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Article Dans Une Revue Diabetes Année : 2006

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

Résumé

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.

Dates et versions

hal-02664129 , version 1 (31-05-2020)

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Citer

Françoise Homo-Delarche, Sophie Calderari, Jean-Claude Irminger, Marie-Noëlle Gangnerau, Josiane Coulaud, et al.. Islet inflammation and fibrosis in a spontaneous model of type 2 diabetes, the GK rat. Diabetes, 2006, 55 (6), pp.1625-1633. ⟨10.2337/db05-1526⟩. ⟨hal-02664129⟩
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