Abstract: Objective: To investigate the ameliorative effect and underlying mechanism of human-origin Lactobacillus combined with inulin in type 2 diabetic mice (T2DM). Methods: Obese/diabetic?(db/db)?mice?were consecutively administrated with a cocktail of four strains (each with a viable count of 1.0×109 CFU/mL) of human-origin Lactobacillus at a dose of 10 mL/(kg mb·d), and fed a basal incorporated with 5% inulin for dietary intervention on mice. Body?mass,?feed intake and fasting blood glucose levels were?measured?once?a?week. At the late stage of intervention, oral glucose tolerance and insulin resistance tests were performed. After completion of the experiment, fasting blood glucose, blood lipids, glycated serum protein (GSP), the mRNA expression of inflammatory factors, and phosphatidylinositol-3-kinase (PI3K) and serine/threonine kinase (AKT) protein expression were measured. Liver, kidney and pancreas tissues were collected and stained with hematoxylin-eosin (HE) to observe histomorphology. Results: Human-origin Lactobacillus coordinated with inulin effectively regulated blood glucose and lipid levels, reduced the expression of GSP and improved insulin resistance. The mRNA expression of pro-inflammatory factors interleukin (IL)-6 and IL-1β were significantly inhibited and the mRNA expression of anti-inflammatory factor IL-10 was promoted. Furthermore, the expression of PI3K and AKT proteins were increased significantly, and pathological damage was significantly improved in liver, kidney and pancrea tissues. Conclusion: Human-origin Lactobacillus coordinated with inulin can alleviate type 2 diabetic symptoms in mice by reducing insulin resistance and inflammatory response, and activating the PI3K/AKT signaling pathway.

Key words: type 2 diabetes; human-origin Lactobacillus; inulin; phosphatidylinositol-3-kinase/serine/threonine kinase pathway