Song Qiaoying, Zhang Kunpeng, Li Shuyan, Weng Shaoting
College of Biotechnology and Food Science, Anyang Institute of Technology, Huanghe Road, Anyang, 455000, China.
Curr Res Food Sci. 2025 Jan 19;10:100977. doi: 10.1016/j.crfs.2025.100977. eCollection 2025.
Polysaccharide, a chain of sugars bound by glycosidic bonds, have a wide range of physiological activities, including hypoglycemic activity. In present study, we established T2DM mice models to explore the effects and mechanism of Maxim polysaccharide (TMSP1) on high-fat diet/streptozotocin (HF-STZ) induced diabetes mice. The results showed that high-fat diet significantly increased the oral glucose tolerance test (OGTT), viscera index, oxidative stress, impaired glucose tolerance, decreased body weight, immune response and short-chain fatty acid (SCFAs) content, and disrupted the balance of intestinal flora structure. However, after 6 weeks of TMSP1 intervention decreased lipid accumulation, ameliorated gut microbiota dysbiosis by increasing SCFAs-producing bacteria and mitigated intestinal inflammation and oxidative stress. Moreover, TMSP1 significantly restored the integrity of the intestinal epithelial barrier and mucus barrier. The results of fecal microbiota transplantation confirmed that TMSP1 exerted hypoglycemic effect through regulating intestinal flora to a certain extent. Collectively, the findings revealed TMSP1 intervention inhibits hyperglycemia by improving gut microbiota disorder, lipid metabolism, and inflammation. Hence, TMSP1 may be an effective measure to ameliorate HF-STZ induced diabetes.
多糖是一种通过糖苷键连接的糖链，具有广泛的生理活性，包括降血糖活性。在本研究中，我们建立了2型糖尿病小鼠模型，以探讨大苞景天多糖（TMSP1）对高脂饮食/链脲佐菌素（HF-STZ）诱导的糖尿病小鼠的影响及机制。结果表明，高脂饮食显著增加了口服葡萄糖耐量试验（OGTT）、脏器指数、氧化应激、糖耐量受损、体重下降、免疫反应和短链脂肪酸（SCFAs）含量，并破坏了肠道菌群结构的平衡。然而，TMSP1干预6周后，脂质积累减少，通过增加产生SCFAs的细菌改善了肠道微生物群失调，减轻了肠道炎症和氧化应激。此外，TMSP1显著恢复了肠道上皮屏障和黏液屏障的完整性。粪便微生物群移植的结果证实，TMSP1在一定程度上通过调节肠道菌群发挥降血糖作用。总的来说，这些发现表明TMSP1干预通过改善肠道微生物群紊乱、脂质代谢和炎症来抑制高血糖。因此，TMSP1可能是改善HF-STZ诱导的糖尿病的有效措施。
