The Ailing β-Cell in Diabetes: Insights From a Trip to the ER: The 2023 Outstanding Scientific Achievement Award Lecture

Author:

Evans-Molina Carmella1234567ORCID

Affiliation:

1. 1Department of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN

2. 2Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN

3. 3Department of Medicine, Indiana University School of Medicine, Indianapolis, IN

4. 4Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN

5. 5Center for Diabetes and Metabolic Diseases, Indiana University School of Medicine, Indianapolis, IN

6. 6Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN

7. 7Roudebush VA Medical Center, Indianapolis, IN

Abstract

The synthesis, processing, and secretion of insulin by the pancreatic β-cell is key for the maintenance of systemic metabolic homeostasis, and loss or dysfunction of β-cells underlies the development of both type 1 diabetes (T1D) and type 2 diabetes (T2D). Work in the Evans-Molina laboratory over the past 15 years has pioneered the idea that regulation of calcium dynamics is critical to β-cell biology and diabetes pathophysiology. In this article, I will share three vignettes from the laboratory that demonstrate our bench-to-bedside approach to determining mechanisms of β-cell stress that could improve therapeutic options and outcomes for individuals living with diabetes. The first of these vignettes will illustrate a role for the sarcoendoplasmic reticulum calcium ATPase (SERCA) pump in the regulation of endoplasmic reticulum (ER) calcium, protein trafficking, and proinsulin processing within the β-cell. The second vignette will highlight how alterations in β-cell calcium signaling intersect with T1D pathogenesis. The final vignette will demonstrate how activation of β-cell stress pathways may serve as an anchor to inform biomarker strategies in T1D. Lastly, I will share my vision for the future of diabetes care, where multiple biomarkers of β-cell stress may be combined with additional immune and metabolic biomarkers to better predict disease risk and improve therapies to prevent or delay T1D development.

Funder

the Richardson Family

U.S. Department of Veterans Affairs

Sigma Beta Sorority

Ball Brothers Foundation

Leona M. and Harry B. Helmsley Charitable Trust

Luke Bracken Wiese Fund in Juvenile Diabetes

IU School of Medicine

National Institutes of Health

Thomas Trust

George and Frances Ball Foundation

JDRF

Riley Children’s Foundation

Publisher

American Diabetes Association

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