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Samuel Stephens, PhD

Assistant Professor
Internal Medicine

Office: 3334 PBDB
Office Phone: 319-335-4843

Lab: 3400 PBDB

Lab Website: https://stephens.lab.uiowa.edu/

My lab studies mechanisms contributing to the loss of nutrient-regulated insulin secretion from pancreatic islet beta-cells in Type 2 diabetes.

Pancreatic islet β-cells are central regulators of whole animal fuel metabolism, coupling nutritional demands and uptake with insulin release. In Type 2 diabetes (T2D), the loss of nutrient-regulated insulin secretion is well-defined as a key event in the transition from the prediabetic state (insulin resistance) to overt diabetes (chronic hyperglycemia); however, the cellular mechanisms leading to β-cell dysfunction are not completely understood, yet could have considerable therapeutic value if β-cell function could be restored. My lab is focused on understanding fundamental aspects of islet β-cell function and survival with the long-term strategy of restoring normal (appropriate) islet hormone release as an effective diabetes treatment. My lab explores 2 broad topic areas relevant to the pancreatic islet as follows: (i) understand the molecular mechanisms regulating insulin trafficking in the β-cell; and (ii) explore the mechanisms contributing to dysregulation of insulin trafficking in the context of human diabetes. To do this, we take a multi-disciplinary approach using genetic mouse models, ex vivo (rodent and human) islet cell culture, and islet transplantation strategies. Our current work is focused on understanding defects in the secretory pathway that contribute to β-cell dysfunction in T2D, with a strong interest in Golgi function and secretory granule formation using imaging techniques (confocal microscopy and TIRF) and genetically encoded biosensors developed by my lab to monitor insulin trafficking.

PubMed link

Department/Program Affiliations:
Internal Medicine
Molecular Medicine