Pittsburgh Liver Research Center,
Department of Medicine,
Division of Gastroenterology,
Hepatology and Nutrition,
Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition
Dr. Juliane I Beier is an Assistant Professor of Medicine in the Division of Gastroenterology, Hepatology & Nutrition at the University of Pittsburgh. She is also member of the Pittsburgh Liver Research Center (PLRC) and was recently named a leader for the junior faculty group within the PLRC. Dr. Beier’s research focuses on interactions of environmental exposures and lifestyles that increase risk of chronic liver disease and which may be preventable.
Her doctoral training at the Heinrich-Heine University in Düsseldorf, Germany focused predominantly on the elucidation of ROS-induced signal transduction pathways. During her postdoctoral career at the University of Louisville in Louisville, KY, USA, she studied the mechanisms by which chronic liver disease initiates and progresses, focusing on all stages of chronic liver disease, including early (steatosis), intermediate (steatohepatitis), and late (fibrosis and cirrhosis) stages of the liver disease using animal models. Together her background with both biochemistry and toxicology laid the perfect foundation for her long-term research goal to explore the mechanisms by which environmental exposures that are not overtly hepatotoxic, may modify the risk of liver disease through experimental and translational studies. Obesity and its associated liver disease (i.e., NAFLD/NASH) are epidemic in the US population; indeed, it is estimated that up to 30% of US adults have underlying liver disease, most likely predominantly due to obesity. The impact of this new status quo in the risk of liver injury caused by environmental exposures is understudied. Importantly, such an interaction would imply that risk may be underestimated at this time. Vinyl chloride (VC) is a known human hepatotoxicant that causes a spectrum of both benign and malignant diseases, including hepatocellular carcinoma (HCC), hemangiosarcoma and toxicant associated steatohepatitis (TASH). However, these direct effects of VC exposure require high occupational exposures and have limited relevance with existing VC safety regulations. The impact of low environmental exposures, in contrast to high occupational exposures to VC, is unknown. Importantly, the effect of low exposure must consider aspects that may modify hepatotoxicity. In this context, the impact of underlying disorders (i.e., obesity) or lifestyle choices (i.e., diet) that may modify risk is critical. The Beier lab has demonstrated that low doses of VC that are not overtly hepatotoxic, may serve as a contributing factor in the development and progression of liver disease.
Interaction of volatile organic compounds and underlying liver disease: a new paradigm for risk.
Biological chemistry 10, 2018 | Pubmed ID: 29924722
Vinyl chloride-induced interaction of nonalcoholic and toxicant-associated steatohepatitis: Protection by the ALDH2 activator Alda-1.
Redox biology 06, 2019 | Pubmed ID: 31026768
Mechanisms of Environmental Contributions to Fatty Liver Disease.
Current environmental health reports 09, 2019 | Pubmed ID: 31134516
Rapamycin attenuates liver injury caused by vinyl chloride metabolite chloroethanol and lipopolysaccharide in mice.
Toxicology and applied pharmacology Nov, 2019 | Pubmed ID: 31499194
Anna L. Lang1,2,
William T. Goldsmith3,4,
Regina D. Schnegelberger5,6,
Gavin E. Arteel6,7,
Juliane I. Beier6,7
1Department of Pharmacology and Toxicology, University of Louisville,
2Hepatobiology and Toxicology Program, University of Louisville,
3Department of Physiology and Pharmacology, West Virginia University,
4Center for Inhalation Toxicology, West Virginia University,
5Department of Pharmacology and Chemical Biology, University of Pittsburgh,
6Pittsburgh Liver Research Center, University of Pittsburgh,
7Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh
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