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Scope: The prevalence of obesity and related disorders has vastly increased throughout the world and prevention of such circumstances thus represents a major challenge. Here, it has been shown that one protein-bound β-glucan (PBG) from the edible mushroom Coriolus versicolor can be a potent anti-obesity component., Methods and Results: PBG can reduce obesity and metabolic inflammation in mice fed with a high-fat diet (HFD). Gut microbiota analysis reveals that PBG markedly increases the abundance of Akkermansia muciniphila, although it does not rescue HFD-induced change in the Firmicutes to Bacteroidetes ratio. It appears that PBG alters host physiology and creates an intestinal microenvironment favorable for A. muciniphila colonization. Fecal transplants from PBG-treated animals in part reduce obesity in recipient HFD-fed mice. Further, PBG is shown to upregulate expression of a set of genes related to host metabolism in microbiota-depleted mice., Conclusion: The data highlight that PBG may exert its anti-obesity effects through a mirobiota-dependent (richness of specific microbiota) and -independent (modulation of host metabolism) manner. The fact that C. versicolor PBGs are approved oral immune boosters in cancers and chronic hepatitis with well-established safety profiles may accelerate PBG as a novel use for obesity treatment., (© 2019 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Bacteriostatic properties of a potential anti-obesity agent cinnamaldehyde (CMN) may present untoward effects on the resident gut microbiota. Here, we evaluated whether the combination of Isomalto-oligosaccharides (IMOs) with CMN prevents unwanted effects of CMN on gut microbiota and associated metabolic outcomes in HFD-fed mice. Male Swiss albino mice divided into four groups (n = 10), were fed on normal chow, or HFD (58% fat kcal), HFD + CMN (10 mg kg -1 ) and HFD + CMN (10 mg kg -1 ) + IMOs (1 g kg -1 ) for 12 weeks. Effects on HFD-induced biochemical, histological, inflammatory and genomic changes in the gastrointestinal tract, liver, and visceral white adipose tissue were studied. Cosupplementation of CMN with IMOs potentiates its preventive action against HFD-induced increase in serum LPS and abundances of selected LPS producing bacteria (Enterobacteriaceae, Escherichia Coli, Cronobacter sp, Citrobacter sp., Klebsiella sp., Salmonella sp.). CMN and IMOs co-administration prevented HFD-induced decrease in selected beneficial gut bacterial abundances (Bifidobacteria, Roseburia sp., Akkermansia muciniphila, Feacalibacterium sp.). CMN's effects against HFD-induced increase in gut permeability, histological and inflammatory changes in the colon were further augmented by cosupplementation of IMOs. Similar effects were observed in hepatic inflammatory markers. Cosupplementation of CMN with IMOs and CMN alone administration prevented HFD-induced changes in peripheral hormones and lipid metabolism-related parameters. This study provides evidence that coadministration of IMOs with CMN potentiates its anti-obesity effect and limits the side effects of CMN on gastrointestinal flora. Further, this study gives us important direction for the development of a concept-based novel class of functional foods/nutraceuticals for improved metabolic health. © BioFactors, 43(6):821-835, 2017., (© 2017 International Union of Biochemistry and Molecular Biology.)

Scope: β-Glucans have been shown to reduce the risk of obesity and diabetes. However, they often contain diverse polysaccharides and other ingredients, leading to elusive experimental data and mechanisms. In this study, a pure β-glucan was obtained from the crude Baker's yeast polysaccharides for investigating its effect on the metabolic disorders in high-fat diet induced obese (DIO)/type 2 diabetic (T2D) mice and the underlying mechanism., Methods and Results: The Fourier transform infrared spectroscopy and nuclear magnetic resonance spectroscopy data indicated that the pure β-glucan (BYGlc) was a linear β-(1→3)-glucan. It was first found that the oral administration of BYGlc into T2D and DIO mice significantly downregulated the blood glucose through suppressing sodium-glucose transporter-1 expression in intestinal mucosa. Meanwhile, BYGlc promoted glycogen synthesis and inhibited fat accumulation in liver, and depressed macrophage infiltration and pro-inflammatory cytokines production measured by histochemistry/immunohistochemistry and ELISA. Additionally, BYGlc remarkably decreased Firmicutes population and increased the proportion of Akkermansia by 16S rDNA analysis., Conclusion: BYGlc showed hypoglycemic activity accompanied by promotion of metabolism and inhibition of inflammation in T2D/DIO mice model. The hypoglycemic mechanisms were first declared to be through suppressing sodium-glucose transporter-1 expression and possibly associated with the altered gut microbiota., (© 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)