ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2008
Gastric relaxation induced by hyperglycemia is mediated by vagal afferent pathways in the rat.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Pooled it
- Article
- Current Concepts in Gastroparesis and Gastric Neuromuscular Disorders-Pathophysiology, Diagnosis, and Management.Diagnostics (Basel, Switzerland) · 2025Review
- Impact of Vagotomy on Postoperative Weight Loss, Alimentary Intake, and Enterohormone Secretion After Bariatric Surgery in Experimental Translational Models.Obesity surgery · 2022Article
- Evidence that hindbrain astrocytes in the rat detect low glucose with a glucose transporter 2-phospholipase C-calcium release mechanism.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- MicroRNA 375 modulates hyperglycemia-induced enteric glial cell apoptosis and Diabetes-induced gastrointestinal dysfunction by targeting Pdk1 and repressing PI3K/Akt pathway.Scientific reports · 2018Article
- Response of catecholaminergic neurons in the mouse hindbrain to glucoprivic stimuli is astrocyte dependent.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- 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
- High fat diet attenuates glucose-dependent facilitation of 5-HT3 -mediated responses in rat gastric vagal afferents.The Journal of physiology · 2016Article
- Central nervous system control of gastrointestinal motility and secretion and modulation of gastrointestinal functions.Comprehensive Physiology · 2014Review
- Mapping glucose-mediated gut-to-brain signalling pathways in humans.NeuroImage · 2014Article
- MicroRNA 375 mediates palmitate-induced enteric neuronal damage and high-fat diet-induced delayed intestinal transit in mice.Gastroenterology · 2014Article
- Melanocortin signaling in the brainstem influences vagal outflow to the stomach.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Modulation of gastrointestinal vagal neurocircuits by hyperglycemia.Frontiers in neuroscience · 2013Article
- Essential elements for glucosensing by gastric vagal afferents: immunocytochemistry and electrophysiology studies in the rat.Endocrinology · 2013Article
- The Neural Mechanism by Which the Dorsal Vagal Complex Mediates the Regulation of the Gastric Motility by Weishu (RN12) and Zhongwan (BL21) Stimulation.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- Glucose-dependent trafficking of 5-HT3 receptors in rat gastrointestinal vagal afferent neurons.Neurogastroenterology and motility · 2012Article
- Severe intestinal ischemia can trigger cardiovascular collapse and sudden death via a parasympathetic mechanism.Shock (Augusta, Ga.) · 2011Article
- Plasticity of vagal brainstem circuits in the control of gastrointestinal function.Autonomic neuroscience : basic & clinical · 2011Review
- Inhibition of gastric motility by hyperglycemia is mediated by nodose ganglia KATP channels.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hyperglycemia has a profound effect on gastric motility. However, little is known about the site and mechanism that sense alteration in blood glucose level. The identification of glucose-sensing neurons in the nodose ganglia led us to hypothesize that hyperglycemia acts through vagal afferent pathways to inhibit gastric motility. With the use of a glucose-clamp rat model, we showed that glucose decreased intragastric pressure in a dose-dependent manner. In contrast to intravenous infusion of glucose, intracisternal injection of glucose at 250 and 500 mg/dl had little effect on intragastric pressure. Pretreatment with hexamethonium, as well as truncal vagotomy, abolished the gastric motor responses to hyperglycemia (250 mg/dl), and perivagal and gastroduodenal applications of capsaicin significantly reduced the gastric responses to hyperglycemia. In contrast, hyperglycemia had no effect on the gastric contraction induced by electrical field stimulation or carbachol (10(-5) M). To rule out involvement of serotonergic pathways, we showed that neither granisetron (5-HT(3) antagonist, 0.5 g/kg) nor pharmacological depletion of 5-HT using p-chlorophenylalanine (5-HT synthesis inhibitor) affected gastric relaxation induced by hyperglycemia. Lastly, N(G)-nitro-L-arginine methyl ester (L-NAME) and a VIP antagonist each partially reduced gastric relaxation induced by hyperglycemia and, in combination, completely abolished gastric responses. In conclusion, hyperglycemia inhibits gastric motility through a capsaicin-sensitive vagal afferent pathway originating from the gastroduodenal mucosa. Hyperglycemia stimulates vagal afferents, which, in turn, activate vagal efferent cholinergic pathways synapsing with intragastric nitric oxide- and VIP-containing neurons to mediate gastric relaxation.
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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.