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

被引：162
|
作者：
Homo-Delarche, Francoise
Calderari, Sophie
Irminger, Jean-Claude
Gangnerau, Marie-Noelle
Coulaud, Josiane
Rickenbach, Katharina
Dolz, Manuel
Halban, Philippe
Portha, Bernard
Serradas, Patricia
机构：
[1] Univ Paris 07, CNRS, UMR 7059, F-75005 Paris, France
[2] Univ Geneva, Med Ctr, Dept Genet Med & Dev, CH-1211 Geneva, Switzerland
来源：
DIABETES | 2006年 / 55卷 / 06期
关键词：
D O I：
10.2337/db05-1526
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
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.
引用
收藏
页码：1625 / 1633
页数：9
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