Dysfunction of insulin producing pancreatic beta cells – The Central Problem in Diabetes – UROP Spring Symposium 2022

Dysfunction of insulin producing pancreatic beta cells – The Central Problem in Diabetes

photo of presenter

Weina Cheng

Pronouns: she/her

Research Mentor(s): Mehboob Hussain
Co-Presenter:
Research Mentor School/College/Department: Internal Medicine, Metabolism, Endocrinology, Diabetes / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 2 – 11am – 11:50am
Room: League Ballroom
Authors:
Presenter: 87

Abstract

Diabetes Mellitus is a worldwide disease of epidemic proportions. Failure of pancreatic beta-cells to produce sufficient insulin to meet metabolic demands is a central component in the pathogenesis of diabetes. Our goal is to understand the molecular mechanisms underlying beta- cell dysfunction and failure. A central aspect of our studies is the observation the incretin hormone action becomes defective in diabetes mellitus. Therefore, we focus our studies on incretin hormone signaling pathways in beta-cells using genetically engineered mouse models (based on Cre/LoxP technology), immortalized cell models as well as isolated mouse and human islets. Diabetes mellitus is associated with low level inflammation with inflammation cytokines being produced in adipose tissue but also locally in the pancreatic islets of Langerhans. Thus, currently the laboratory is examining how inflammatory mediators alter beta-cell function as well as incretin hormone action in beta cells. A critical component for these studies is to have a a reliable and efficient means to identify mutant mice from normal, wild type mice. We use PCR-based genotyping techniques to positively identify mutations in mice. This methodology can also be used to identify genetically engineered cells models that we generate using CRISPR/Cas9 techniques. We are establishing mouse models that lack tumor necrosis factor a receptors in pancreatic beta cells. We are examining whether mice lacking TNFa receptors on beta cells will be resistant to diabetes mellitus when under diet-induced obesity. My contribution to the work will be in participating in the genotype analysis of the mice, participating in generating diet induced obese by feeding high fat/high sucrose content diet to the mice and analyzing tissue samples from these mice using immunohistological techniques

Presentation link

Biomedical Sciences, Interdisciplinary, Natural/Life Sciences

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