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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.