scholarly journals Gut Microbiota Prevents Sugar Alcohol-Induced Diarrhea

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 2029
Author(s):  
Kouya Hattori ◽  
Masahiro Akiyama ◽  
Natsumi Seki ◽  
Kyosuke Yakabe ◽  
Koji Hase ◽  
...  

While poorly-absorbed sugar alcohols such as sorbitol are widely used as sweeteners, they may induce diarrhea in some individuals. However, the factors which determine an individual’s susceptibility to sugar alcohol-induced diarrhea remain unknown. Here, we show that specific gut bacteria are involved in the suppression of sorbitol-induced diarrhea. Based on 16S rDNA analysis, the abundance of Enterobacteriaceae bacteria increased in response to sorbitol consumption. We found that Escherichia coli of the family Enterobacteriaceae degraded sorbitol and suppressed sorbitol-induced diarrhea. Finally, we showed that the metabolism of sorbitol by the E. coli sugar phosphotransferase system helped suppress sorbitol-induced diarrhea. Therefore, gut microbiota prevented sugar alcohol-induced diarrhea by degrading sorbitol in the gut. The identification of the gut bacteria which respond to and degrade sugar alcohols in the intestine has implications for microbiome science, processed food science, and public health.

2021 ◽  
pp. 1-17
Author(s):  
Axel Walter ◽  
Simon Friz ◽  
Christoph Mayer

<i>Escherichia coli</i> is unable to grow on polymeric and oligomeric chitin, but grows on chitin disaccharide (GlcNAc-GlcNAc; <i>N,N</i>′-diacetylchitobiose) and chitin trisaccharide (GlcNAc-GlcNAc-GlcNAc; <i>N,N</i>′<i>,N</i>′′-triacetylchitotriose) via expression of the <i>chb</i> operon (<i>chbBCARFG</i>). The phosphotransferase system (PTS) transporter ChbBCA facilitates transport of both saccharides across the inner membrane and their concomitant phosphorylation at the non-reducing end, intracellularly yielding GlcNAc 6-phosphate-GlcNAc (GlcNAc6P-GlcNAc) and GlcNAc6P-GlcNAc-GlcNAc, respectively. We revisited the intracellular catabolism of the PTS products, thereby correcting the reported functions of the 6-phospho-glycosidase ChbF, the monodeacetylase ChbG, and the transcriptional regulator ChbR. Intracellular accumulation of glucosamine 6P-GlcNAc (GlcN6P-GlcNAc) and GlcN6P-GlcNAc-GlcNAc in a <i>chbF</i> mutant unraveled a role for ChbG as a monodeacetylase that removes the <i>N-</i>acetyl group at the non-reducing end. Consequently, GlcN6P- but not GlcNAc6P-containing saccharides likely function as coactivators of ChbR. Furthermore, ChbF removed the GlcN6P from the non-reducing terminus of the former saccharides, thereby degrading the inducers of the <i>chb</i> operon and facilitating growth on the saccharides. Consequently, ChbF was unable to hydrolyze GlcNAc6P-residues from the non-reducing end, contrary to previous assumptions but in agreement with structural modeling data and with the unusual catalytic mechanism of the family 4 of glycosidases, to which ChbF belongs. We also refuted the assumption that ChiA is a bifunctional endochitinase/lysozyme ChiA, and show that it is unable to degrade peptidoglycans but acts as a bona fide chitinase in vitro and in vivo, enabling growth of <i>E. coli</i> on chitin oligosaccharides when ectopically expressed. Overall, this study revises our understanding of the chitin, chitin oligosaccharide, and chitin disaccharide metabolism of <i>E. coli</i>.


2021 ◽  
Vol 22 (10) ◽  
pp. 5228
Author(s):  
Aparna Shil ◽  
Havovi Chichger

Artificial sweeteners (AS) are synthetic sugar substitutes that are commonly consumed in the diet. Recent studies have indicated considerable health risks which links the consumption of AS with metabolic derangements and gut microbiota perturbations. Despite these studies, there is still limited data on how AS impacts the commensal microbiota to cause pathogenicity. The present study sought to investigate the role of commonly consumed AS on gut bacterial pathogenicity and gut epithelium-microbiota interactions, using models of microbiota (Escherichia coli NCTC10418 and Enterococcus faecalis ATCC19433) and the intestinal epithelium (Caco-2 cells). Model gut bacteria were exposed to different concentrations of the AS saccharin, sucralose, and aspartame, and their pathogenicity and changes in interactions with Caco-2 cells were measured using in vitro studies. Findings show that sweeteners differentially increase the ability of bacteria to form a biofilm. Co-culture with human intestinal epithelial cells shows an increase in the ability of model gut bacteria to adhere to, invade and kill the host epithelium. The pan-sweet taste inhibitor, zinc sulphate, effectively blocked these negative impacts. Since AS consumption in the diet continues to increase, understanding how this food additive affects gut microbiota and how these damaging effects can be ameliorated is vital.


