Effects of Aerobic Exercise on Inflammation and Gut Microbiota in Obese Mice: A Metagenomic and Metabolomic Analysis

Background Aerobic exercise can ameliorate insulin resistance. However, the mechanism by which aerobic exercise regulates the gut microbiome to ameliorate IR and obesity remains unexplored. Methods The Obese mice model was established with a high-fat diet in C57BL/6 male mice. 26 mice were randomly divided into a control group (group A, N = 8) and a high-fat diet group (HFD group, N = 18). The successfully modeled mice were divided into the model group (group B, N = 8) and the exercise group (group C, N = 8). Group C underwent a 6-week treadmill exercise program (12 m/min, 60 minutes per day, 5 days per week). After the intervention, the morphology of the colon tissue was observed through hematoxylin-eosin staining, and the levels of blood lipids and inflammatory indicators in the serum were detected by ELISA. The changes in the intestinal microbiota of the mice were also examined using metagenomic sequencing and UPLC-MS non-targeted metabolomics techniques. Results Compared with the control group, the body weight, TC, TG, LDL-C, blood glucose, insulin, and insulin resistance in the model group significantly increased ( P  < 0.01), while the levels of pro-inflammatory cytokines TXNIP, TNF-α, NLRP3, IL-1β, and IL-18 significantly increased ( P  < 0.05 or P  < 0.01). Compared with the model group, aerobic exercise can reduce the body weight, TC, blood glucose, insulin, insulin resistance, TXNIP, TNF-α and other indicators in obese mice ( P  < 0.05 or P  < 0.01). Moreover, aerobic exercise can improve the imbalance of the intestinal flora in obese mice and restore the disorder of metabolites. The metabolic pathways including arachidonic acid metabolism and histidine metabolism showed the most significant differences after the intervention of aerobic exercise. Conclusions In conclusion, aerobic exercise can ameliorate the glucose and lipid metabolism, insulin resistance, inflammatory response, and regulate the intestinal microecology and metabolic disorders in obese mice. The mechanism may be closely related to increasing the diversity of intestinal flora, regulating the metabolism of arachidonic acid and histidine.