Similarly, LBP (glucan type) remarkably downregulated the level of Proteobacteria, and reduced the LPS/TLR4/NF-κB signaling path in high-fat diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD) in Sprague–Dawley (SD) rats [79]. Here, LBP is linked to metabolic dysfunction-associated steatotic liver disease.