Related Experiment Video
Updated: May 7, 2026

Observing Islet Function and Islet-Immune Cell Interactions in Live Pancreatic Tissue Slices
Published on: April 12, 2021
Expression of mesenchymal and α-cell phenotypic markers in islet β-cells in recently diagnosed diabetes
Michael G White1, Helen L Marshall, Rebecca Rigby
1Corresponding author: James A.M. Shaw, jim.shaw@ncl.ac.uk.
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 glucagon, and vimentin and glucagon were demonstrated in all cases. These phenotypes were not present in nondiabetic control subjects.
Conclusions:
Coexpression of mesenchymal and α-cell phenotypic markers in human diabetic islet β-cells has been confirmed, providing circumstantial evidence for β-cell dedifferentiation and possible reprogramming to α-cells in clinical diabetes.
Related Concept Videos
Type I Diabetes II: Pathophysiology
Type I Diabetes I: Introduction
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
Insulin and C-peptide are co-secreted in...
Type II Diabetes II: Pathophysiology
Type II Diabetes Mellitus III: Clinical Manifestations and Diagnosis
Type I Diabetes III: Clinical Manifestations

