Glucagon-like peptide-1 inhibits gastric emptying via vagal afferent-mediated central mechanisms
Open accessAbstract
Exogenous administration of glucagon-like peptide-1-(7—36) amide (GLP-1), an insulinotropic hormone, inhibits gastric emptying and acid secretion in humans. The role of GLP-1 as a regulator of gastric function is elusive. In gastric fistula rats, vagal afferent denervation and peripheral administration of the GLP-1 receptor antagonist exendin(9—39) amide enhanced emptying of a glucose meal, whereas intracerebroventricular exendin was ineffective. The rate of saline emptying was attenuated by peripheral as well as by central administration of GLP-1, and pretreatment with exendin by the respective routes reversed the inhibition by GLP-1. Vagal afferent denervation abolished the central and peripheral action of GLP-1 on gastric emptying. Neither peripheral cholinergic nor adrenergic blockade altered the delay of methyl cellulose meal emptying by intracisternal GLP-1 injection. Acid secretion in conscious pylorus-ligated rats was inhibited by intracisternal GLP-1 administration, whereas systemic GLP-1 was ineffective. These results support the notion that GLP-1 receptors participate in the central and peripheral regulation of gastric function. Furthermore, vagal afferent nerves mediate the inhibitory action of GLP-1 on gastric motor function. GLP-1 may be a candidate brain-gut peptide that acts as a physiological modulator of gastric function.
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Peripherally, GLP-1 activates GLP-1 receptors on afferent vagal fibers, initiating signals that inhibit gastrointestinal motility within the peripheral nervous system.
“Peripherally, as an incretin and enterogastrone secreted from the gut, GLP-1 activates GLP-1 receptors on afferent vagal fibers, initiating signals that inhibit gastrointestinal motility within the PNS [26].”
From Delayed gastric emptying induced by glucagon-like peptide-1 receptor agonists and its implications for perioperative risk during anesthesia (2026) · cites this paper as [26]
The Discussion reports that peripheral GLP-1 appears to inhibit gastric emptying through vagal afferents, and the Abstract reports that vagal afferent denervation abolished this effect. The paper does not establish that GLP-1 receptors are located on those fibers or that the inhibitory signaling occurs wholly within the PNS; it also implicates central mechanisms. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThere is evidence that GLP-1, administered peripherally or centrally, inhibits vagal activity in animals and humans.
“In addition to regulating glycemia, there is evidence that the neuropeptide GLP-1, administered peripherally or centrally, inhibits vagal activity in animals and humans (19, 50, 51) and increases sympathetic activity in rats (52, 53).”
From Effects of glucagon-like peptide-1, yohimbine, and nitrergic modulation on sympathetic and parasympathetic activity in humans (2008) · cites this paper as [19]
The Abstract (p. G920) reports that central and peripheral GLP-1 inhibited gastric emptying in rats, and that vagal afferent denervation abolished both effects. This supports vagal involvement, but the paper does not show that GLP-1 inhibits vagal nerve activity itself or establish that effect in humans. (LLM, conf=0.86)
Experimental — accuracy not yet measuredGLP-1 RAs delay gastric emptying by inhibiting gastrointestinal motility through both peripheral and central nervous system mechanisms.
“GLP-1 RAs delay gastric emptying by inhibiting gastrointestinal motility through both PNS and CNS.”
From Delayed gastric emptying induced by glucagon-like peptide-1 receptor agonists and its implications for perioperative risk during anesthesia (2026) · cites this paper as [26]
The Abstract and Discussion report that centrally and peripherally administered GLP-1 delayed gastric emptying in rats, with vagal afferents mediating the effect on gastric motor function. The study tested GLP-1 itself, not GLP-1 receptor agonists as a broader class, so it does not establish the claim for all GLP-1 RAs. (LLM, conf=0.84)
Experimental — accuracy not yet measuredGLP-1 and 5-HT activate GLP-1 and 5-HT3 receptors on intestinal vagus nerve endings as key gut-brain axis signals, triggering vagal reflexes that slow gastric emptying and induce satiation.
