| Literature DB >> 25447052 |
Teresa Vanessa Fiorentino1, Michael Owston2, Gregory Abrahamian3, Stefano La Rosa4, Alessandro Marando4, Carla Perego5, Eliana S Di Cairano5, Giovanna Finzi4, Carlo Capella4, Fausto Sessa4, Francesca Casiraghi6, Ana Paez7, Ashwin Adivi8, Alberto Davalli9, Paolo Fiorina10, Rodolfo Guardado Mendoza11, Anthony G Comuzzie12, Mark Sharp2, Ralph A DeFronzo8, Glenn Halff3, Edward J Dick2, Franco Folli13.
Abstract
In this study, we aimed to evaluate the effects of exenatide (EXE) treatment on exocrine pancreas of nonhuman primates. To this end, 52 baboons (Papio hamadryas) underwent partial pancreatectomy, followed by continuous infusion of EXE or saline (SAL) for 14 weeks. Histological analysis, immunohistochemistry, Computer Assisted Stereology Toolbox morphometry, and immunofluorescence staining were performed at baseline and after treatment. The EXE treatment did not induce pancreatitis, parenchymal or periductal inflammatory cell accumulation, ductal hyperplasia, or dysplastic lesions/pancreatic intraepithelial neoplasia. At study end, Ki-67-positive (proliferating) acinar cell number did not change, compared with baseline, in either group. Ki-67-positive ductal cells increased after EXE treatment (P = 0.04). However, the change in Ki-67-positive ductal cell number did not differ significantly between the EXE and SAL groups (P = 0.13). M-30-positive (apoptotic) acinar and ductal cell number did not change after SAL or EXE treatment. No changes in ductal density and volume were observed after EXE or SAL. Interestingly, by triple-immunofluorescence staining, we detected c-kit (a marker of cell transdifferentiation) positive ductal cells co-expressing insulin in ducts only in the EXE group at study end, suggesting that EXE may promote the differentiation of ductal cells toward a β-cell phenotype. In conclusion, 14 weeks of EXE treatment did not exert any negative effect on exocrine pancreas, by inducing either pancreatic inflammation or hyperplasia/dysplasia in nonhuman primates.Entities:
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Year: 2014 PMID: 25447052 PMCID: PMC4278248 DOI: 10.1016/j.ajpath.2014.09.009
Source DB: PubMed Journal: Am J Pathol ISSN: 0002-9440 Impact factor: 4.307