BME Seminar - Wed., Sept. 18

Event Date: September 18, 2013
Time: 9:30-10:20 a.m.
Location: MJIS 1001, WL campus
Debbie C. Thurmond, Ph.D., Associate Director of Basic Diabetes Research Group, Herman B. Wells Center for Pediatric Research and Professor of Biochemistry & Molecular Biology and Cellular & Integrative Physiology will present a seminar entitled "Exploiting Syntaxin 4 to increase beta-cell function for diabetes treatment" on Wednesday, September 16th, at 9:30 a.m. in MJIS 1001.

(The seminar will be teleconferenced to SL-220 at IUPUI.)

ABSTRACT: Type 1 diabetes has an incidence rate of about 30,000 annual cases in the USA and is characterized by the declining function and loss of the insulin-producing β cells of the islet resulting in a need for life-long insulin replacement therapy.  Current treatment of T1D patients for hyperglycemia involves insulin injection, however this treatment results in constant non-regulated insulin delivery, which fails to mimic the body’s native pattern of insulin delivery.  As a result, hypoglycemic episodes are a significant health hazard in T1D.  Islet transplantation is an exciting alternative to insulin injection, although one major constraint is that each transplant requires islets from several donors.  Evidence suggests that β cells become less efficient and exhibit dysfunction early in the disease progression of T1D.  Indeed, even modest β cell function at entry in the Diabetes Control and Complications Trial correlated with reduced incidences of retinopathy, nephropathy and hypoglycemic complications.  For these reasons there is great interest in developing strategies to enhance insulin secretory function from the patient’s residual β cells, and for transplantation success to ‘build a more efficient β cell’, so that fewer islets would be required per patient.  Toward these goals for a restorative/cure, we have investigated the potential for enrichment of a protein crucial for the regulated release of insulin from the β cell, named ‘Syntaxin 4’.  Syntaxin 4 resides at the surface of the β cell to facilitate insulin release – our recent studies show that the cellular content of Syntaxin 4 correspondingly improves the function of the β cell, making each cell more efficient.  Syntaxin 4 enrichment can also restore malfunctioning islets from diabetic humans to normal in the petri dish.  Our goals for this project are to determine the mechanism by which Syntaxin 4 enrichment exerts these beneficial effects, and whether it is a safe and effective means to prevent and/or treat type 1 diabetes in living mammals.  Another exciting prospect of this project is the possible use of Syntaxin 4 abundance as a biomarker of pre-clinical type 1 diabetes.  Our pilot studies show an association between the incidence of type 1 diabetes and attenuated Syntaxin 4 levels in blood-borne platelets.  Thus our goal is to build upon this finding to determine if Syntaxin 4 could be useful as a screen for pre-clinical type 1 diabetes, which could ultimately be remedied by Syntaxin 4 enrichment therapies to preserve and restore function to the body’s own β cells.

~BME Faculty Hosts: Alyssa Panitch and Jenna Rickus~

***Coffee and juice will be provided at West Lafayette***