Biliverdin reductase and bilirubin in hepatic disease

Author:

Weaver Lauren1ORCID,Hamoud Abdul-rizaq1,Stec David E.2ORCID,Hinds Terry D.1ORCID

Affiliation:

1. Department of Physiology and Pharmacology, Center for Hypertension and Personalized Medicine, University of Toledo College of Medicine, Toledo, Ohio

2. Department of Physiology and Biophysics, Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, Mississippi

Abstract

The buildup of fat in the liver (hepatic steatosis) is the first step in a series of incidents that may drive hepatic disease. Obesity is the leading cause of nonalcoholic fatty liver disease (NAFLD), in which hepatic steatosis progresses to liver disease. Chronic alcohol exposure also induces fat accumulation in the liver and shares numerous similarities to obesity-induced NAFLD. Regardless of whether hepatic steatosis is due to obesity or long-term alcohol use, it still may lead to hepatic fibrosis, cirrhosis, or possibly hepatocellular carcinoma. The antioxidant bilirubin and the enzyme that generates it, biliverdin reductase A (BVRA), are components of the heme catabolic pathway that have been shown to reduce hepatic steatosis. This review discusses the roles for bilirubin and BVRA in the prevention of steatosis, their functions in the later stages of liver disease, and their potential therapeutic application.

Funder

HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)

HHS | NIH | National Center on Minority Health and Health Disparities (NCMHD)

HHS | NIH | National Institute of General Medical Sciences (NIGMS)

Publisher

American Physiological Society

Subject

Physiology (medical),Gastroenterology,Hepatology,Physiology

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