Hypoglycemic activity of the Baker's yeast β-glucan in obese/type 2 diabetic mice and the underlying mechanism

cope 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.