Format

Send to

Choose Destination
See comment in PubMed Commons below
Diabetes. 2006 Jun;55(6):1625-33.

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

Author information

  • 1Unité Mixte de Recherche 7059, National Center for Scientific Research, Diderot University, Paris, France. francoise.homo-delarche@paris7.jussieu.fr

Erratum in

  • Diabetes. 2006 Sep;55(9):2665.

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.

PMID:
16731824
DOI:
10.2337/db05-1526
[PubMed - indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire
    Loading ...
    Support Center