Samuel Stephens, PhD

Contact Information

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

Brief description of current research:

The regulated release of the pancreatic islet hormones glucagon and insulin coordinate changes in nutrient availability during fasting/feeding to maintain whole animal nutrient status.  Chronic dysregulation of islet hormone release and loss of islet cell mass result in persistent hyperglycemia and the development of diabetes.  My research is focused on understanding fundamental aspects of islet cell function and survival with the long-term strategy of restoring normal (appropriate) islet hormone release as an effective diabetes treatment.  My laboratory explores 4 broad topic areas relevant to the pancreatic islet as follows: (i) understand the molecular mechanisms responsible for the fidelity of insulin secretory granule formation; (ii) explore the mechanisms contributing to dysregulation of secretory granule biogenesis in the context of human diabetes; (iii)  examine the generation of mitochondrial-derived coupling factors necessary to sustain fuel-stimulated insulin secretion; and (iv) investigate cell survival mechanisms utilized by pancreatic islets to circumvent apoptosis and promote cell recovery in the context of islet dysfunction.  To do this, we take a multi-disciplinary approach using genetic mouse models, ex vivo (rodent and human) islet cell culture, pharmacological tools, and cellular and molecular biology. 

3 most influential diabetes/obesity/metabolism publications:

  • Stephens SB, Edwards RJ, Sadahiro M, Lin WJ, Jiang C, Salton SR, Newgard CB. The prohormone VGF regulates β-cell function via secretory granule biogenesis. Cell Reports. 2017; 20(10):2480-2489
  • Hayes HL, Peterson BS, Haldeman JM, Newgard CB, Hohmeier HE, Stephens SB. Delayed apoptosis allows islet β-cells to implement an autophagic mechanism to promote cell survival. PLoS One. 2017; 12(2): e0172567.
  • Stephens SB, Schisler JC, Hohmeier HE, An J, Sun AY, Pitt GS, and Newgard CB. A VGF-derived peptide attenuates development of type 2 diabetes via enhancement of islet β-cell survival and function. Cell Metabolism. 2012; 16(1):33-43


“Over and over again, scientific discoveries have provided answers to problems that had no apparent connection with the phenomena that gave rise to the discovery.” -Isaac Asimov