| Morphofunctional changes underlying intestinal dysmotility in diabetic RIP-I/hIFNβ transgenic mice. | |
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MedLine Citation:
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PMID: 22050417 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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The pathogenetic mechanisms underlying gastrointestinal dysmotility in diabetic patients remain poorly understood, although enteric neuropathy, damage to interstitial cells of Cajal (ICC) and smooth muscle cell injury are believed to play a role. The aim of this study was to investigate the morphological and functional changes underlying intestinal dysmotility in RIP-I/hIFNβ transgenic mice treated with multiple very low doses of streptozotocin (20 mg/kg, i.p., 5 days). Compared with vehicle-treated mice, streptozotocin-treated animals developed type 1 diabetes mellitus, with sustained hyperglycaemia for 3.5 months, polyphagia, polydipsia and increased faecal output without changes in faecal water content (metabolic cages). Diabetic mice had a longer intestine, longer ileal villi and wider colonic crypts (conventional microscopy) and displayed faster gastric emptying and intestinal transit. Contractility studies showed selective impaired neurotransmission in the ileum and mid-colon of diabetic mice. Compared with controls, the ileal and colonic myenteric plexus of diabetic mice revealed ultrastructural features of neuronal degeneration and HuD immunohistochemistry on whole-mount preparations showed 15% reduction in neuronal numbers. However, no immunohistochemical changes in apoptosis-related markers were noted. Lower absolute numbers of neuronal nitric oxide synthase- and choline acetyltransferase-immunopositive neurons and enhanced vasoactive intestinal polypeptide and substance P immunopositivity were observed. Ultrastructural and immunohistochemical analyses did not reveal changes in the enteric glial or ICC networks. In conclusion, this model of diabetic enteropathy shows enhanced intestinal transit associated with intestinal remodelling, including neuroplastic changes, and overt myenteric neuropathy. Such abnormalities are likely to reflect neuroadaptive and neuropathological changes occurring in this diabetic model. |
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Authors:
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Anna Domènech; Gianandrea Pasquinelli; Roberto De Giorgio; Alessandra Gori; Fàtima Bosch; Martí Pumarola; Marcel Jiménez |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-11-3 |
Journal Detail:
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Title: International journal of experimental pathology Volume: - ISSN: 1365-2613 ISO Abbreviation: - Publication Date: 2011 Nov |
Date Detail:
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Created Date: 2011-11-4 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9014042 Medline TA: Int J Exp Pathol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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© 2011 The Authors. International Journal of Experimental Pathology © 2011 International Journal of Experimental Pathology. |
Affiliation:
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Department of Animal Medicine and Surgery, Universitat Autònoma de Barcelona, Bellaterra, Spain Department of Radiological and Histocytopathological Sciences, Ospedale St.Orsola-Malpighi, Università di Bologna, Bologna, Italy Department of Clinical Medicine, Ospedale St.Orsola-Malpighi, Università di Bologna, Bologna, Italy Center of Animal Biotechnology and Gene Therapy, Universitat Autònoma de Barcelona, Bellaterra, Spain Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, Bellaterra, Spain Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Instituto de Salud Carlos III, Barcelona, Spain. |
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