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Remedi Lab

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    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.

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    The Bionic Mouse

    The Bionic Mouse

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    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).

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    Neonatal Diabetes Mellitus is Genetic and Inherited

    Neonatal Diabetes MellitusGenetically Modified Mice

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    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).

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    Diabetic Glucotoxicity

    Diabetic Glucotoxicity
    Tamoxifen InductionIslets 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).

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

    Loss of β Cell Identity

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    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.

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    Antidiabetic Sulfonylureas: Transient vs Permanent Neonatal Diabetes?

    Glibenclamide Injection

    Sulfonylureas Treatment Very Early

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    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)

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    The Hyperactive Mouse

    The Hyperactive Mouse

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 Hyperactivity, impaired motor coordination and balance, decreased muscle strength (unpublished data).

  • Remedi Lab

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    Principal Investigator
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    Maria S. Remedi, PhD Principal Investigator

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    Maria S. Remedi, Ph.D.
    Assistant Professor of Medicine and Cell Biology & Physiology
    mremedi@dom.wustl.edu
    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

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

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    Remedi Lab–Team 2016
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    Remedi Lab Team 2016

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    Maria Remedi, PhD

    Maria Remedi

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    Chris Emfinger

    Chris Emfinger
    PhD student

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    Zihan Yan

    Zihan Yan
    Research Assistant

    Theresa Harter

    Theresa Harter
    Lab Manager

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    Amanda Piaruli

    Amanda Piaruli
    Medical Student Drexel Univ.
    NIH Medical Student Research Program

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    Eric Hilker

    Eric Hilker
    Truman Univ.
    Summer student

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    Yixi Wang

    Yixi Wang
    Washington Univ.
    Summer student

    Felesha Clake

    Felesha Clake
    High School student


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    Remedi Lab–Team 2015
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    Christopher Emfinger, PhD

    Christopher Emfinger
    (Ph.D. student)

    Zihan Yan

    Zihan Yan
    (Research Technician II)

    Alecia Welscher

    Alecia Welscher
    (Research Technician I)

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    Undergraduate Students
    Leah Yuan

    Leah Yuan
    (Washington University)

    Nihar Shah

    Nihar Shah
    (Washington University)

    Mariana Alisio

    Mariana Alisio
    (Washington University)

    Hannah Conway

    Hannah Conway
    (Washington University)

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    Former Lab Members

    Zhiyu Wang (Clinical Fellow, Washington University)
    Nathan York (Undergraduate student, University of Missouri)
    Jonathan Friedman (Undergraduate student, Washington University)