressors of colonization by pathogenic bacteria, and 6) modulators of colitis. Insights into basic biophysical principles, including the bioavailability of B‐vitamins and their derivatives in the distal gut are still not fully elucidated. Here, the function of single B‐vitamin in the distal gut including their roles in relation to bacteria are briefly reviewed. The prospect of extending analytical methods to better understand the role of B‐vitamins in the gut is also explored.

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Many species of bacteria induce secretory and inflammatory diarrhea (1). The increased intestinal fluid secretion in diarrhea appears to result from the active secretion of chloride (1-3), a principal anion, but the way in which diarrhea is caused by individual bacterial infections has not been completely elucidated. Vibrio parahaemolyticus is a Gram-negative halophilic bacterium that naturally occurs in marine and estuarine environments (4). It is a human pathogen that causes food-borne acute gastroenteritis, often associated with the consumption of raw or undercooked seafood (5, 6). Clinical symptoms of V. parahaemolyticus infections include watery diarrhea, abdominal cramps, nausea, vomiting, headaches, fever, and chills (7,8). THERMOSTABLE DIRECT HEMOLYSIN (TDH) AND TDH-RELATED HEMOLYSIN (TRH)The majority of V. parahaemolyticus clinical isolates from patients with diarrhea has produced TDH and/or TRH, which are encoded by the tdh and trh genes, respectively (9). Strong associations have been found between gastroenteritis and these two proteins (10, 11). Therefore, TDH and TRH are regarded as major virulence factors of V. parahaemolyticus.V. parahaemolyticus TDH (Vp-TDH) is a proteinaceous toxin composed of 165 amino acids with one disulfide bond near the carboxyl terminus (12). The protein is a dimer, which lacks lipid and carbohydrate moieties, and has a molecular weight of c. 42 kDa by gel filtration and 21 kDa by denaturing sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) (13,14). Vp-TDH exhibits β-hemolytic activity on Wagatsuma medium, which has been termed the Kanagawa phenomenon (KP). Purified Vp-TDH is heat-stable, even at 100! !for REVIEW Diarrhea induced by infection of Vibrio parahaemolyticusTakaaki Shimohata and Akira Takahashi Department of Preventive Environment and Nutrition, Institute of Health Biosciences, the University of Tokushima Graduate School, Tokushima, JapanAbstract : Vibrio parahaemolyticus is a human pathogen that naturally inhabits marine and estuarine environments. Infection with V. parahaemolyticus is often associated with the consumption of raw or undercooked seafood, causing gastroenteritis with watery diarrhea. The presence of two type III secretion system (T3SS) proteins, thermostable direct hemolysin (TDH) and TDH-related hemolysin (TRH), has been closely associated with the severity of diarrheal illness. TDH and TRH have various biological activities including hemolytic activity, cardiotoxicity, and enterotoxicity. T3SS1 is involved in cytotoxicity to host cells and orchestrates a multifaceted host cell infection by induction of autophagy, cell rounding, and cell lysis. T3SS2 is thought to be related to the enterotoxicity of V. parahaemolyticus. The activities of inducing diarrhea of each of the virulence factors were summarized in this review.

The sugar alcohol xylitol inhibits the growth of some bacterial species including Streptococcus mutans. It is used as a food additive to prevent caries. We previously showed that 1.5–4.0 g/kg body weight/day xylitol as part of a high-fat diet (HFD) improved lipid metabolism in rats. However, the effects of lower daily doses of dietary xylitol on gut microbiota and lipid metabolism are unclear. We examined the effect of 40 and 200 mg/kg body weight/day xylitol intake on gut microbiota and lipid metabolism in mice. Bacterial compositions were characterized by denaturing gradient gel electrophoresis and targeted real-time PCR. Luminal metabolites were determined by capillary electrophoresis electrospray ionization time-of-flight mass spectrometry. Plasma lipid parameters and glucose tolerance were examined. Dietary supplementation with low- or medium-dose xylitol (40 or 194 mg/kg body weight/day, respectively) significantly altered the fecal microbiota composition in mice. Relative to mice not fed xylitol, the addition of medium-dose xylitol to a regular and HFD in experimental mice reduced the abundance of fecal Bacteroidetes phylum and the genus Barnesiella, whereas the abundance of Firmicutes phylum and the genus Prevotella was increased in mice fed an HFD with medium-dose dietary xylitol. Body composition, hepatic and serum lipid parameters, oral glucose tolerance, and luminal metabolites were unaffected by xylitol consumption. In mice, 40 and 194 mg/kg body weight/day xylitol in the diet induced gradual changes in gut microbiota but not in lipid metabolism.