This facilitates the translocation of microbial products such as LPS and trimethylamine N-oxide (TMAO), which return to the liver, perpetuating hepatic injury and fibrosis.290,291 Bile acid receptors, farnesoid X receptor (FXR) and TGR5, mediate this feedback loop; FXR activation bolsters barrier integrity and GLP-1 secretion, whereas TGR5 curbs inflammation via cAMP signaling—both of which are compromised in liver disease states such as primary sclerosing cholangitis (PSC).292. This evidence concerns the gene NR1H4 and pancreatic serous cystadenoma.