Maria S. Remedi, Ph.D.

Assistant Professor
Internal Medicine
Endocrinology/Metabolism
Cell Biology and Physiology

Molecular Cell Biology Program
Neurosciences Program
Developmental, Regenerative and Stem Cell Biology Program

  • 314 362-6636

  • 314-747-0437

  • 8127

  • Southwest Tower 8th floor, lab room # 846

  • mremedi@wustl.edu

  • http://endo.wustl.edu/maria-s-remedi-ph-d/

  • Diabetes, disease, channels, brain, neurons, hormones, growth, death, obesity, physiology

  • Channels: diabetes, obesity and brain disorders

Research Abstract:

The broad context of my ongoing research has been focused on understanding the physiological and pathological roles of ATP-sensitive potassium (KATP) channels. KATP channels are expressed in many tissues (brain, heart, muscle and pancreas) linking metabolism to membrane electrical activity. Mutations on ATP-sensitive K+ (KATP) channels are the main cause of several human diseases including Neonatal Diabetes Mellitus, Congenital Hyperinsulinism, brain disorders and Cantu syndrome. In pancreatic β--cells, KATP channels critically link
glucose metabolism to insulin secretion. In the last few years, I focused my research on the role and consequences of altered KATP channels in insulin secretion; and more recently, on understanding the underlying mechanism/s of pancreatic β-cell exhaustion and glucotoxicity in diabetes . I have been also studying the consequences of altered KATP channels in extra-pancreatic tissues (heart, vasculature).

Selected Publications:

Wang, Z., York, N.W., Nichols C.G. and Remedi M.S. (2014) Pancreatic β-cell Dedifferentiation in Diabetes and Re-differentiation following Insulin Therapy. Cell Metabolism, 19: 872–882. PMID: 24746806.

Marshall, B.A., Green R.P, Wambach, J., White, N.H., Remedi, M.S. and Nichols, C.G. Remission of severe neonatal diabetes by very early treatment with sulfonylurea. Diabetes Care, In Press 2014.

Last Updated: 10/30/2015 10:22:20 AM

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