The role of bilio-pancreatic limb in nonalcoholic steatohepatitis improvement after duodenal–jejunal bypass in rats.

Nonalcoholic fatty liver disease, which is highly associated with obesity, includes nonalcoholic steatohepatitis. Lipopolysaccharides from the intestine would induce inflammation in the liver in nonalcoholic fatty liver disease. This study aimed to examine the role of the bilio-pancreatic limb in the effect of duodenal–jejunal bypass on nonalcoholic steatohepatitis, with respect to the gut–liver axis, using a rat model. Nonalcoholic steatohepatitis model rats were randomly assigned into 3 groups as follows: 1 sham group and 2 duodenal–jejunal bypass groups. The 2 duodenal–jejunal bypass groups were defined according to the bilio-pancreatic limb length: 30 cm (30-DJB group) and 0 cm (0-DJB group). Pathology findings and blood biochemistry, inflammatory cytokine and lipopolysaccharides receptor mRNA in the liver and common channel, and lipopolysaccharide-binding protein level in the portal vein were assessed. The reduction in plasma alanine aminotransferase and nonalcoholic fatty liver disease activity score in the 30-DJB group was not observed in the 0-DJB group, similar to the sham group. In the liver tissue, mRNA of inflammatory cytokines and lipopolysaccharide receptors, the area occupied by CD68-positive macrophages, and the number of CD3-positive T-lymphocytes on immunostaining were lower in the 30-DJB group; however, these findings were not observed in the 0-DJB group, and lipopolysaccharide-binding protein levels in the portal vein and mRNA expressions of inflammation-related genes in the common channel showed similar tendencies. The bilio-pancreatic limb plays an important role in the beneficial effect of duodenal–jejunal bypass for nonalcoholic steatohepatitis. The bilio-pancreatic limb may suppress lipopolysaccharides-related cascades in the liver by reducing intestinal inflammation. [ABSTRACT FROM AUTHOR]