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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

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

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.[1]

References

  1. Islet Inflammation and Fibrosis in a Spontaneous Model of Type 2 Diabetes, the GK Rat. Homo-Delarche, F., Calderari, S., Irminger, J.C., Gangnerau, M.N., Coulaud, J., Rickenbach, K., Dolz, M., Halban, P., Portha, B., Serradas, P. Diabetes (2006) [Pubmed]
 
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