Lactobacillus paracasei improves dietary fatty liver by reducing insulin resistance and inflammation in obese mice model

Long term high-fat diet (HFD) will lead to obesity and its complications, such as lipid metabolism disorder, insulin resistance and inflammation. The purpose of this study is to demonstrate the mechanism of Lactobacillus paracasei Jlus66 to improve dietary fatty liver in obese mice model. C57BL/6J male mice were randomly divided into three groups (Control, HFD and HFD + Jlus66). Proteins of many pathways related to insulin resistance (IRS-1, AKT, GSK3 beta, GLUT4 and PTP1B), to jejunum permeability (Zo-1, Claudin-1 and Occludin) were detected by using western blotting. Correspondingly, genes of inflammation (Inos, Tnf-alpha and Il-1 beta), mitochondrial dysfunc-tion (Cox5b, Cox7a1, CoxII, Cox8b, Cycs and Sirt1) and oxidative stress (yGcs, Mnsod, Nqo-1, Gpx1 and Ho-1) were detected by using RT-qPCR. As results, Jlus66 effectively improved lipid metabolism disorder and mitochondrial dysfunction, ameliorated insulin resistance and inflammatory response in the liver, jejunum and adipose tissue of HFD-induced obese mice model. Moreover, Jlus66 treated also protected jejunum barrier integrity and alleviated oxidative stress. In conclusion, Jlus66 might be a nutritional strategy for obesity and its complications.

Automated summary

This study demonstrates that Lactobacillus paracasei Jlus66 can effectively improve lipid metabolism disorder, mitochondrial dysfunction, insulin resistance, and inflammatory response in a mouse model of obesity.