Background: Huang-Lian-Jie-Du-Decoction (HLJDD), a prescription of traditional Chinese medicine, has been clinically used to treat diabetes for thousands of years and its mechanism was reported to be related to gut microbiota. However, no study has explored the effect of HLJDD on the gut microbiota in type 2 diabetes mellitus (T2DM) yet. Therefore, in this study, we investigated the modulation of gut microbiota induced by HLJDD treatment in T2DM in order to unveil the underlying mechanism.Methods: A combination of high-fat diet (HFD) and streptozotocin (STZ) was used to induce T2DM in rats. Bacterial communities in the fecal samples from the control group, the T2DM model group, and the HLJDD-treated T2DM group were analyzed by 16S gene sequencing, followed with a subset sample analyzed by shotgun sequencing.Results: The HLJDD treatment significantly ameliorated hyperglycemia and inflammation in T2DM rats. Additionally, our results indicated that HLJDD treatment could not only restore the gut dysbiosis in T2DM rats, which was proved by an increasing amount of short chain fatty acids (SCFAs)-producing and anti-inflammatory bacteria such as Parabacteroides, Blautia, and Akkermansia as well as a decreasing amount of conditioned pathogenic bacteria (e.g., Aerococcus, Staphylococcus, and Corynebacterium), but also modulate the dysregulated function of gut microbiome in T2DM rats, including an up-regulation in bile acid biosynthesis as well as a reduction in glycolysis/gluconeogenesis and nucleotide metabolism.Conclusion: HLJDD treatment could ameliorate hyperglycemia and restore the dysregulated microbiota structure and function to a normal condition mainly by increasing SCFAs-producing bacteria and reducing conditioned pathogenic bacteria in T2DM rats, which provides insights into the mechanism of HLJDD treatment for T2DM from the view of gut microbiota.

Background and Aim Inflammatory bowel disease results from a dysregulated immune response to intestinal microbial flora in individuals with genetic predisposition(s). This study aimed to determine the effects of compound polysaccharides (CP) containing yam polysaccharide and inulin on the rat model of colitis induced by 2,4,6‐trinitrobenzenesulfonic acid (TNBS) and to explain the mechanism in terms of gut microbiota composition and function. Methods Male SD rats were divided into three groups: the control group, the model group, and the CP group. Disease activity index, serum myeloperoxidase level, and the composition and function of gut microbiota were analyzed. Results The data in the study showed CP reduced inflammation in the rat model of colitis induced by TNBS and ameliorated the experimental colitis. The results also indicated that CP not only reversed TNBS‐induced gut dysbiosis‐indexed by increased short‐chain fatty acids (SCFAs)‐producing bacteria, lactic acid‐producing bacteria, and decreased Bacteroides, Proteobacteria as well as sulfate‐reducing bacteria, but also restored the dysregulated microbiota function of colitic rats into a normal condition, including an improvement on basic metabolism and a reduction on oxidative stress, cell motility, signal transduction, xenobiotics biodegradation, and metabolism as well as pathogenesis processes. Conclusions Compound polysaccharides ameliorated the experimental colitis of rats induced by TNBS by modulating the gut microbiota composition and function profiles, which makes it possible to be used as prebiotic agents to treat gut dysbiosis in colitis individuals.

GA enema can treat UC by influencing microbiota-mediated metabolism.

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Compound polysaccharides may be used as a functional food to modulate the composition and metabolism of gut microbiota, and to help maintain the health of the intestinal microecosystem.

Functional dyspepsia (FD) is one of the most prevalent functional gastrointestinal disorders (FGIDs).Accumulated evidence has shown that FD is a metabolic disease that might relate to gut microbiota, but the relationship between microbiome and the host metabolic changes is still uncertain. To clarify the host-microbiota co-metabolism disorders related to FD, an integrated approach combining 1 H NMRbased metabolomics profiles, polymerase chain reaction-denaturing gradient gel electrophoresis (PCR-DGGE) and 16S rRNA gene sequencing was used to investigate the relationship among FD, metabolism of gut microbiota and the host. 34 differential urinary metabolites and 19 differential fecal metabolites, which affected the metabolism of energy, amino acids, nucleotides and short chain fatty acids (SCFAs), were found to have associated with FD. Based on the receiver operating characteristic (ROC) analysis, 10 biomarkers were screened out as diagnostic markers of FD. Meanwhile, the concentrations of Flintibacter, Parasutterella, Eubacterium and Bacteroides significantly increased in the FD group, whereas Eisenbergiella, Butyrivibrio, Intestinimonas, Saccharofermentans, Acetivibrio, Lachnoanaerobaculum and Herbinix significantly decreased. Furthermore, the above altered microbiota revealed a strong correlation with the intermediate products of the tricarboxylic acid (TCA) cycle, amino acids and SCFAs. In our study, it suggested that the energy metabolism was mainly disturbed in FD rats. Our findings also demonstrated that FD might be the result of gut microbiota and metabolism disorders, which was potentially valuable to enrich our understanding of the pathogenesis of FD.