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

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.