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Articles in PresS, published online ahead of print October 31, 2001
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00323.2001
Submitted on July 23, 2001
Accepted on October 18, 2001
1 Third Department of Internal Medicine, University of Occupational and Environmental Health, Japan, School of Medicine, Kitakyushu, Fukuoka, Japan
* To whom correspondence should be addressed. E-mail: mac-otsk{at}med.uoeh-u.ac.jp.
The recently established Otsuka Long-Evans Tokushima Fatty (OLETF) rat, a model of naturally occurring obesity-diabetes, exhibits progressive accumulation of connective tissue in the pancreas. The present study was designed to determine the pathogenic role of transforming growth factor-ß1 (TGF-ß1) in the development of pancreatic fibrosis in OLETF rats by investigating the serial changes in the expression of TGF-ß1 and extracellular matrix (ECM) in the pancreas. The progressive proliferation of connective tissue arose from interstitial region surrounding islets at 20 weeks of age, and extended to the exocrine pancreas adjacent to the islets. TGF-ß1 mRNA levels in OLETF rats markedly increased at 20 weeks and reached a peak value at 30 weeks of age. Fibronectin (FN), and procollagen types I and III mRNAs peaked at 20 weeks of age, and remained at higher levels than those in the non-diabetic counterparts Long-Evans Tokushima Otsuka (LETO) rats until 50 weeks of age. Immunoreactivities for TGF-ß1 and FN were found in islets of OLETF rats at 20 weeks of age, and were seen in acinar and interstitial cells at 50 weeks of age. TGF-ß1 protein was also found in inflammatory cells. Moreover, immunoreactivity for 
smooth muscle actin was located at the interstitial region surrounding islets. Proliferation of the connective tissue in the pancreas of OLETF rat closely correlated with the expression of TGF-ß1 and ECM. Our results suggest that the development of pancreatic fibrosis in OLETF rat extends from endocrine to exocrine pancreas, and that TGF-ß1 is involved in pancreatic fibrosis of OLETF rats. TGF-ß1 may promote the accumulation of ECM, resulting in pancreatic fibrosis.
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