In addition to these three professorships, Dr. Abel is also the Chair of the Department of Internal Medicine, Director of the Division of Endocrinology & Metabolism, the John B. Stokes III Chair in Diabetes Research, and the François M. Abboud Chair in Internal Medicine.

Dr. Abel earned his medical degree from the University of the West Indies, followed by a D.Phil at Oxford, where he was a Rhodes Scholar. He trained in internal medicine at Northwestern University, and then moved to Boston, where he was affiliated with Harvard and the Beth Israel Deaconess Medical Center. In 2000, he was recruited to the University of Utah. Among the many hats he wore at Utah, Dr. Abel oversaw the Metabolism Interest Group, which received a T32 grant from the NIH to train graduate students. In 2013, he moved to the University of Iowa, where he has largely focused on expanding their diabetes research program.

Platelets are the small blood cells without any nucleus. Their primary function in the body is to clot (clump together) at the site of an injury, to plug the hole. After the platelets migrate to the wound and attach to something nearby, they are “activated,” which involves a set of changes to metabolism and morphology (shape) to promote clumping. One change that occurs during platelet activation is a dramatic increase in the amount of glucose needed by the cell. In order to use this extra glucose, the platelet must also increase the amount of glucose that it is receiving from outside.

In a recent paper, Dr. Abel and colleagues investigated the role of a glucose transporter protein (GLUT3), which helps platelets take up glucose. In inactive platelets, the vast majority of the GLUT3 is inside granules (membrane-bound spheres of proteins) within the cell. When platelets are activated, the membrane of the granules fuses to the plasma membrane of the cell, which would hypothetically result in all of that sequestered GLUT3 being moved to the outer membrane of the cell — where it could increase the amount of glucose getting in. However, there are two waves of granule fusion after activation, and it was unclear how much each one contributed to the observed effect.

Using mice that had no GLUT3 specifically in their platelets, Dr. Abel and others were able to show that the movement of GLUT3 from the granules to the cell surface is definitely required for increasing the amount of glucose getting into the cell after activation. Platelets without GLUT3 had trouble clotting, being activated, and fusing their granules. In addition to the contributions to the basic science, the authors were also able to show a potential therapeutic target: the mice whose platelets had no GLUT3 had reduced symptoms of autoimmune inflammatory arthritis and survived better after a pulmonary embolism (blood clot in the lungs).