Geniposide protects pancreatic INS‐1E β cells from hIAPP‐induced cell damage: Potential involvement of insulin degrading‐enzyme. (10th November 2014)

• Record Type: Journal Article
• Authors: Zhang, Yonglan; Yin, Fei; Liu, Jianhui; Wang, Yanwen
• Is Part Of: Cell biology international. Volume 39:Number 4(2015)
• Page Start: 373
• Page End: 378
• Publication Date: 2014-11-10
• Subjects: cytotoxicity -- geniposide -- human islet amyloid peptide -- type 2 diabetes mellitus (T2DM); Cytology -- Periodicals; Cells -- Periodicals; 571.605
• DOI: 10.1002/cbin.10394
• Languages: English
• ISSNs: 1065-6995

Abstract

Abstract: Islet amyloid deposition is increasingly seen as a pathogenic feature of type 2 diabetes mellitus (T2DM), with the deposits containing the unique amyloidogenic peptide islet amyloid polypeptide (IAPP, also known as amylin). The fibril precursors of IAPP contribute to its cytotoxicity on pancreatic β cells and be important in causing β‐cell dysfunction in T2DM. However, the development of effective this study, inhibitors against the toxicity of IAPP has been extremely challenging. We have found that pre‐incubation with geniposide dose‐dependently prevented human IAPP (hIAPP)‐induced cell damage in INS‐1E cells, and bacitracin, an inhibitor of IDE activity, prevented significantly the protective effects of geniposide in pancreatic INS‐1E cells significantly. Geniposide induced the expression of insulin‐degrading enzyme (IDE), a key degrading protein of hIAPP, but had no significant effect on the aggregation of hIAPP. These findings indicate that geniposide prevents hIAPP‐induced cytotoxicity in INS‐1E cells involving upregulation of IDE expression.