ArticleCell and tissue research2015
Prolonged high fat diet ingestion, obesity, and type 2 diabetes symptoms correlate with phenotypic plasticity in myenteric neurons and nerve damage in the mouse duodenum.
Article in Cell and tissue research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 74 citations in OpenAlex.
- Postbiotic Stool Filtrates From Patients With Type 2 Diabetes Impair Mouse Intestinal Muscle Contractility Ex Vivo and Alter Enteric Cholinergic Neuronal Activity in Vivo.Neurogastroenterology and motility · 2026Article
- Central control of gastrointestinal functions in health and disease.Physiological reviews · 2026Review
- Impact of obesity on the short-term outcomes of robotic surgery for rectal cancer: a Japanese multicenter study.Surgery today · 2026Article
- Obesity-Related Oxidative Stress and Antioxidant Properties of Natural Compounds in the Enteric Nervous System: A Literature Overview.Antioxidants (Basel, Switzerland) · 2026Review
- Rewiring the Brain Through the Gut: Insights into Microbiota-Nervous System Interactions.Current issues in molecular biology · 2025Review
- Enteric neuropathy in diabetes: Implications for gastrointestinal function.World journal of gastroenterology · 2024Article
- Gastrointestinal dysfunction in the valproic acid induced model of social deficit in rats.Autonomic neuroscience : basic & clinical · 2024Article
- Impaired colonic motility in high-glycemic diet-induced diabetic mice is associated with disrupted gut microbiota and neuromuscular function.Endocrine connections · 2023Article
- Chronic early life stress alters the neuroimmune profile and functioning of the developing zebrafish gut.Brain, behavior, & immunity - health · 2023Article
- The enteric nervous system.Physiological reviews · 2023Review
- Chinese medicine, Qijudihuang pill, mediates cholesterol metabolism and regulates gut microbiota in high-fat diet-fed mice, implications for age-related macular degeneration.Frontiers in immunology · 2023Article
- High-fat diet impairs duodenal barrier function and elicits glia-dependent changes along the gut-brain axis that are required for anxiogenic and depressive-like behaviors.Journal of neuroinflammation · 2021Article
- High-fat Diet Enhances Gastric Contractility, but Abolishes Nesfatin-1-induced Inhibition of Gastric Emptying.Journal of neurogastroenterology and motility · 2021Article
- Role of Gut Microbiota on Onset and Progression of Microvascular Complications of Type 2 Diabetes (T2DM).Nutrients · 2020Review
- Role of sex hormones and their receptors on gastric Nrf2 and neuronal nitric oxide synthase function in an experimental hyperglycemia model.BMC gastroenterology · 2020Article
- High-fat diet-induced alterations to gut microbiota and gut-derived lipoteichoic acid contributes to the development of enteric neuropathy.Neurogastroenterology and motility · 2020Article
- Caspase-11-mediated enteric neuronal pyroptosis underlies Western diet-induced colonic dysmotility.The Journal of clinical investigation · 2020Article
- Microevolutionary Dynamics of Chicken Genomes under Divergent Selection for Adiposity.iScience · 2020Article
- Food, microbes, sex and old age: on the plasticity of gastrointestinal innervation.Current opinion in neurobiology · 2020Review
- Characterization of Mechanical Allodynia and Skin Innervation in a Mouse Model of Type-2 Diabetes Induced by Cafeteria-Style Diet and Low-Doses of Streptozotocin.Frontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Symptoms of diabetic gastrointestinal dysmotility indicate neuropathy of the enteric nervous system. Long-standing diabetic enteric neuropathy has not been fully characterized, however. We used prolonged high fat diet ingestion (20 weeks) in a mouse model to mimic human obese and type 2 diabetic conditions, and analyzed changes seen in neurons of the duodenal myenteric plexus. Ganglionic and neuronal size, number of neurons per ganglionic area, density indices of neuronal phenotypes (immunoreactive nerve cell bodies and varicosities per ganglion or tissue area) and nerve injury were measured. Findings were compared with results previously seen in mice fed the same diet for 8 weeks. Compared to mice fed standard chow, those on a prolonged high fat diet had smaller ganglionic and cell soma areas. Myenteric VIP- and ChAT-immunoreactive density indices were also reduced. Myenteric nerve fibers were markedly swollen and cytoskeletal protein networks were disrupted. The number of nNOS nerve cell bodies per ganglia was increased, contrary to the reduction previously seen after 8 weeks, but the density index of nNOS varicosities was reduced. Mice fed high fat and standard chow diets experienced an age-related reduction in total neurons, with bias towards neurons of sensory phenotype. Meanwhile, ageing was associated with an increase in excitatory neuronal markers. Collectively, these results support a notion that nerve damage underlies diabetic symptoms of dysmotility, and reveals adaptive ENS responses to the prolonged ingestion of a high fat diet. This highlights a need to mechanistically study long-term diet-induced nerve damage and age-related impacts on the ENS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.