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Rohit Kohli, MDAssociate ProfessorCo-Director, Steatohepatitis Center Department of Pediatrics; Division of Gastroenterology, Hepatology and NutritionVisit the Kohli Lab
Dr. Kohli’s studies the pathogenesis of obesity-related fatty liver disease. Reactive oxygen species (ROS) have been shown to initiate various cell signaling cascades and he has demonstrated in cultured hepatocytes that increased mitochondrial ROS production is the initial signal that results in cellular steatosis mediated through the PI3-K pathway. Dr. Kohli’s lab has further demonstrated the role of refined carbohydrates (fructose and sucrose) in increasing ROS and liver fibrosis in a novel murine model of obesity and nonalcoholic steatohepatitis (NASH). This model also brought to light a potential “biomarker” for disease progression, oxidized CoEnzyme Q, whose plasma levels increased in parallel to the increase in ROS seen in liver tissue. Dr. Kohli has also published changes in bile acid physiology after bariatric surgery using small rodent models of weight loss surgery.
Dr. Kohli collaborates with Dr. Seeley investigating bile acids in the treatment of obesity and with Dr. Tschöp on energy expenditure studies. Additionally, he works with Drs. Balistreri and Xanthakos studying NASH. Anticipated Core Use: Gene and Protein Expression, Bioinformatics, and Integrative Morphology Cores.
click image to enlarge
Frozen liver sections demonstrate red fluorescence staining for reactive oxygen species. HF = high fat; HFHC = High-fat high-carbohydrate. Figure from Hepatology, 2010;52:934-44.
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