Chaozhou Branch of Chemistry and Chemical Engineering Guangdong Laboratory, Chaozhou 521000, China.
School of Food Science and Engineering, South China University of Technology, Guangzhou 510640, China.
Food Funct. 2021 Nov 29;12(23):11898-11912. doi: 10.1039/d1fo01838h.
The aim of the current work was to investigate the anti-diabetic effects and underlying mechanisms of polysaccharides (UPP) based on a type 2 diabetes (T2DM) rat model. The starch loading test showed that UPP administration could reduce blood glucose fluctuations caused by eating. Analysis of diabetic symptoms and biochemical profiles showed that UPP intervention markedly decreased fasting blood glucose level, mitigated insulin resistance, improved glucose tolerance, dyslipidemia and liver and kidney damage in diabetic rats. The 16S rRNA analysis demonstrated that UPP intervention could markedly change the intestinal microflora composition, causing increases in , , _R-7_group, , _norank, _UCG-013, and _UCG-014, and a decrease in . Furthermore, RT-qPCR analysis results clarified that UPP administration distinctly activated the IRS/PI3K/AKT signaling pathway, restrained PEPCK, G-6-Pase and Egr-1 genes, and affected the relative expression of HMGCR and LDLR genes. This study demonstrates that UPP could be applied as an adjuvant agent for the management of T2DM.
本研究旨在通过 2 型糖尿病（T2DM）大鼠模型，探讨多糖（UPP）的抗糖尿病作用及其潜在机制。淀粉负荷试验表明，UPP 给药可降低进食引起的血糖波动。对糖尿病症状和生化特征的分析表明，UPP 干预可显著降低空腹血糖水平，减轻胰岛素抵抗，改善糖尿病大鼠的葡萄糖耐量、血脂异常以及肝肾功能损伤。16S rRNA 分析表明，UPP 干预可显著改变肠道微生物群落组成，使 、 、 _R-7_group、 、 _norank、_UCG-013 和 _UCG-014 增加，而 减少。此外，RT-qPCR 分析结果表明，UPP 给药可明显激活 IRS/PI3K/AKT 信号通路，抑制 PEPCK、G-6-Pase 和 Egr-1 基因，并影响 HMGCR 和 LDLR 基因的相对表达。本研究表明，UPP 可作为 T2DM 治疗的辅助剂。
