ArticleInternational journal of experimental pathology2011
Morphofunctional changes underlying intestinal dysmotility in diabetic RIP-I/hIFNβ transgenic mice.
Article in International journal of experimental pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 44 citations in OpenAlex.
- Blunting of Colon Contractions in Diabetics with Gastroparesis Quantified by Wireless Motility Capsule Methods.PloS one · 2015Trial
- β3 Adrenoceptor Agonism Prevents Hyperoxia-Induced Colonic Alterations.Biomolecules · 2023Article
- Gut Region-Specific Interleukin 1β Induction in Different Myenteric Neuronal Subpopulations of Type 1 Diabetic Rats.International journal of molecular sciences · 2023Article
- Prucalopride might improve intestinal motility by promoting the regeneration of the enteric nervous system in diabetic rats.International journal of molecular medicine · 2022Article
- CNS-Sparing Histamine HBiomolecules · 2022Article
- CD44 fucosylation on bone marrow-derived mesenchymal stem cells enhances homing and promotes enteric nervous system remodeling in diabetic mice.Cell & bioscience · 2021Article
- Enhanced Store-Operated CaFrontiers in physiology · 2021Article
- Effect of Hyperglycemia on Purinergic and Nitrergic Inhibitory Neuromuscular Transmission in the Antrum of the Stomach: Implications for Fast Gastric Emptying.Frontiers in medicine · 2018Article
- Diabetes and the Small Intestine.Current treatment options in gastroenterology · 2017Review
- Diabetes Mellitus and the Colon.Current treatment options in gastroenterology · 2017Review
- Article
- Diabetes-induced mechanophysiological changes in the small intestine and colon.World journal of diabetes · 2017Review
- α-lipoic acid suppresses neuronal excitability and attenuates colonic hypersensitivity to colorectal distention in diabetic rats.Journal of pain research · 2017Article
- Circulating IGF-I and IGFBP3 Levels Control Human Colonic Stem Cell Function and Are Disrupted in Diabetic Enteropathy.Cell stem cell · 2015Article
- Hepatic insulin gene therapy prevents diabetic enteropathy in STZ-treated CD-1 mice.Molecular therapy. Methods & clinical development · 2015Article
- Enteric motor pattern generators involve both myogenic and neurogenic mechanisms in the human colon.Frontiers in physiology · 2015Article
- Interleukin-6 (IL-6) mediated the increased contraction of distal colon in streptozotocin-induced diabetes in rats via IL-6 receptor pathway.International journal of clinical and experimental pathology · 2015Article
- Diabetic gastrointestinal motility disorders and the role of enteric nervous system: current status and future directions.Neurogastroenterology and motility · 2014Review
- Interstitial cells of Cajal: update on basic and clinical science.Current gastroenterology reports · 2014Review
- Myosin Va but Not nNOSα is Significantly Reduced in Jejunal Musculomotor Nerve Terminals in Diabetes Mellitus.Frontiers in medicine · 2014Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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