2020 ◽  
Vol 15 (1) ◽  
pp. 52-56
Author(s):  
Sri Winarti ◽  
Agung Pasetyo

The consumption of prebiotics is known to affect the balance of gut microbiota. The purpose of this study was to explore how a galactomannan-rich effervescent drink can affect the population of Lactobacillus, Bifidobacterium, E. coli, and the concentration of short-chain fatty acids in the cecum of rats. Twenty-eight male Wistar rats (aged 2 months) were divided equally into 7 groups and treated orally each day for 15 days with 2 mL effervescent drinks with increasing levels of prebiotic galactomannan. The dosage of 500 mg galactomannan increased the growth of Lactobacillus spp. and Bifidobacterium spp. with inhibition of the growth of E.coli with increased formation of short-chain fatty acids such as acetate, propionate, and butyrate in the cecum of rats.


2019 ◽  
Vol 14 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Banin Maghfirotin Marta ◽  
Utami Tyas ◽  
Cahyanto Muhammad Nur ◽  
Widada Jaka ◽  
Rahayu Endang Sutriswati

Consumption of probiotics is known to influence the gut microbiota. The aim of this study was to assess the effect of probiotic powder containing Lactobacillus plantarum Dad-13 on bacterial composition in the gut by examining fecal samples of school-age children in Yogyakarta, Indonesia. This is a randomized, double-blind, placebo-controlled study. A total of 40 healthy subjects were recruited for this study and were divided into two groups: placebo group and probiotic group. The placebo group consumed skim milk and the probiotic group consumed probiotic powder containing L. plantarum Dad-13 (2 × 109 CFU/g) for 65 days. The results showed that placebo intake had no significant effect on gut microbiota; however, probiotic caused a significant increase in L. plantarum and Lactobacillus population, while decreasing the population of E. coli and non-E. coli coliform bacteria by 55% and 75%, respectively and Bifidobacteria count did not change significantly. The study concluded that consumption of probiotic powder L. plantarum Dad-13 could increase propionic acid thereby decreasing the gut pH which has an effect on the microbial population.


2005 ◽  
Vol 32 (7) ◽  
pp. 643 ◽  
Author(s):  
Xinli Li ◽  
Tamás Borsics ◽  
H. Michael Harrington ◽  
David A. Christopher

We have isolated and characterised AtCNGC10, one of the 20 members of the family of cyclic nucleotide (CN)-gated and calmodulin (CaM)-regulated channels (CNGCs) from Arabidopsis thaliana (L.) Heynh. AtCNGC10 bound CaM in a C-terminal subregion that contains a basic amphiphillic structure characteristic of CaM-binding proteins and that also overlaps with the predicted CN-binding domain. AtCNGC10 is insensitive to the broad-range K+ channel blocker, tetraethylammonium, and lacks a typical K+-signature motif. However, AtCNGC10 complemented K+ channel uptake mutants of Escherichia coli (LB650), yeast (Saccharomyces cerevisiae CY162) and Arabidopsis (akt1-1). Sense 35S-AtCNGC10 transformed into the Arabidopsis akt1-1 mutant, grew 1.7-fold better on K+-limited medium relative to the vector control. Coexpression of CaM and AtCNGC10 in E. coli showed that Ca2+ / CaM inhibited cell growth by 40%, while cGMP reversed the inhibition by Ca2+ / CaM, in a AtCNGC10-dependent manner. AtCNGC10 did not confer tolerance to Cs+ in E. coli, however, it confers tolerance to toxic levels of Na+ and Cs+ in the yeast K+ uptake mutant grown on low K+ medium. Antisense AtCNGC10 plants had 50% less potassium than wild type Columbia. Taken together, the studies from three evolutionarily diverse species demonstrated a role for the CaM-binding channel, AtCNGC10, in mediating the uptake of K+ in plants.


