It has been proven that β-glucan produced by Schizophyllum commune has beneficial effects on obesity, obesity-associated constipation, and colitis conditions; however, the protective effect of the compound on host at basal state is yet to be investigated. C57BL/6 J mice were fed with a normal diet (ND), normal diet supplemented with 3 g/kg (BG_low), and 5 g/kg (BG_high) of β-glucan (BG) for 12 weeks. Body weight, food and water intake and fecal status were monitored weekly. Intestine was stained by Periodic acid–Schiff (PAS) and Alcian Blue to evaluate the mucin layer thickness and goblet cell population. Morphological changes in internal organs and intestinal motility were also assessed, while serum biomarkers for liver injury and glucose level were analyzed. On the other hand, fecal microbiota and associated metabolic activities were also investigated. β-glucan bulked feces, decreased fecal moisture, and proliferated goblet cells resulted in a thickened lubricating mucin layer; however, the intestinal transit rate did not increase. The abundance of beneficial bacteria was increased while the harmful strains was decreased in a dose-dependent manner by the effect of β-glucan. Specific short chain fatty acid (SCFA)-producing strains, such as Roseburia, Ruminococcus, and Bifidobacteria, were selectively increased by β-glucan. In addition, consumption of β-glucan lowered level of obesity-associated biomarkers. Schizophyllum commune β-glucan showed an insignificant change in transit rate in healthy conditions when compared with obesity, despite similar effects on increasing mucus production and bulked feces. Nonetheless, the outcomes proposed protective effects against obesity, diabetes, inflammatory bowel diseases (IBD), and constipation, in which the modification of the gut microbiota by β-glucan is the largest contributor.

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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.

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