Fagopyrum tataricum ethanol extract ameliorates symptoms of hyperglycemia by regulating gut microbiota in type 2 diabetes mellitus mice

Type 2 diabetes mellitus (T2DM) is typically accompanied by sudden weight loss, dyslipidemia-related indicators, decreased insulin sensitivity, and altered gut microbial communities. Fagopyrum tataricum possesses many biological activities, such as antioxidant, hypolipidemic, and hypotensive activities. However, only a few studies have attempted to elucidate the regulatory effects of F. tataricum ethanol extract (FTE) on intestinal microbial communities and its potential relationships with T2DM. In this study, we established a T2DM mouse model and investigated the regulatory effects of FTE on hyperglycemia symptoms and intestinal microbial communities. FTE intervention significantly improved the levels of fasting blood glucose, the area under the curve of oral glucose tolerance test (OGTT), and glycosylated serum protein, as well as pancreas islet function correlation index. In addition, FTE effectively improved hepatic and cecum injuries and insulin secretion due to T2DM. It was also revealed that the potential hypoglycemic mechanism of FTE was involved in the regulation of protein kinase B (AKT-1) and glucose transporter 2 (GLUT-2). Furthermore, compared with the Model group, the FTE-H intervention exhibited a significantly decreased ratio of Firmicutes to Bacteroidetes at the phylum level, reduced relative abundance of pernicious bacteria at the genus level, such as Desulfovibrio, Oscillibacter, Blautia, Parabacteroides, and Erysipelatoclostridium, and ameliorated inflammatory response and insulin resistance. Moreover, the correlation between gut microbiota and hypoglycemic indicators was predicted. The results showed that Lachnoclostridium, Lactobacillus, Oscillibacter, Bilophila, and Roseburia have the potential to be used as bacterial markers for T2DM. In conclusion, our research showed that FTE alleviates hyperglycemia symptoms by regulating the expression of AKT-1 and GLUT-2, as well as intestinal microbial communities in T2DM mice.