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Keywords
Diabetes, beta-cell death, metabolites, glucolipotoxicity, pro-inflammatory cytokines
Abstract
The pathogenesis of type 1 (T1D) and type 2 diabetes (T2D) is associated with progressive beta-cell death and loss of insulin secretion, making functional betacell mass preservation a priority in the treatment of diabetes. T1D beta-cell death is primarily mediated by autoimmune exposure of beta-cells to proinflammatory cytokines such as IL-1b, TNFa, and IFNg (1, 2). Beta-cell loss in T2D, however, is characterized by damage caused by a destructive metabolic state of persistent hyperglycemia and elevated free fatty acid (FFA) levels (2, 3). Our lab has shown that the monomeric flavonoid epicatechin and its metabolites hippuric acid, homovanillic acid, and 5-phenylvaleric acid enact diverse beneficial effects on beta-cell viability, including reduction of oxidative stress and increased mitochondrial respiration, both important sites of intervention in the prevention of beta-cell death (5). This study aims to explore potential protective effects of epicatechin and its gut bacteria derived metabolites against cytokine or glucolipotoxic (GLT) mediated beta-cell death. This study’s findings will have important implications for differing therapeutic approaches to T1D and T2D, as well as insight regarding potential areas of intervention against both major antagonists of beta-cell death.
BYU ScholarsArchive Citation
Bench, Aubree and Tessem, Jeffery S., "The Effect of Epicatechin and its Microbial Metabolites on Differing Pathways of Beta-Cell Death in Type I and Type II Diabetes" (2024). Library/Life Sciences Undergraduate Poster Competition 2024. 4.
https://scholarsarchive.byu.edu/library_studentposters_2024/4
Document Type
Poster
Publication Date
2024-03-21
Language
English
College
Life Sciences
Department
Nutrition, Dietetics, and Food Science
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