Ontology highlight
ABSTRACT: Objective
Relative contributions of reversible β-cell dysfunction and true decrease in β-cell mass in type 2 diabetes remain unclear. Definitive rodent lineage-tracing studies have identified β-cell dedifferentiation and subsequent reprogramming to α-cell fate as a novel mechanism underlying β-cell failure. The aim was to determine whether phenotypes of β-cell dedifferentiation and plasticity are present in human diabetes.Research design and methods
Immunofluorescence colocalization studies using classical endocrine and mesenchymal phenotypic markers were undertaken using pancreatic sections and isolated islets from three individuals with diabetes and five nondiabetic control subjects.Results
Intraislet cytoplasmic coexpression of insulin and vimentin, insulin and g
SUBMITTER: White MG
PROVIDER: S-EPMC3816907 | biostudies-literature | 2013 Nov
REPOSITORIES: biostudies-literature