Author information

1. Research Division, Central Texas Veterans Health Care System, Temple, TX, USA; Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, TX, USA.
2. Research Division, Central Texas Veterans Health Care System, Temple, TX, USA; Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, TX, USA; Department of Internal Medicine, Dell Medical School, The University of Texas at Austin, Austin, TX, USA. Electronic address: sharon.demorrow@austin.utexas.edu.

Abstract

Hepatic encephalopathy describes an array of neurological complications that arise due to liver insufficiency. The pathogenesis of hepatic encephalopathy shares a longstanding association with hyperammonemia and inflammation, and recently, aberrant bile acid signaling has been implicated in the development of key features of hepatic encephalopathy. These key features include neuronal dysfunction, neuroinflammation and blood-brain barrier permeability. This review summarizes the findings of recent studies demonstrating a role for bile acids in the pathogenesis of hepatic encephalopathy via one of three main bile acid receptors and speculates on the possible downstream consequences of aberrant bile acid signaling.