Courtney Lowe
Pronouns: her/she
Research Mentor(s): Corentin Cras-Meneur
Co-Presenter:
Research Mentor School/College/Department: Internal Medicine Division of Metabolism, Endocrinology & Diabetes / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 1 – 10am – 10:50am
Room: League Ballroom
Authors: Courtney Lowe, Corentin Cras-Meneur
Presenter: 36
Abstract
Type 1 Diabetes results from an immune attack targeting the pancreatic ß-cells that produce insulin. In the absence of ß-cells, patients can no longer regulate their blood glucose and have to self-manage it lifelong through insulin injections. With the aid of prediabetic mice that have been crossed with mice bearing a fluorescent reporter on the insulin itself–allowing us to track insulin content and secretion live–we can understand what is happening to the ß-cells upon glucose stimulation in models of early onset type-1 diabetes. The main question we wanted to address here was to understand what matters most at this stage. Are the mice becoming diabeteic simply because they are losing ß-cells, or is the inflammation affecting the function of the remaining cells. The answers to these questions will guide us in the pharmaceutical approach to help patients early on. This study measures the ß-cell in a qualitative and quantitative way by anesthetizing these mice, exteriorizing the pancreas through laparotomy, and observing how their islets react during a glucose challenge. We analyze their response through a live-imaging microscope, which allows us to quantify the insulin content through fluorescent imaging. The images are acquired on a grid to recompose a high resolution mosaic. We then use morphometry analysis software to compile, tile and , and quantify the images using , background subtraction, thresholding, and particle analysis to identify each group of ß-cell and track their content over the course of the glucose challenge. At the end of the experiment, the mouse is euthanized and we can collect and image the whole pancreas. This allows us to assess both the function of individual pancreatic islets and the overall isletmass The data from various mice is presently being analyzed. Based on our preliminary data, we can say some diabetic mice seem to be impaired even before the ß-cell mass drops. This would fall in line with the goal of determining what is happening to the ß-cells. We will use the information to direct our approach on therapies for ß-cells and diabetic patients. In finding treatments that increase secretion and reduce the stress on ß-cells, we hope to slow down the onset of full blown type 1 diabetes.
Biomedical Sciences, Interdisciplinary
