Brian DeBosch, MD, PhD
The DeBosch laboratory uses mouse genetic, physiological, cell biological and multi-omic techniques to understand the signaling pathways that are activated downstream of blocking hepatocyte glucose transporters. We found that inhibiting hepatocyte glucose transport and the adaptive responses that are engaged are sufficient to convey key aspects of the physiological response to caloric restriction. This includes upregulation of hepatic fat oxidation, autophagy and secretion of the anti-diabetic peptide — FGF21. Our goal is to understand and then utilize these responses to treat metabolic diseases, including non-alcoholic fatty liver disease, cardiovascular disease and type 2 diabetes mellitus.
Lori R. Holtz, MD
Work in our lab focuses on the integrated use of epidemiology, bioinformatics, and molecular virology to address questions in the developing childhood gut.
Kim Hung Ho Liss, MD
Childhood liver disease; liver transplantation; nonalcoholic fatty liver disease; ischemia-reperfusion injury
Mark E. Lowe, MD, PhD
Dietary fat digestion and mechanisms of chronic pancreatitis.
David Perlmutter, MD
David Perlmutter is internationally recognized for his research on the pathobiology of α1-antitrypsin deficiency, a rare disease in which a misfolded protein causes chronic liver failure and hepatocellular carcinoma. His work has led to advances in understanding the basic mechanisms of liver fibrosis and carcinoma and novel therapeutic strategies. Together with collaborators he has discovered a pipeline of drugs that can eliminate misfolded proteins and reverse the liver disease in model organisms. One of these drugs has advanced to phase II/III clinical trials. The class of drugs may also be utilized for other diseases caused by misfolded proteins, including Alzheimer’s disease and other age-dependent degenerative diseases.
David Rudnick, MD, PhD
Our laboratory is interested in elucidating the molecular signaling mechanisms of liver regeneration. In addition to liver mass being precisely regulated in proportion to body mass, this organ is also able to regenerate the anatomic and functional deficits incurred by many forms of injury or disease (e.g. toxin exposure, trauma, infection). We use rodent partial hepatectomy and other models to investigate the mechanisms responsible for this remarkable regenerative potential, and have focused our recent efforts on defining and investigating the functional relevance of extrahepatic signals that influence regulation of liver mass and regeneration. In addition, we began a translational line of investigation in which lessons learned about liver regeneration in this basic model are applied to analyses of human liver diseases. Such studies led us to identify a novel metabolomic marker of liver regeneration and evaluate its utility in predicting clinical outcomes in pediatric acute liver failure.
Phillip I. Tarr, MD
Our laboratory is focused on several inter-related projects. Our major effort is to determine if the microbes that populate the guts of newborn premature infants play a role in the development of necrotizing enterocolitis (NEC), which is a catastrophic necroinflammatory lesion that remains 30% fatal, and affects about 7% of very low birth weight infants. We use a combination of metagenomic sequencing, statistics, and clinical data to confirm or refute associations between the acquisition of this biomass, and its specific constituents.
Todd N. Wylie
Current focus is to collaborate with clinicians and basic scientists in improving medical practice through the application of high-throughput multi-omics and associated computational methods. Involved in many collaborative efforts studying the microbiome and its association with disease.
Xunjun Xiao, PhD
My primary research interest is to understand the molecular mechanisms of dietary fat digestion by pancreatic lipases in young children to improve fat digestion for better growth and development. My secondary research interest is to define the role of proteotoxicity in the pathophysiology of chronic pancreatitis using mutant misfolded pancreatic lipases as study model for finding potential novel therapies.