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This review discusses the effects of short-chain fatty acids (SCFAs) and trimethylamine-N-oxide (TMAO) on metabolic diseases, focusing on non-alcoholic fatty liver disease (NAFLD) and cardiovascular disease, and suggests dietary modification as a promising therapeutic strategy. SCFAs, a product of fiber fermentation by microbiota, foster intestinal cell populations, upregulate mucin production, and secure the gut barrier. In contrast, TMAO, a microbiota-produced metabolite from choline, phosphatidylcholine, and l-carnitine, induces atherosclerosis by decreasing cholesterol clearance. An unmanageable abundance of TMAO is potentially harmful to patients with NAFLD owing to its ability to regulate the synthesis and transport of bile acids. The production of SCFAs and TMAO is strongly dependent on the microbial community; therefore, dietary modifications, such as reduction in meat intake, and prebiotic and probiotic consumption that can shape the gut microbiome are considered as promissing therapeutic approaches. This review focuses on well-known prebiotics, such as inulin, fructooligosaccharides, and β-glucan, and probiotics, such as VSL#3 mixture, Lactobacillus rhamnosus GG, Bifidobacterium, and Lactobacillus spp. These additives facilitate microbiota modification, gut homeostasis, intestinal barrier maintenance, and promotion of cholesterol excretion, which may protect the liver from steatosis, inflammation, and fibrosis. Controversial results from previous studies suggest that personalized approaches should be used for dietary modifications. [ABSTRACT FROM AUTHOR]

Purpose: Probiotics and prebiotics are commonly used to improve the gut microbiota. Since prebiotics can support the growth of probiotics, co-administration of these is called synbiotics. It has been demonstrated that obesity-induced gut dysbiosis can worsen inflammatory bowel disease symptoms. This study evaluated how modulation of gut microbiota with Schizophyllum commune-derived β-glucan (BG), probiotics (PRO), and synbiotics containing both BG and PRO (SYN) could improve the symptoms of obesity-associated colitis and hepatic manifestation. Methods: Mice were fed a normal diet (ND), high-fat diet (HFD), and HFD with different additives (BG, PRO, and SYN) for 12 weeks, followed by 5 days of colitis induction. Mice were sacrificed before and after colitis induction. During the experiment, body weight, food and water consumption, and rectal bleeding were monitored. Proteins from the colon were subjected to western blotting, and serum biomarkers such as alanine transaminase, alkaline phosphatase, triglycerides, and total cholesterol were analyzed. Colon and liver samples were sectioned for histological analysis. The fecal microbiota was analyzed based on partial 16S rRNA gene sequences. Results: Although BG and PRO secured intestinal tight junctions, these two treatments did not modulate inflammatory cell infiltration and inflammatory markers (i.e., IL-6 and TNF-α). In contrast, SYN demonstrated stronger and broader effects in reducing colonic inflammation. While BG treatment increased the abundance of indigenous Lactobacillus, PRO treatment decreased bacterial diversity by suppressing the growth of several species of bacteria. SYN treatment groups, however, supported the growth of both indigenous and supplemented bacteria while maintaining bacterial diversity. Conclusion: Obesity-associated colitis can be improved by modulating gut bacteria with β-glucan and probiotics. The co-administration of both outperformed β-glucan and probiotic treatment alone by fostering both indigenous and supplemented probiotic strains. [ABSTRACT FROM AUTHOR]

Synbiotics synergistically favors beneficial effects of prebiotics and probiotics towards host metabolic health by modulating gut ecosystem. In this study, we sought to examine the effects of prebiotics (Schizophyllum commune derived β-(1,3/1,6)-glucan), probiotics (concoction made of eight different bacterial strains) and synbiotics (prebiotics + probiotics) on gut microbiota and its associated metabolic functions through 16S rRNA gene sequences analysis. Results showed that probiotics strains used in this study were detected more in the synbiotic and probiotic treatments, while prebiotic dietary intervention increased the total bacterial abundance and metabolisms related to host immune strengthening. Probiotics and synbiotics dietary interventions enhanced similar metabolisms relating to butanediol and s-adenosyl-l-methionine biosynthesis. Probiotics treatment also showed depleted metabolic activities related to SCFA productions, that were not depleted in prebiotics treatment. With varying differential abundance patterns and metabolic activities across the treatments, our results suggest that synbiotic treatment provide more beneficial effects over probiotics and prebiotics. [ABSTRACT FROM AUTHOR]

Purpose: Western diet, rich in carbohydrates and fat, is said to be a major factor underlying metabolic syndrome. Interventions with prebiotics, the key modulators of the gut microbiota, have paramount impact on host-associated metabolic disorders. Herein, we investigated the effect of fungus-derived (1,3)/(1,6)-β-glucan, a highly soluble dietary fiber, on high-fat diet (HFD)-induced metabolic distress. Methods: Male C57BL/6 J mice were fed with different diet groups (n = 11): control diet, HFD, 3 g/kg or 5 g/kg of β-glucan-incorporated HFD. At the end of experimental study period (12th week), body weight, feces weight and fecal moisture content were observed. Further, colonic motility was measured using activated charcoal meal study. Proteins extracted from liver and intestine tissues were subjected to western blot technique. Paraffin-embedded intestinal tissues were sectioned for histochemical [Periodic acid-Schiff (PAS) and Alcian blue (AB) staining] analysis. Fecal microbiota analysis was performed using MOTHUR bioinformatic software. Results: β-glucan consumption exhibited anti-obesity property in mice groups fed with HFD. In addition, β-glucan ameliorated HFD-induced hepatic stress, colonic motility and intestinal atrophy (reduction in colon length, goblet cells, and mucosal layer thickness). Further, β-glucan incorporation shifted bacterial community by increasing butyrate-producing bacteria such as Anaerostipes, Coprobacillus, and Roseburia and decreasing reportedly obesity-associated bacteria such as Parabacteroides and Lactococcus. Conclusion: Altogether, the outcomes of this present pre-clinical animal study show β-glucan to be a promising therapeutic candidate in the treatment of HFD-induced metabolic distress. Further comprehensive research has to be conducted to brace its clinical relevance, reproducibility and efficacy for aiding human health. [ABSTRACT FROM AUTHOR]

A correction to this paper has been published: https://doi.org/10.1007/s00394-021-02537-9 [ABSTRACT FROM AUTHOR]