The pathogenic mechanism of diabetes varies with the degree of overexpression and oligomerization of human amylin in the pancreatic islet β cells

S Zhang, Hong Liu, Chia Lin Chuang, Xiaoling Li, M Au, Lin Zhang, Anthony R. J. Phillips, David W. Scott, Garth Cooper

    Research output: Contribution to journalArticlepeer-review

    135 Downloads (Pure)

    Abstract

    The aggregation of human amylin (hA) to form cytotoxic structures has been closely associated with the causation of type 2 diabetes. We sought to advance understanding of how altered expression and aggregation of hA might link β-cell degeneration with diabetes onset and progression, by comparing phenotypes between homozygous and hemizygous hA-transgenic mice. The homozygous mice displayed elevated islet hA that correlated positively with measures of oligomer formation (r=0.91; P
    Original languageEnglish
    Article numberfj.14-251744.
    Pages (from-to)5083-5096
    Number of pages13
    JournalThe F A S E B Journal
    Volume28
    Issue number12
    DOIs
    Publication statusPublished - 19 Aug 2014

    Keywords

    • gene-dosage effect, apoptosis, peptide, aggregation, transgenic mice, insulin resistance

    Fingerprint

    Dive into the research topics of 'The pathogenic mechanism of diabetes varies with the degree of overexpression and oligomerization of human amylin in the pancreatic islet β cells'. Together they form a unique fingerprint.

    Cite this