ArticleEndocrinology2013
Essential elements for glucosensing by gastric vagal afferents: immunocytochemistry and electrophysiology studies in the rat.
Article in Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Gut instincts: Multi-level control and neural pathways involved in gastrointestinal interoception.Autonomic neuroscience : basic & clinical · 2026Review
- The critical role of gut-brain signalling in eating behaviour and obesity.Nature reviews. Gastroenterology & hepatology · 2026Review
- The Vagus Nerve Regulates Immunometabolic Homeostasis in the Ovine Fetus near Term: The Impact on Terminal Ileum.Biology · 2024Article
- Autonomic control of energy balance and glucose homeostasis.Experimental & molecular medicine · 2022Review
- The physiological control of eating: signals, neurons, and networks.Physiological reviews · 2022 · on this mapArticle
- Intact vagal gut-brain signalling prevents hyperphagia and excessive weight gain in response to high-fat high-sugar diet.Acta physiologica (Oxford, England) · 2021Article
- Deletion of the insulin receptor in sensory neurons increases pancreatic insulin levels.Experimental neurology · 2018Article
- Distinct Expression of Phenotypic Markers in Placodes- and Neural Crest-Derived Afferent Neurons Innervating the Rat Stomach.Digestive diseases and sciences · 2018Article
- High glucose increases action potential firing of catecholamine neurons in the nucleus of the solitary tract by increasing spontaneous glutamate inputs.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Plasticity of vagal afferent signaling in the gut.Medicina (Kaunas, Lithuania) · 2017Review
- KATP channels in the nodose ganglia mediate the orexigenic actions of ghrelin.The Journal of physiology · 2015Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Glucosensing nodose ganglia neurons mediate the effects of hyperglycemia on gastrointestinal motility. We hypothesized that the glucose-sensing mechanisms in the nodose ganglia are similar to those of hypothalamic glucose excited neurons, which sense glucose through glycolysis. Glucose metabolism leads to ATP-sensitive potassium channel (K(ATP)) channel closure and membrane depolarization. We identified glucosensing elements in the form of glucose transporters (GLUTs), glucokinase (GK), and K(ATP) channels in rat nodose ganglia and evaluated their physiological significance. In vitro stomach-vagus nerve preparations demonstrated the gastric vagal afferent response to elevated glucose. Western blots and RT-PCR revealed the presence of GLUT1, GLUT3, GLUT4, GK, and Kir6.2 in nodose ganglia neurons and gastric branches of the vagus nerve. Immunocytochemistry confirmed the expression of GLUT3, GK, and Kir6.2 in nodose ganglia neurons (46.3 ± 3%). Patch-clamp studies detected glucose excitation in 30% (25 of 83) of gastric-projecting nodose ganglia neurons, which was abolished by GLUT3 or GK short hairpin RNA transfections. Silencing GLUT1 or GLUT4 in nodose ganglia neurons did not prevent the excitatory response to glucose. Elevated glucose elicited a response from 43% of in vitro nerve preparations. A dose-dependent response was observed, reaching maximum at a glucose level of 250 mg/dl. The gastric vagal afferent responses to glucose were inhibited by diazoxide, a K(ATP) channel opener. In conclusion, a subset of neurons in the nodose ganglia and gastric vagal afferents are glucoresponsive. Glucosensing requires a GLUT, GK, and K(ATP) channels. These elements are transported axonally to the gastric vagal afferents, which can be activated by elevated glucose through modulation of K(ATP) channels.
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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.