ArticleGastroenterology2017
Hyperglycemia Increases Interstitial Cells of Cajal via MAPK1 and MAPK3 Signaling to ETV1 and KIT, Leading to Rapid Gastric Emptying.
Article in Gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 74 citations in OpenAlex.
- Investigating the role of IGF-1 in diabetic gastroparesis: a preliminary review.Acta diabetologica · 2026Review
- Enhanced Spatial Mapping of Mouse Gastric Muscle Layers Using a Modified Swiss Roll Technique.Journal of visualized experiments : JoVE · 2025Article
- Obesity induces phenotypic switching of gastric smooth muscle cells through the activation of the PPARD/PDK4/ANGPTL4 pathway.Journal of biomedical science · 2025Article
- Effects of DA-9701 (motilitone®) on gastric emptying, glycemic control, and oxidative stress in diabetic rats.PloS one · 2025Article
- Investigation of the Pharmacodynamic Components ofInternational journal of molecular sciences · 2024Article
- Gastrointestinal Dysmotility Predisposes to Colitis through Regulation of Gut Microbial Composition and Linoleic Acid Metabolism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Common Pathophysiological Mechanisms and Treatment of Diabetic Gastroparesis.Journal of neurogastroenterology and motility · 2024Review
- Role of mechanoregulation in mast cell-mediated immune inflammation of the smooth muscle in the pathophysiology of esophageal motility disorders.American journal of physiology. Gastrointestinal and liver physiology · 2024Review
- Protocol for gene knockdown using siRNA in organotypic cultures of murine gastric muscle.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2024Article
- Plasticity of colonic enteric nervous system following spinal cord injury in male and female rats.Neurogastroenterology and motility · 2023Article
- Review
- Late dumping syndrome preceded by Coxsackievirus B4 infection and cholecystectomy.Journal of surgical case reports · 2023Article
- Tracking Gut Motility in Organ and Cultures.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Gene Networks of Hyperglycemia, Diabetic Complications, and Human Proteins Targeted by SARS-CoV-2: What Is the Molecular Basis for Comorbidity?International journal of molecular sciences · 2022Article
- The Antiemetic Mechanisms of Gingerols against Chemotherapy-Induced Nausea and Vomiting.Evidence-based complementary and alternative medicine : eCAM · 2022Review
- Article
- High-fat Diet Enhances Gastric Contractility, but Abolishes Nesfatin-1-induced Inhibition of Gastric Emptying.Journal of neurogastroenterology and motility · 2021Article
- Xiangbinfang granules enhance gastric antrum motilityWorld journal of gastroenterology · 2021Article
- Wnt-induced, TRP53-mediated Cell Cycle Arrest of Precursors Underlies Interstitial Cell of Cajal Depletion During Aging.Cellular and molecular gastroenterology and hepatology · 2021Article
- Supplementation of 17β-Estradiol Normalizes Rapid Gastric Emptying by Restoring Impaired Nrf2 and nNOS Function in Obesity-Induced Diabetic Ovariectomized Mice.Antioxidants (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
23 authors at 3 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsDepletion of interstitial cells of Cajal (ICCs) is common in diabetic gastroparesis. However, in approximately 20% of patients with diabetes, gastric emptying (GE) is accelerated. GE also occurs faster in obese individuals, and is associated with increased blood levels of glucose in patients with type 2 diabetes. To understand the fate of ICCs in hyperinsulinemic, hyperglycemic states characterized by rapid GE, we studied mice with mutation of the leptin receptor (Lepr
methodsMice were given breath tests to analyze GE of solids. ICCs were studied by flow cytometry, intracellular electrophysiology, isometric contractility measurement, reverse-transcription polymerase chain reaction, immunoblot, immunohistochemistry, enzyme-linked immunosorbent assays, and metabolite assays; cells and tissues were manipulated pharmacologically and by RNA interference. Viable cell counts, proliferation, and apoptosis were determined by methyltetrazolium, Ki-67, proliferating cell nuclear antigen, bromodeoxyuridine, and caspase-Glo 3/7 assays. Sdhc was disrupted in 2 different strains of mice via cre recombinase.
resultsIn obese, hyperglycemic, hyperinsulinemic female Lepr
conclusionsHyperglycemia increases ICCs via oxidative metabolism-dependent, MAPK1- and MAPK3-mediated stabilization of ets variant 1 and increased expression of KIT, causing rapid GE. Increases in ICCs might contribute to the acceleration in GE observed in some patients with diabetes.
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Registered trials
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