2021 ◽  
Vol 28 ◽  
Author(s):  
Divakar Sharma ◽  
Manisha Aswal ◽  
Nayeem Ahmad ◽  
Manish Kumar ◽  
Asad U Khan

Background: Antimicrobial resistance is a worldwide problem after the emergence of colistin resistance since it was the last option left to treat carbapenemase-resistant bacterial infections. The mcr gene and its variants are one of the causes for colistin resistance. Besides mcr genes, some other intrinsic genes are also involved in colistin resistance but still need to be explored. Objective: The aim of this study was to investigate differential proteins expression of colistin-resistant E. coli clinical isolate and to understand their interactive partners as future drug targets. Methods: In this study, we have employed the whole proteome analysis through LC-MS/MS. The advance proteomics tools were used to find differentially expressed proteins in the colistin-resistant Escherichia coli clinical isolate compared to susceptible isolate. Gene ontology and STRING were used for functional annotation and protein-protein interaction networks, respectively. Results: LC-MS/MS analysis showed overexpression of 47 proteins and underexpression of 74 proteins in colistin-resistant E. coli. These proteins belong to DNA replication, transcription and translational process; defense and stress related proteins; proteins of phosphoenol pyruvate phosphotransferase system (PTS) and sugar metabolism. Functional annotation and protein-protein interaction showed translational and cellular metabolic process, sugar metabolism and metabolite interconversion. Conclusion: We conclude that these protein targets and their pathways might be used to develop novel therapeutics against colistin-resistant infections. These proteins could unveil the mechanism of colistin resistance.


2017 ◽  
Vol 23 (1) ◽  
pp. 76-83
Author(s):  
Wei Yang ◽  
Bin Wei ◽  
Ru Yan

Amoxapine has been demonstrated to be a potent inhibitor of Escherichia coli β-glucuronidase. This study aims to explore the factors causing unsatisfactory efficacy of amoxapine in alleviating CPT-11–induced gastrointestinal toxicity in mice and to predict the outcomes in humans. Amoxapine (100 µM) exhibited poor and varied inhibition on β-glucuronidase activity in gut microbiota from 10 healthy individuals and their pool (pool, 11.9%; individuals, 3.6%−54.4%) with IC50 >100 µM and potent inhibition toward E. coli β-glucuronidase (IC50 = 0.34 µM). p-Nitrophenol formation from p-nitrophenyl-β-D-glucuronide by pooled and individual gut microbiota fitted classical Michaelis-Menten kinetics, showing similar affinity (Km = 113–189 µM) but varied catalytic capability (Vmax = 53–556 nmol/h/mg). Interestingly, amoxapine showed distinct inhibitory effects (8.7%–100%) toward β-glucuronidases of 13 bacterial isolates (including four Enterococcus, three Streptococcus, two Escherichia, and two Staphylococcus strains; gus genes belonging to OTU1, 2 or 21) regardless of their genetic similarity or bacterial origin. In addition, amoxapine inhibited the growth of pooled and individual gut microbiota at a high concentration (6.3%–30.8%, 200 µM). Taken together, these findings partly explain the unsatisfactory efficacy of amoxapine in alleviating CPT-11–induced toxicity and predict a poor outcome of β-glucuronidase inhibition in humans, highlighting the necessity of using a human gut microbiota community for drug screening.


2020 ◽  
Vol 20 (1) ◽  
pp. 179-189
Author(s):  
Leszek Tymczyna ◽  
Beata Trawińska ◽  
Marta Kowaleczko ◽  
Anna Chmielowiec-Korzeniowska ◽  
Jerzy Lechowski

AbstractThe aim of the study was to assess the gut microbiota and selected haematological and biochemical blood parameters of weaned piglets following dietary supplementation with a probiotic and vitamin C. the piglets were divided into a control group (group C) and an experimental group (group E), with 30 piglets in each group. All animals received the same feed ad libitum. The animals in the control group (group C) received feed with no added probiotic and vitamin C. the piglets in the experimental group (group E) were given a supplement containing a probiotic (Bacillus cereus 1×109 CFU/kg) in the amount of 1.5 g/piglet/day and vitamin c in the amount of 300 mg/piglet/day. The supplement was administered for 28 days. The total numbers of bacteria of the family Enterobacteriaceae and of the genus Lactobacillus were determined in faeces. The erythrocyte count, haemoglobin level, haematocrit, leukocyte count, and percentages of neutrophils and lymphocytes were determined in the blood. The biochemical analysis concerned the concentration of triacylglycerols, total cholesterol, and LDL and HDL cholesterol. In group E a significant decrease (P<0.01) in the total number of Enterobacteriaceae bacteria was observed in the faeces of the piglets, accompanied by an increase in the number of lactobacilli relative to group C. E. coli was found to predominate over other microorganisms. Salmonella choleraesuis bacteria were present in the faeces of both groups before administration of the supplement, but were not found after its use. The supplement with probiotic and vitamin C caused a significant increase in the erythrocyte, haemoglobin and haematocrit levels in the blood of the piglets and a significant decrease in the concentration of triacylglycerols, total cholesterol and LDL cholesterol.


