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

Scope: beta-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 andmechanisms. In this study, a pure beta-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 beta-glucan (BYGlc) was a linear beta-(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.