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马铃薯抗性淀粉通过调节炎症、糖脂代谢和肠道微生物环境改善 2 型糖尿病。

Potato resistant starch improves type 2 diabetes by regulating inflammation, glucose and lipid metabolism and intestinal microbial environment.

机构信息

College of Food Science and Technology, Hebei Agricultural University, 289th Lingyusi Street, Lianchi District, Baoding 071000, China; College of Chemical Engineering and Biotechnology, Xing Tai University, 88th Quanbei East Street, Xiangdu District, Xingtai 054001, China.

College of Food Science and Technology, Hebei Agricultural University, 289th Lingyusi Street, Lianchi District, Baoding 071000, China; Hebei Technology Innovation Centre of Agricultural Products Processing, Baoding 071000, China.

出版信息

Int J Biol Macromol. 2024 Nov;281(Pt 3):136389. doi: 10.1016/j.ijbiomac.2024.136389. Epub 2024 Oct 9.

DOI:10.1016/j.ijbiomac.2024.136389
PMID:39389507
Abstract

This study established a type 2 diabetes mellitus (T2DM) mouse model and assessed the influence of Potato resistant starch 3 (PRS3) intervention. The results showed that PRS3 significantly improved glucose tolerance and insulin resistance, alleviated abnormal lipid metabolism and oxidative stress, inhibited inflammatory factor expression in the liver and pancreas, and reduced pathological damage to the pancreas and liver. Moreover, PRS3 increased fecal short-chain fatty acid content and altered the gut microbiota. At the phylum level, PRS3 increased the relative abundance of Firmicutes and Verrucomicrobiota and decreased the relative abundance of Desulfobacterota, Proteobacteria, Bacteroides, and Actinobacteriota. At the species level, PRS3 increased the relative abundance of Faecalibaculum_rodentium, uncultured_bacterium_g_Dubosiella, uncultured_bacterium_g__Olsenella, and Akkermansiamuciniphila and reduced the relative abundance of unclassified_g_Lactobacillus, unclassified_g_Cornebacterium, Lactobacillus_murinus, and Lachnospiraceae_bacterium_10_1. This study provides a theoretical basis for elucidating the glucose-lowering mechanisms of PRS3.

摘要

本研究建立了 2 型糖尿病(T2DM)小鼠模型,并评估了马铃薯抗性淀粉 3(PRS3)干预的影响。结果表明,PRS3 显著改善了葡萄糖耐量和胰岛素抵抗,缓解了异常的脂质代谢和氧化应激,抑制了肝脏和胰腺中炎症因子的表达,减轻了胰腺和肝脏的病理损伤。此外,PRS3 增加了粪便短链脂肪酸含量,并改变了肠道微生物群。在门水平上,PRS3 增加了厚壁菌门和疣微菌门的相对丰度,降低了脱硫杆菌门、变形菌门、拟杆菌门和放线菌门的相对丰度。在属水平上,PRS3 增加了 Faecalibaculum_rodentium、未培养菌属 g_Dubosiella、未培养菌属 g__Olsenella 和 Akkermansiamuciniphila 的相对丰度,降低了未分类 g_Lactobacillus、未分类 g_Cornebacterium、乳杆菌属 murinus 和 Lachnospiraceae 细菌 10_1 的相对丰度。本研究为阐明 PRS3 的降血糖机制提供了理论依据。

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