Maria S. Remedi, PhD

Assistant Professor of Medicine and Cell Biology & Physiology

Remedi Lab


Dr. Remedi was born and raised in Argentina. She obtained a dual degree, a M.S. in Biochemistry (equivalent) and a Pharmacist Degree at National University of Cordoba in Argentina. Dr. Remedi obtained a Ph.D. in Chemical Sciences at the same University. As a Ph.D. student, she was awarded with a prestigious fellowship from the Science and Technology Council in Argentina to study metabolic pathways in a parasite that causes Chagas disease. Dr. Remedi then moved to USA to study Diabetes Mellitus and Congenital Hyperinsulinism with Dr. Colin Nichols, Department of Cell Biology and Physiology at Washington University School of Medicine. During her postdoctoral training she obtained an American Diabetes Association Minority Fellowship Award to work in the progression of diabetes with Dr. Michael McDaniel, Department of Pathology and Immunology at Washington University. As a Junior Faculty in the Department of Cell Biology and Physiology, Dr. Remedi has been studying the role and consequences of altered ion channels in diabetes and hyperinsulinism, making major advances in these fields. Dr. Remedi and her husband Arturo Alisio have three children: Gustavo, Mariana and Carolina. Dr. Remedi joined the Department of Medicine faculty at Washington University in St. Louis in July of 2015.

Research Interests

I am currently an Assistant Professor of Medicine at Washington University. Diabetes mellitus, a chronic degenerative metabolic disease, has reached epidemic proportions in the past 30 years. I have a long standing interest in studying development and progression of diabetes. Collaboration with clinicians promoted a unique experience that has highly motivated me to devote my research in addressing fundamental questions in diabetes.

My laboratory is currently focused on understanding the underlying mechanisms of diabetes, pancreatic β-cell failure and secondary consequences of glucotoxicity in different forms of diabetes. We are using multiple genetically modified animal models of diabetes that I have previously generated, a spectrum of molecular biology techniques and classical physiology to assess the consequences of altered metabolism-excitation coupling in insulin secreting β-cells in the development and progression of diabetes. We are utilizing interdisciplinary resources and translational approaches to address mouse, patient and disease-oriented issues.

In a mouse model of insulin secretory deficiency induced diabetes we have recently shown that loss of β-cell mass in long-standing diabetes is not due to β-cell death, as frequently assumed, but instead to β-cell dedifferenciation to progenitor cells (cells that cannot produce insulin). Strikingly, we have also demonstrated reversibility of this process, with the same dedifferentiated cells re-differentiating to mature insulin containing β-cells after lowering of blood glucose by insulin treatment, thus challenging the current paradigm of permanent β-cell damage in diabetes. These results nicely correlate with the recovery of oral antidiabetic-drug responsivity in diabetic patients after intensive insulin therapy. We are further studying the underlying mechanism/s of diabetic glucotoxicity, and recovery, in pancreatic and extra-pancreatic tissues (brain, muscle, fat).

The contribution of environmental factors, obesity and nutritional programming in early life could affect metabolic and physiological functions throughout life, processes that we are also investigating in mice. Moreover, diabetes has been associated with brain abnormalities as several forms of dementia including Alzheimer’s disease, epilepsy, developmental delay and cognitive dysfunction. We are currently investigating these associations in various mouse models.

By closely collaborating with clinicians nationally and internationally we hope to elucidate the underlying mechanisms of β-cell dysfunction in human diabetes, with the expectation to be able to improve the quality of life of these patients using the most appropriate treatment to prevent, delay or reverse this process.