Cao Yan, Zou Siwei, Xu Hui, Li Mengxia, Tong Zan, Xu Min, Xu Xiaojuan
College of Chemistry and Molecular Sciences, Wuhan University, Wuhan, China.
Department of Physiology, Wuhan University School of Basic Medical Sciences, Wuhan, China.
Mol Nutr Food Res. 2016 Dec;60(12):2678-2690. doi: 10.1002/mnfr.201600032. Epub 2016 Aug 12.
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.
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.
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.
β-葡聚糖已被证明可降低肥胖和糖尿病风险。然而，它们通常含有多种多糖和其他成分，导致实验数据和机制难以捉摸。在本研究中，从粗制面包酵母多糖中获得了一种纯β-葡聚糖，以研究其对高脂饮食诱导的肥胖（DIO）/2型糖尿病（T2D）小鼠代谢紊乱的影响及其潜在机制。
傅里叶变换红外光谱和核磁共振光谱数据表明，纯β-葡聚糖（BYGlc）是一种线性β-(1→3)-葡聚糖。首次发现，给T2D和DIO小鼠口服BYGlc可通过抑制肠黏膜中钠-葡萄糖转运蛋白-1的表达显著下调血糖。同时，BYGlc促进肝脏糖原合成并抑制脂肪积累，并通过组织化学/免疫组织化学和ELISA检测抑制巨噬细胞浸润和促炎细胞因子的产生。此外，通过16S rDNA分析，BYGlc显著降低了厚壁菌门的数量，并增加了阿克曼氏菌的比例。
在T2D/DIO小鼠模型中，BYGlc表现出降血糖活性，同时促进代谢并抑制炎症。首次宣称其降血糖机制是通过抑制钠-葡萄糖转运蛋白-1的表达，并且可能与肠道微生物群的改变有关。
