Peroxisome proliferator-activated receptor-alpha activation and dipeptidyl peptidase-4 inhibition target dysbiosis to treat fatty liver in obese mice

Figure 7 Main findings of the study. All treatments alleviated fatty liver by countering gut dysbiosis and rescuing the intestinal barrier integrity. The reduced lipopolysaccharide (LPS) influx to the liver caused reduced inflammasome and CD206 macrophage activation. Peroxisome proliferator-activated receptor-alpha activation and DPP-4 inhibition can be regarded as viable tools to treat leaky gut and prevent LPS-driven hepatic steatosis. PPAR: Peroxisome proliferator-activated receptor; DPP-4: Dipeptidyl peptidase-4; LPS: Lipopolysaccharide; LBP: Lipopolysaccharide-binding protein; TLR4: Toll-Like receptor 4; ZO-1: Zonula occludens 1; NLRP3: NLR family pyrin domain containing 3; CD206: Cluster of differentiation 206; IL: Interleukin. Created with Biorender: www.biorender.com.