“GLP-1 and 5-HT also activate GLP-1 and 5-HT 3 receptors on intestinal vagus nerve endings as key signals in the “gut-brain axis, ” which, in turn, triggers vagal reflexes to slow the subsequent emptying of carbohydrate from the stomach, and induce satiation (12,13).”
From Gut mechanisms linking intestinal sweet sensing to glycemic control (2018) · cites this paper as [12]
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GLP-1-Based Strategies: A Physiological Analysis of Differential Mode of Action
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Andrews, C. N., Bharucha, A. E., Camilleri, M., Low, P. A., Seide, B. M., Burton, D. D., Nickander, K. K., Baxter, K. L., & Zinsmeister, A. R. (2007) · Neurogastroenterology & Motility · doi:10.1111/j.1365-2982.2007.00923.x · Cited by 26 · see citing works
Chronic high fat diet impairs glucagon like peptide-1 sensitivity in vagal afferents
Al Helaili, A., Park, S. J., & Beyak, M. J. (2020) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2020.08.045 · Cited by 17 · see citing works
Isbil-Buyukcoskun, N., & Gulec, G. (2005) · Regulatory Peptides · doi:10.1016/j.regpep.2004.12.019 · Cited by 10 · see citing works
Kassir, R., Ezzat, A., & Fakhro, J. (2025) · Obesity Surgery · doi:10.1007/s11695-025-07833-5 · Cited by 1 · see citing works
Kang, D., & Choi, D. (2026) · The Korean Journal of Internal Medicine · doi:10.3904/kjim.2025.277 · Cited by 1 · see citing works
“…delay gastric emptying by inhibiting gastrointestinal motility through both PNS and CNS. Peripherally, as an incretin and enterogastrone secreted from the gut, GLP-1 activates GLP-1 receptors on afferent vagal fibers, initiating signals that inhibit gastrointestinal motility within the PNS [26].”
- Authors
- I˙meryüz, N., Yeğen, B. Ç., Bozkurt, A., Coşkun, T., Villanueva-Peñacarrillo, M. L., & Ulusoy, N. B.
- Affiliations
- Departments ofGastroenterology and
- Marmara University (TR)
- Fundacion Jimenez Diaz, Departamento de Metabolismo Nutricion y Hormonas, 28040 Madrid, Spain
- Venue
- American Journal of Physiology-Gastrointestinal and Liver Physiology
- Publisher
- American Physiological Society
- Published
- 1997-10-01
- Volume
- 273
- Issue
- 4
- Pages
- G920-G927
- ISSN
- 0193-1857 (ISSN-L)
- 1522-1547
- OpenAlex
- W2141362365
- Cited by
- 432
- References
- 33
- Citations by year
- 2026: 10 · 2025: 15 · 2024: 19 · 2023: 11 · 2022: 9 · 2021: 12 · 2020: 11 · 2019: 10 · 2018: 18 · 2017: 21 · 2016: 18 · 2015: 20 · 2014: 23 · 2013: 23 · 2012: 15
- FWCI
- 6.86
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal of Physiology-Gastrointestinal and Liver Physiology (publishedVersion)
- PubMed (publishedVersion)
- Dspace Repository (Marmara Üniversitesi) (submittedVersion, other-oa)
- Funders
- Marmara Üniversitesi
- Topics
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- glucagon-like peptide-1, gastric emptying, vagal afferent nerves, exendin-9-39, GLP-1 receptor, acid secretion, brain-gut peptides, gastric motility, vagal denervation, intracisternal administration, pylorus-ligated rats, gastric fistula
- MeSH terms
- Animals, Blood Glucose, Capsaicin, Cerebral Ventricles, Denervation, Female, Gastric Acid, Gastric Emptying, Gastric Mucosa, Gastrointestinal Hormones, Glucose, Injections, Intraventricular, Peptide Fragments, Peptides, Stomach, Vagus Nerve, Venoms, Rats, Sprague-Dawley, Visceral Afferents, Rats, Glucagon-Like Peptide 1
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