Islet Inflammation and Fibrosis in a Spontaneous Model of Type 2 Diabetes, the GK Rat-Reference-Cited by-同舟云学术

Islet Inflammation and Fibrosis in a Spontaneous Model of Type 2 Diabetes, the GK Rat

Published:2006-06-01 Issue:6 Volume:55 Page:1625-1633
ISSN:0012-1797
Container-title:Diabetes
language:en
Short-container-title:

Author:

Homo-Delarche Françoise¹,Calderari Sophie¹,Irminger Jean-Claude²,Gangnerau Marie-Noëlle¹,Coulaud Josiane¹,Rickenbach Katharina²,Dolz Manuel¹,Halban Philippe²,Portha Bernard¹,Serradas Patricia¹

Affiliation:

1. Unité Mixte de Recherche 7059, National Center for Scientific Research, Diderot University, Paris, France

2. Department of Genetic Medecine and Development, University Medical Center, Geneva, Switzerland

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.

Publisher

American Diabetes Association

Subject

Endocrinology, Diabetes and Metabolism,Internal Medicine

Link

https://journals.org/diabetes/diabetes/article-pdf/55/6/1625/660665/zdb00606001625.pdf

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