HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Homo-Delarche, F. Articles by Serradas, P. Search for Related Content PubMed PubMed Citation Articles by Homo-Delarche, F. Articles by Serradas, P. Social Bookmarking                What's this?

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

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

Address correspondence and reprint requests to Francoise Homo-Delarche, CNRS UMR 7059, Université Paris 7/D. Diderot, 2, place Jussieu, 75005 Paris, France. E-mail: francoise.homo-delarche{at}paris7.jussieu.fr

Abbreviations: ECM, extracellular matrix; MHC, major histocompatibility complex; vWF, von Willebrand factor

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.

CiteULike    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				J. A. Ehses, A. Perren, E. Eppler, P. Ribaux, J. A. Pospisilik, R. Maor-Cahn, X. Gueripel, H. Ellingsgaard, M. K.J. Schneider, G. Biollaz, et al. Increased Number of Islet-Associated Macrophages in Type 2 Diabetes Diabetes, September 1, 2007; 56(9): 2356 - 2370. [Abstract] [Full Text] [PDF]

				H. Ghanaat-Pour, Z. Huang, M. Lehtihet, and A. Sjoholm Global expression profiling of glucose-regulated genes in pancreatic islets of spontaneously diabetic Goto-Kakizaki rats J. Mol. Endocrinol., August 1, 2007; 39(2): 135 - 150. [Abstract] [Full Text] [PDF]

				X. Li, L. Zhang, S. Meshinchi, C. Dias-Leme, D. Raffin, J. D. Johnson, M. K. Treutelaar, and C. F. Burant Islet Microvasculature in Islet Hyperplasia and Failure in a Model of Type 2 Diabetes Diabetes, November 1, 2006; 55(11): 2965 - 2973. [Abstract] [Full Text] [PDF]