Poster Presentation by Ashley Turnage
Sophomore, Chemical and Biological Engineering
Author: Gabriel Ibanez, Senior, Quantitative Biosciences and Engineering
Mentor: Susanta Sarkar, Physics
Abstract:
Insulin resistance, i.e., dysregulation of insulin-mediated glucose metabolism in tissues, particularly in muscle, fat, and liver, leads to diabetes. About 38.0% of adults ages 18 or above have prediabetes, and 11.3% of the total population has diabetes in the United States. The biological network related to insulin resistance involves many proteins, including insulin receptor (IR). In this context, the reduced tyrosine kinase activity of IR and decreased cell surface IR presentation are two key mechanisms that scientists link to insulin resistance. Based on the literature and our preliminary experiments, we hypothesize that matrix metalloproteases (MMPs) fragment IR and prevent insulin from binding IR. Degradation of IRs expedites the dysregulation of insulin-mediated glucose metabolism, ultimately causing diabetes. If we can identify the fragmentation of IRs by MMP1, the most studied MMP, then we can modulate MMP activity by changing its dynamics using allosteric ligands. We will quantify the degradation of IR by MMP1 under different experimental conditions.