The silent epidemic of non-alcoholic fatty liver.

Non-alcoholic fatty liver disease (NAFLD) is highly prevalent. To date, up to 25% of the general population has NAFLD. This disease is characterized by the accumulation of lipids in hepatocytes, and with the onset of inflammation and fibrosis in the liver that are strongly associated with the increase in cardiovascular disease and diabetes. NAFLD also increases mortality and is becoming the leading cause of liver transplantation because it can progress to cirrhosis and liver cancer. Currently, it is a challenge to detect early cases of NAFLD, and we do not have a specific treatment to reduce or reverse NAFLD yet. However, due to the efforts of the scientific community in the last decades, several mouse models have been developed that allow us to reproduce the progression of NAFLD as occurs in humans.

These tools have increased significantly the study of the molecular mechanisms that promote NAFLD and contribute to the development of potential therapies for NAFLD. The great advantage of the mouse models is that we can alter the expression of genes in different liver cells (hepatocytes, macrophages, hepatic stellate cells, and endothelial cells) from birth or in adults (inducible models). In addition, we can induce NAFLD with genetic models that have predisposition to develop it, or with special diets. In my laboratory we are exploring the role of a nuclear receptor in hepatocytes, and how it contributes to the development of NAFLD. Using mouse models, we have shown that this receptor decreases the efficacy of a drug that has been tested in humans to reverse fatty liver disease. Our results are leading us to study in detail how the metabolism of specific amino acids and their related molecules are regulated in hepatocytes. This could help us to learn more about the progression of NAFLD and develop research projects that identify possible therapies.

Dr. Cordoba-Chacon earned a Master of Science in Biochemistry (2006), and another in Cellular and Molecular Biotechnology, and Genetics (2007) and a PhD in the Biomedicine program of the University of Córdoba in 2011. In 2011 he moved to University of Illinois at Chicago as a postdoctoral research fellow to study the metabolic effects of growth hormone on the physiology of the beta-pancreatic cell and on hepatic metabolism. Since 2017, Dr. Cordoba-Chacon leads a research group in the division of endocrinology, diabetes, and metabolism of the department of medicine at the University of Illinois at Chicago, where he studies the molecular mechanisms that promote the development of non-alcoholic fatty liver disease, and control glucose production in models with lipodystrophy. His research group is funded by the National Institute of Diabetes, Digestive and Kidney Diseases (NIDDK), the University of Chicago Diabetes Research and Training Center (DRTC), and the Central Society for Clinical and Translational Research (CSCTR).

Dr. Cordoba-Chacon has published numerous research articles, obtained several scholarships and post-doctoral contracts from the Alfonso Martín Escudero Foundation, the Endocrine Society, and the Chicago Biomedical Consortium, as well as the Early Investigator Award and the Eugenia Rosemberg Award from the Endocrine Society and the Young Investigator Award from the University of Illinois at Chicago Obesity and Diabetes Research Day.