Kelle H. Moley, MD
Photo: Kelle Harbert Moley

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Elected 2005
From animal and human studies it is clear that mammalian embryos are vulnerable to injury during the pre-implantation stages of development. Glucose transport and metabolism are critical for blastocyst formation and further development. The primary focus of my laboratory is how early pre-implantation glucose transport and metabolism affect the fate and outcome of pregnancy at a molecular level. Glucose enters the blastocyst via one of several facilitative glucose transporters, GLUT1-3, and the novel transporters GLUT8 and GLUT9 which we recently cloned. We have shown that maternal hyperglycemia leads to down regulation of GLUT1-3 at the blastocyst stage in the mouse and that this event triggers apoptosis via pathways involving BAX, p53, TRAIL and caspases. We have also shown that, in the diabetic state, this increase in apoptosis results in fetal resorption or malformations. Both these adverse pregnancy outcomes are more common in diabetic women. One focus of my lab is how decreased intracellular glucose triggers apoptosis and how this manifests as pregnancy loss or malformation. We have also demonstrated that hyperinsulinemia and high IGF-1 levels, associated with polycystic ovary syndrome, lead to decreased insulin-stimulated glucose transport and increased apoptosis at a blastocyst stage. We are interested in how GLUT8, the only known insulin-regulated GLUT at this stage, and the insulin signaling pathways in the mouse are involved in apoptosis, blastocyst development and metabolism. Dysregulation of this transporter is responsible for apoptosis at this stage and thus may be related to the increased miscarriage rate experienced by these women.

Honors / awards

National Academy of Medicine (2014)