Session 2F: The Effect of High Mobility Group Box 1 Protein on Oxidative Stress and Subsequent Type 2 Diabetes in the Gut

Session Number

Session 2F: 2nd Presentation

Advisor(s)

Eugene Chang, University of Chicago

Location

Room A115

Start Date

28-4-2017 10:00 AM

End Date

28-4-2017 11:15 AM

Abstract

The majority of glutathione, an important antioxidant, appears in the body in its reduced form (GSH), with 10% appearing in its oxidized form of glutathione disulfide (GSSG). A deficiency in glutathione results in oxidative stress and plays a major role in the pathogenesis of type 2 diabetes. Furthermore, oxidative stress is an important cause of intestinal epithelial cell death. High mobility group box 1 protein (HMGB1) has been shown to mitigate disease and inhibit apoptosis. This investigation sought to determine the effect of HMGB1 on oxidative stress in the gut to determine HMGB1’s role in the pathogenesis of type 2 diabetes. The oxidative stress of HMGB1 f/f and HMGB1 f/f vil-CRE mice was measured using a GSH/GSSG ratio assay kit on ileal mucosal scrapings, cecal contents, stoop samples, and tissue taken from the liver. Future investigations could investigate the role of HMGB1 in conjunction with diet by also using mice that are fed either a high fat diet or a regular chow diet.

Comments

Additional team members: Dr. Jeannette Messer, Dr. Xiaorong Zhu, and Noelle Patno

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Apr 28th, 10:00 AM Apr 28th, 11:15 AM

Session 2F: The Effect of High Mobility Group Box 1 Protein on Oxidative Stress and Subsequent Type 2 Diabetes in the Gut

Room A115

The majority of glutathione, an important antioxidant, appears in the body in its reduced form (GSH), with 10% appearing in its oxidized form of glutathione disulfide (GSSG). A deficiency in glutathione results in oxidative stress and plays a major role in the pathogenesis of type 2 diabetes. Furthermore, oxidative stress is an important cause of intestinal epithelial cell death. High mobility group box 1 protein (HMGB1) has been shown to mitigate disease and inhibit apoptosis. This investigation sought to determine the effect of HMGB1 on oxidative stress in the gut to determine HMGB1’s role in the pathogenesis of type 2 diabetes. The oxidative stress of HMGB1 f/f and HMGB1 f/f vil-CRE mice was measured using a GSH/GSSG ratio assay kit on ileal mucosal scrapings, cecal contents, stoop samples, and tissue taken from the liver. Future investigations could investigate the role of HMGB1 in conjunction with diet by also using mice that are fed either a high fat diet or a regular chow diet.