26337-Linnemann, Amelia
Faculty

Amelia K. Linnemann, PhD

Assistant Professor of Pediatrics

Address
MS 2031
PENB
IN
Indianapolis, IN

Bio

Dr. Linnemann recently established her research program as an Assistant Professor in the Herman B Wells Center for Pediatric Research at Indiana University School of Medicine. In addition to numerous awards throughout her career Dr. Linnemann is currently funded by a prestigious K01 Career Development Award from the National Institutes of Health (NIH). The primary focus of the Linnemann laboratory is to understand mechanisms of pancreatic β-cell death/survival, islet compensatory adaptation to cellular stress, and how these factors contribute to diabetes pathogenesis.

Titles & Appointments

  • Assistant Professor of Pediatrics
  • Adjunct Assistant Professor of Anatomy, Cell Biology & Physiology
  • Adjunct Assistant Professor of Biochemistry & Molecular Biology
  • Education
    2012 FEL University of Wisconsin School of Medicine and Public Health
    2009 PhD Wayne State University
    2002 BS University of Detroit Mercy
  • Research

    Research in the Linnemann lab is focused on diabetes; specifically the study of the insulin producing pancreatic beta-cells under conditions of inflammatory stress. The beta-cells must adapt rapidly to changing conditions in the body in order to maintain blood glucose within a normal range. When pancreatic islets are exposed to additional stress and demand due to factors such as inflammation or obesity, some beta-cells are better able to adapt and respond in such a way that allows them to survive. An inability to adapt contributes significantly to the development of diabetes. Thus, we are particularly interested in how higher level metabolic signals contribute to molecular crosstalk within the islet and influence beta-cell adaptation to stress. In an effort to develop therapies that prevent beta-cell failure in type 1 and type 2 diabetes, projects in the lab are focused on 3 major areas:

    1. Identifying mechanisms of adaptive stress response in the pancreatic islet that enable beta-cell survival.
    2. Studying paracrine signaling in the islet under conditions of stress and increased demand.
    3. Understanding the regulation of core mediators of autophagy and how this process contributes to beta-cell homeostasis and survivial.
  • Professional Organizations
    American Association for the Advancement of Science
    American Diabetes Association
    Endocrine Society

Research Labs

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Faculty Labs