Author(s):  
Shiju Xiao ◽  
Guangzhong Zhang ◽  
Chunyan Jiang ◽  
Xin Liu ◽  
Xiaoxu Wang ◽  
...  

BackgroundIncreasing evidence has shown that alterations in the intestinal microbiota play an important role in the pathogenesis of psoriasis. The existing relevant studies focus on 16S rRNA gene sequencing, but in-depth research on gene functions and comprehensive identification of microbiota is lacking.ObjectivesTo comprehensively identify characteristic gut microbial compositions, genetic functions and relative metabolites of patients with psoriasis and to reveal the potential pathogenesis of psoriasis.MethodsDNA was extracted from the faecal microbiota of 30 psoriatic patients and 15 healthy subjects, and metagenomics sequencing and bioinformatic analyses were performed. The Kyoto Encyclopedia of Genes and Genomes (KEGG) database, cluster of orthologous groups (COG) annotations, and metabolic analyses were used to indicate relative target genes and pathways to reveal the pathogenesis of psoriasis.ResultsCompared with healthy individuals, the gut microbiota of psoriasis patients displayed an alteration in microbial taxa distribution, but no significant difference in microbial diversity. A distinct gut microbial composition in patients with psoriasis was observed, with an increased abundance of the phyla Firmicutes, Actinobacteria and Verrucomicrobia and genera Faecalibacterium, Bacteroides, Bifidobacterium, Megamonas and Roseburia and a decreased abundance of the phyla Bacteroidetes, Euryarchaeota and Proteobacteria and genera Prevotella, Alistipes, and Eubacterium. A total of 134 COGs were predicted with functional analysis, and 15 KEGG pathways, including lipopolysaccharide (LPS) biosynthesis, WNT signaling, apoptosis, bacterial secretion system, and phosphotransferase system, were significantly enriched in psoriasis patients. Five metabolites, hydrogen sulfide (H2S), isovalerate, isobutyrate, hyaluronan and hemicellulose, were significantly dysregulated in the psoriatic cohort. The dysbiosis of gut microbiota, enriched pathways and dysregulated metabolites are relevant to immune and inflammatory response, apoptosis, the vascular endothelial growth factor (VEGF) signaling pathway, gut-brain axis and brain-skin axis that play important roles in the pathogenesis of psoriasis.ConclusionsA clear dysbiosis was displayed in the gut microbiota profile, genetic functions and relative metabolites of psoriasis patients. This study is beneficial for further understanding the inflammatory pathogenesis of psoriasis and could be used to develop microbiome-based predictions and therapeutic approaches.


2011 ◽  
Vol 16 (31) ◽  
Author(s):  
A M Hauri ◽  
U Götsch ◽  
I Strotmann ◽  
J Krahn ◽  
G Bettge-Weller ◽  
...  

During the recent outbreak of Shiga toxin-producing Escherichia coli (STEC) O104:H4 in Germany most cases notified in the State of Hesse (6 million inhabitants) were linked to satellite clusters or had travelled to the outbreak area in northern Germany. Intensified surveillance was introduced to rapidly identify cases not linked to known clusters or cases and thus to obtain timely information on possible further contaminated vehicles distributed in Hesse, as well to describe the risk of secondary transmission among known cases. As of 2 August 2011*, 56 cases of haemolytic uraemic syndrome (HUS) including two fatal cases, and 124 cases of STEC gastroenteritis meeting the national case definitions have been reported in Hesse. Among the 55 HUS and 81 STEC gastroenteritis cases that met the outbreak case definition, one HUS case and eight STEC gastroenteritis cases may have acquired their infection through secondary transmission. They include six possible transmissions within the family, two possible nosocomial and one possible laboratory transmission. Our results do not suggest an increased transmissibility of the outbreak strain compared to what is already known about E. coli O157 and other STEC serotypes.


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