Central and peripheral regulation of gastric acid secretion by peptide YY

@article{Yang2002CentralAP,
  title={Central and peripheral regulation of gastric acid secretion by peptide YY},
  author={Hong Yang},
  journal={Peptides},
  year={2002},
  volume={23},
  pages={349-358}
}
  • Hong Yang
  • Published 1 February 2002
  • Biology, Medicine
  • Peptides
Involvement of apolipoprotein A-IV and cholecystokinin1 receptors in exogenous peptide YY3 36-induced stimulation of intestinal feedback.
TLDR
The data suggest a role for apo A-IV and the CCK(1)R in PYY(3-36)-induced activation of the vagal afferent pathway and inhibition of gastric emptying, but this is likely not the pathway mediating the effects of PYY (3- 36) on food intake.
Gastric secretion
  • M. Schubert
  • Biology, Medicine
    Current opinion in gastroenterology
  • 2013
TLDR
An improved understanding of the pathways and mechanisms regulating gastric acid secretion should lead to the development of novel therapies to prevent and treat acid-peptic disorders as well as circumvent the adverse effects of currently used antisecretory medications.
Reduced ghrelin, islet amyloid polypeptide, and peptide YY expression in the stomach of gastrin-cholecystokinin knockout mice.
TLDR
Lack of gastrin plus CCK but not gastrin alone reduced ghrelin secretion in response to fasting through both direct and indirect mechanisms.
Neuropeptide Y and Peptide YY Inhibit Excitatory Synaptic Transmission in the Rat Dorsal Motor Nucleus of the Vagus
TLDR
Differences in the receptor subtypes utilized and in the mechanism of action of NPY and PYY may indicate functional differences in their roles within the circuitry of the dorsal vagal complex (DVC).
Modulation of inhibitory neurotransmission in brainstem vagal circuits by NPY and PYY is controlled by cAMP levels
  • K. Browning, R. Travagli
  • Biology
    Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
  • 2009
TLDR
The results suggest that, similar to opioid peptides, the effects of pancreatic polypeptides on GABAergic transmission depend upon the levels of cAMP within gastric inhibitory vagal circuits.
Gastric protective effect of peripheral PYY through PYY preferring receptors in anesthetized rats.
TLDR
Investigation of the influence of intravenous peptide YY on the gastric injury induced by 45% ethanol in urethane-anesthetized rats indicates that PYY-infused intravenously at doses reported to mimic postprandial peak blood levels prevents ethanol-induced Gastric injury through vagal independent pathways and PYY -preferring receptors.
Brainstem neuropeptides and vagal protection of the gastric mucosal against injury: role of prostaglandins, nitric oxide and calcitonin-gene related peptide in capsaicin afferents.
  • Y. Taché
  • Biology
    Current medicinal chemistry
  • 2012
TLDR
Gastric prostaglandins and CGRP/NO pathways represent a common final mechanism through which brain peptides confer vagally mediated gastroprotection against injury.
Altered expression of aquaporin 4 and H+/K+‐ATPase in the stomachs of peptide YY (PYY) transgenic mice
TLDR
This study investigated the expression of AQP4 (aquaporin 4) water channel and H+/K+‐ATPase in stomachs from both control and transgenic mice to investigate the inhibitory effects of these molecules on gastrointestinal and pancreatic fluid secretion.
The role of gut hormone peptide YY in energy and glucose homeostasis: twelve years on.
TLDR
This narrative review critically discusses recent findings relating to the role of PYY in mediating the beneficial effects of bariatric surgery, the role in glucose homeostasis, the roles of hepatoportal PYYIn mediating its central physiological effects, the specific modulation of brain regions by PYY, and the exercise-induced PYY response.
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References

SHOWING 1-10 OF 99 REFERENCES
Peptide YY inhibits gastric acid secretion stimulated by the autonomic nervous system.
Peptide YY (PYY), a new peptide found primarily in mucosal endocrine cells of the terminal ileum and colon, inhibits pentagastrin-stimulated gastric acid secretion in several species, including man.
Central inhibitory action of peptide YY on gastric motility in rats.
TLDR
The results support the view that physiological concentrations of PYY may inhibit proximal gut function as part of the "ileal brake" mechanism by acting directly on vagovagal control circuits in the dorsal medulla.
Inhibition of human gastric acid secretion by peptide YY and secretin.
TLDR
It is suggested that the interaction of PYY and secretin on pentagastrin-stimulated gastric acid secretion in normal man is of the additive type.
Effect of peptide YY on gastric acid secretion, gastrin and somatostatin release in the rat.
TLDR
The study shows that PYY suppressed acid secretion in the rat, suggesting that endogenous somatostatin or gastrin is unlikely to mediate the inhibitory effect of PYY on acid production.
PYY and NPY: control of gastric motility via action on Y1 and Y2 receptors in the DVC
TLDR
The results show that Y2 agonist applied to the DVC during conditions of TRH‐stimulated gastric motility mimicked the suppressive effects of PYY applied under the same conditions and hypothesize that the confounding observations are due to agonist effects on two different receptor types – Y1 and Y2, which are both present in the dorsal vagal complex (DVC).
Inhibition of Gastric Acid Secretion by Peptide YY Is Independent of Gastric Somatostatin Release in the Rat 1
TLDR
It is indicated that PYY can inhibit gastric acid secretion independently of release of gastric somatostatin in the rat.
Inhibitory action of peptide YY on gastric acid secretion.
TLDR
PYY inhibit pentagastrin-stimulated gastric acid secretion in the face of atropine, vagotomy, or indomethacin treatment, indicating that the inhibitory action of PYY on gastric Acid secretion is in part independent of long and short cholinergic pathways.
Evidence for regulation of peptide-YY release by the proximal gut.
TLDR
The results of these experiments indicate that the release of PYY from the distal ileum and colon is controlled, at least in part, by an extramural neural, endocrine, or a combination of both types of mechanisms which originate in the foregut.
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