An official website of the United States government
Publication Information
Affiliation
Division of Gastroenterology and Hepatology, University of California, San Francisco, San Francisco, California. Electronic address: monika.sarkar@ucsf.edu.; Department of Biostats and Epidemiology, Johns Hopkins University, Baltimore, Maryland.; Division of Gastroenterology and Hepatology, Duke University, Durham, North Carolina.; Division of Pediatric Gastroenterology and Hepatology, Columbia University, New York, New York.; Department of Pathology, University of California, San Francisco, San Francisco, California.; National Primate Research Center, University of Wisconsin, Madison, Wisconsin.; Division of Gastroenterology and Hepatology, University of California, San Francisco, San Francisco, California; Division of Gastroenterology and Hepatology, University of Southern California, Los Angeles, California.; Division of Endocrinology and Metabolism, Saint Louis University, Saint Louis, Missouri.
Authors
Sarkar Monika, Yates Katherine, Suzuki Ayako, Lavine Joel, Gill Ryan, Ziegler Toni, Terrault Norah, Dhindsa Sandeep
Studies
Abstract
With rising prevalence of obesity and diabetes, nonalcoholic fatty liver disease (NAFLD) is now a leading cause of chronic liver disease. One-third of obese or diabetic men have subnormal free and bioavailable testosterone concentrations.1 Several studies have further shown low testosterone to be associated with imaging-confirmed NAFLD in men,2 although it is unknown whether low testosterone confers increased risk of more clinically relevant manifestations of NAFLD, including nonalcoholic steatohepatitis (NASH) and NASH fibrosis. We therefore aimed to evaluate the association of testosterone with histologic features of NAFLD among a representative cohort of men from the multicenter NASH Clinical Research Network (NASH CRN).