Premium
Hypoglycemic activity of the Baker's yeast β‐glucan in obese/type 2 diabetic mice and the underlying mechanism
Author(s) -
Cao Yan,
Zou Siwei,
Xu Hui,
Li Mengxia,
Tong Zan,
Xu Min,
Xu Xiaojuan
Publication year - 2016
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201600032
Subject(s) - glucan , glycogen , gut flora , medicine , endocrinology , diabetes mellitus , type 2 diabetes , polysaccharide , chemistry , population , glucose transporter , carbohydrate metabolism , biochemistry , biology , pharmacology , insulin , environmental health
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.