My research focuses on the development of liver injury and disease as a consequence of obesity or alcohol consumption. We are focused on the role of the macrophage in the development of alcoholic steatohepatitis (ASH) and nonalcoholic steatohepatitis (NASH). We have developed a myeloid specific deletion of phosphoenolpyruvate carboxykinase (Pckl). These mice are resistant to diet-induced obesity and alcohol-induced liver injury. The deletion of Pck1 in the macrophage alters the gut microbiota and reduces the expression of trimethylamine (TMA) and trimethylamine N-oxide (TMAO). TMA is an important gut microbe-dependent metabolite, that is generated from dietary choline, betaine and L-carnitine and is converted to TMAO by hepatic flavin monooxygenases (FMOs). Multiple studies have shown a strong association between high levels of plasma TMA and TMAO with cardiovascular disease. Currently we are investigating the mechanism by which the deleted gene (Pck1 ) in the macrophage alters the gut microbiota and its metabolism.
My research involves metabolism, CAAT/enhancer binding protein beta (C/EBP beta), transcription, Phosphoenolpyruvate carboxykinase (PEPCK), knockout animal models, and perinatal metabolism.
Development of new interactive teaching pedagogies
Cross-talk between gut microbiota and macrophages
NIAAA, Alcohol and tissue injury: from mechanisms to treatments (NOAC), Director of Animal Core 12/05/2020-11/30-2025
Awards and Honors
- 2010-present: Editorial Board of World Journal of Diabetes
- 2010-present: Wellcome Trust Scientific Peer Grant Review; London, UK
- 2014-present: NIH/NIAAA AA-1 Biomedical Research Study Section NIH-NIDDK Integrative Nutrition and Metabolic Processes Study Section
- 2015-present: Adjunct Departments of Pathobiology and Gastroenterology, Cleveland Clinic Foundation