Remedi Lab

The major focus of the Remedi laboratory is to study in vivo physiology in various mouse models of diabetes to unravel the underlying mechanisms of pancreatic β-cell failure in glucotoxic stages, and their consequences in both pancreatic and extra-pancreatic tissues. Development of secondary loss of β-cell mass and antidiabetic drug sensitivity in long-standing diabetic patients is not completely understood. Recently, much attention has been gathered on cell plasticity challenging the current paradigms of how diabetes progresses.

Remedi Lab 2021

The Bionic Mouse

Mice lacking the glycolytic enzyme glucokinase in the pancreas normally never live beyond a few days. The white mouse in the picture lacks glucokinase, but also lacks potassium channels. For this reason it bypasses the need for glucose metabolism in insulin secretion. It remains small and unhealthy but -critically- it can survive (Remedi et al. 2005 Diabetes 54, 2925–2931).

Neonatal Diabetes Mellitus is Genetic and Inherited

A genetically modified mouse model of Neonatal Diabetes Mellitus reiterated the main features of the human disease: increased blood glucose with development of severe diabetes induced by lack of insulin secretion in response to glucose. As diabetes progresses, these mice show reduction in body weight, among other whole body abnormalities (Remedi et al. 2009 Cell Metabolism, 9, 140-151).

Diabetic Glucotoxicity


Islets from normal mouse pancreas contain lots of insulin that is released to maintain blood glucose at normal levels. Mice –and people– that express a genetic mutation in potassium channel suffer Neonatal Diabetes Mellitus. The mouse model reveals complex secondary changes, including unexpected disappearance of insulin and glucagon from the islets. Importantly, these consequences are prevented by maintenance of normal blood glucose by either islet transplantation or chronic antidiabetic sulfonylurea therapy (Remedi et al. 2009 Cell Metabolism, 9, 140-151).

Loss of β-cell Identity: to be or not to be? A Reversible Process

The marked reduction of insulin-containing β-cells in severely diabetic mice (untreated) is not due to increased cell death (TUNEL), but instead to β-cell dedifferentiation to islet progenitor cells (Neurogenin3, Ngn3 positive red nuclei). Strikingly, this process is reversible with the same dedifferentiated cells re-differentiating to mature insulin-containing β-cells following normalization of blood glucose by intensive insulin therapy (treated) (Wang et al. 2014, Cell Metabolism 19:872-882), challenging the paradigm of permanent β-cell damage in long-standing diabetes.

Antidiabetic Sulfonylureas: Transient vs Permanent Neonatal Diabetes?

Antidiabetic sulfonylurea therapy at disease onset can cause remission of Neonatal Diabetes in mice (Remedi at al., 2008 PLoS Medicine 5(10):1473-1485; Remedi et al. 2011, Diabetes 60: 2515-22). Strikingly, remission of Neonatal Diabetes has also been shown in patients treated with sulfonylureas very early (Marshall et al. 2015, Diabetes care 38:e38-e39)

The Hyperactive Mouse

Neurological features in mice expressing mutant channels in the brain. Hyperactivity, impaired motor coordination and balance, decreased muscle strength (unpublished data).

Contact Information

Principal Investigator

Maria S. Remedi, PhD

Maria S. Remedi, PhD

Associate Professor of Medicine and Cell Biology & Physiology

Office Location

848 Southwest Tower (Medical campus)

Office Phone (314) 362-6636

Fax (314) 362-7641

Laboratory Location

846 Southwest Tower (Medical campus)

Lab Phone (314) 747-0437

Mailing Address

660 S. Euclid Ave.

Campus Box 8127

St. Louis, MO 63110

Currently seeking graduate students, post-docs and research fellows.

Sophia Chen

Sophia Chen

Undergraduate Research

Rikki  Z. Drexler

Rikki Z. Drexler

Undergraduate Student

Sumit Patel

Sumit Patel

Doctoral Student, DBBS Pre Doc Trainee

Rashaun Williams, PhD

Rashaun Williams, PhD

Postdoctoral Research Scholar

Yuqi Zhang

Yuqi Zhang

Graduate Research Assistant | Remedi Lab

Former Lab Members

Carly Feldman – Undergraduate Research. 2020-2022

Zeenat Asghar Shyr – Postdoctoral Fellow. 2016-2019

Manuela Fortunato – Research Technician. 2017-2018

Christopher Emfinger – PhD student, graduated in 2018

Hannah Conway – Research Technician I, 2016-2019

Alecia Welscher – Research Technician I, 2014-2016

Zhiyu Wang – Clinical Fellow, Washington University

Reka Lorincz – Visiting PhD student, University of Innsbruck – Austria 2017-2018

Stephanie Schiffert   NIH Medical Student Summer Research Program, University of Central Florida. 2019

William McAlister- NIH Medical Student Summer Research Program, Brody School of Medicine. 2018

Erin Lindsey – NIH Medical Student Summer Research Program, Saint Louis University. 2017

Amanda Piaruli – NIH Medical Student Summer Research Program, Drexel University. 2016

Undergraduate students

Gabrielle McGinn – Undergraduate student, Washington University. 2019-2020

Matt Fuess – Undergraduate student, Washington University. 2018-2020

Erin Egan – Undergraduate student, Washington University. 2017-2019

Yixi Wang – Undergraduate Student, Washington University. 2016-2018

Arsam Nadeem – Undergraduate Student St. Louis College of Pharmacy. 2016

Leah Yuan – Undergraduate Student, Washington University. 2015-2017

Betsy Abraham- Undergraduate Student St. Louis College of Pharmacy. 2016

Nihar Shah –Undergraduate student, Washington University. 2015-2016

Jonathan Friedman – Undergraduate student, Washington University. 2012-2014

Summer Students

Bailee Rasmussen – Undergraduate summer student, Utah State University. 2019

Eric Hilker – Undergraduate summer student, Truman University 2016

 Mariana Alisio – Undergraduate summer student – Washington University, 2015

Hannah Conway – Undergraduate summer student, Loyola University, 2015

Nathan York – Undergraduate summer student, University of Missouri, 2011, 2012

Felesha Clake – High School student, St Louis, 2015