Scientific article
English

Islet inflammation and fibrosis in a spontaneous model of type 2 diabetes, the GK rat

Published inDiabetes, vol. 55, no. 6, p. 1625-1633
Publication date2006
Abstract

The molecular pathways leading to islet fibrosis in diabetes are unknown. Therefore, we studied gene expression in islets of 4-month-old Goto-Kakizaki (GK) and Wistar control rats. Of 71 genes found to be overexpressed in GK islets, 24% belong to extracellular matrix (ECM)/cell adhesion and 34% to inflammatory/immune response families. Based on gene data, we selected several antibodies to study fibrosis development during progression of hyperglycemia by immunohistochemistry. One-month-old GK and Wistar islets appeared to be similar. Two-month-old GK islets were strongly heterogenous in terms of ECM accumulation compared with Wistar islets. GK islet vascularization, labeled by von Willebrand factor, was altered after 1 month of mild hyperglycemia. Numerous macrophages (major histocompatibility complex class II(+) and CD68(+)) and granulocytes were found in/around GK islets. These data demonstrate that marked inflammatory reaction accompanies GK islet fibrosis and suggest that islet alterations in this nonobese model of type 2 diabetes develop in a way reminiscent of microangiopathy.

Keywords
  • Animals
  • Cell Adhesion/genetics
  • Diabetes Mellitus, Type 2/genetics/metabolism/ pathology
  • Disease Models, Animal
  • Extracellular Matrix/metabolism
  • Fibrosis
  • Gene Expression Profiling
  • Hyperglycemia/genetics/metabolism/pathology
  • Immunohistochemistry
  • Inflammation/genetics/immunology/metabolism
  • Islets of Langerhans/immunology/metabolism/ pathology
  • Macrophages/metabolism/pathology
  • Male
  • Oligonucleotide Array Sequence Analysis
  • Rats
  • Rats, Wistar
  • Reverse Transcriptase Polymerase Chain Reaction
Citation (ISO format)
HOMO-DELARCHE, Francoise et al. Islet inflammation and fibrosis in a spontaneous model of type 2 diabetes, the GK rat. In: Diabetes, 2006, vol. 55, n° 6, p. 1625–1633. doi: 10.2337/db05-1526
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Identifiers
Journal ISSN0012-1797
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