scholarly journals Peripheral PYY inhibits intracisternal TRH-induced gastric acid secretion by acting in the brain

2000 ◽  
Vol 279 (3) ◽  
pp. G575-G581 ◽  
Author(s):  
Hong Yang ◽  
Keishi Kawakubo ◽  
Helen Wong ◽  
Gordon Ohning ◽  
John Walsh ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Peptide Yy ◽  
Vagal Stimulation ◽  
Inhibitory Effect ◽  
Supporting Evidence ◽  
Intracisternal Injection ◽  
Site Of Action ◽  
The Brain

The site of action of peripheral peptide YY (PYY)-induced inhibition of vagally stimulated gastric acid secretion was studied using immunoneutralization with PYY antibody in urethan-anesthetized rats. Gastric acid secretion (59 ± 7 μmol/90 min) stimulated by intracisternal injection of the stable thyrotropin-releasing hormone (TRH) analog RX-77368 (14 pmol/rat) was dose-dependently inhibited by 52%, 69%, and 83% by intravenous infusion of 0.25, 0.5, and 1.0 nmol · kg−1 · h−1 PYY, respectively. PYY or PYY3–36 (2.4 pmol/rat) injected intracisternally also inhibited the acid response to intracisternal RX-77368 by 73% and 80%, respectively. Intravenous pretreatment with PYY antibody (4.5 mg/rat), which shows a 35% cross-reaction with PYY3–36 by RIA, completely prevented the inhibitory effect of intravenously infused PYY (1 nmol · kg−1 · h−1). When injected intracisternally, the PYY antibody (280 μg/rat) reversed intracisternal PYY (2.4 pmol)- and intravenous PYY (1 nmol · kg−1 · h−1)-induced inhibition of acid response to intracisternal RX-77368 by 64% and 93.5%, respectively. These results provide supporting evidence that peripheral PYY inhibits central vagal stimulation of gastric acid secretion through an action in the brain.

scholarly journals Intestinal fat-induced inhibition of meal-stimulated gastric acid secretion depends on CCK but not peptide YY

1999 ◽  
Vol 276 (2) ◽  
pp. G550-G555 ◽  
Author(s):  
Xiao-Tuan Zhao ◽  
John H. Walsh ◽  
Helen Wong ◽  
Lijie Wang ◽  
Henry C. Lin
Keyword(s):  
Small Intestine ◽  
Gastric Emptying ◽  
Acid Secretion ◽  
Receptor Antagonist ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Peptide Yy ◽  
Inhibitory Effect ◽  
Proximal Half

Fat in small intestine decreases meal-stimulated gastric acid secretion and slows gastric emptying. CCK is a mediator of this inhibitory effect (an enterogastrone). Because intravenously administered peptide YY (PYY) inhibits acid secretion, endogenous PYY released by fat may also be an enterogastrone. Four dogs were equipped with gastric, duodenal, and midgut fistulas. PYY antibody (anti-PYY) at a dose of 0.5 mg/kg or CCK-A receptor antagonist (devazepide) at a dose of 0.1 mg/kg was administered alone or in combination 10 min before the proximal half of the gut was perfused with 60 mM oleate or buffer. Acid secretion and gastric emptying were measured. We found that 1) peptone-induced gastric acid secretion was inhibited by intestinal fat ( P < 0.0001), 2) inhibition of acid secretion by intestinal fat was reversed by CCK-A receptor antagonist ( P < 0.0001) but not by anti-PYY, and 3) slowing of gastric emptying by fat was reversed by CCK-A antagonist ( P< 0.05) but not by anti-PYY. We concluded that inhibition of peptone meal-induced gastric acid secretion and slowing of gastric emptying by intestinal fat depended on CCK but not on circulating PYY.

Peptide YY interacts with secretin and duodenal acidification to inhibit gastric acid secretion

1987 ◽  
Vol 18 (3-4) ◽  
pp. 155-163 ◽  
Author(s):  
Felix Lluis ◽  
Guillermo Gomez ◽  
Masaki Fujimura ◽  
George H. Greeley ◽  
Courtney M. Townsend ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Peptide Yy ◽  
Duodenal Acidification

Hepatic modulation of insulin-induced gastric acid secretion and EMG activity in rats

1980 ◽  
Vol 238 (5) ◽  
pp. R346-R352 ◽  
Author(s):  
J. Granneman ◽  
M. I. Friedman
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Emg Activity ◽  
Glucose Levels ◽  
Hepatic Portal Vein ◽  
Inhibited Acid ◽  
Hepatic Portal ◽  
The Brain

Intravenous infusions of fructose, a hexose that does not cross the blood-brain barrier, suppressed insulin-induced gastric acid secretion and electromyographic (EMG) activity despite continuing hypoglycemia. Hepatic portal vein infusions of 0.15 M fructose inhibited acid output while the same concentration delivered via the jugular vein did not, suggesting a hepatic site of action of the hexose. Only infusions of fructose that began before onset of the insulin-induced gastric responses were effective, whereas glucose infusions, which elevated plasma glucose levels, readily reversed ongoing gastric activity. The suppressive effects of fructose on gastric activity were prevented by prior section of the hepatic branch of the vagus nerve. In contrast, hepatic vagotomy did not prevent suppression of gastric responses by infusions of glucose, a hexose utilized by both brain and liver. These results suggest that receptors in the brain may initiate and terminate insulin-induced gastric acid secretion and motor activity, whereas sensors in the liver may inhibit these responses.

Structural requirements of peptide YY for biological activity at enteric sites

1992 ◽  
Vol 263 (5) ◽  
pp. G695-G701 ◽  
Author(s):  
K. Yoshinaga ◽  
T. Mochizuki ◽  
N. Yanaihara ◽  
K. Oshima ◽  
M. Izukura ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Insulin Release ◽  
Peptide Yy ◽  
Exocrine Secretion ◽  
Pancreatic Exocrine Secretion ◽  
Structural Requirements ◽  
Pancreatic Exocrine

Peptide YY (PYY) is a colonic hormone consisting of 36 amino acids that is a potent inhibitor of pancreatic exocrine, gastric acid, and insulin secretion. The objective of the present experiments was to characterize the structural requirements of PYY for inhibition of pancreatic exocrine, gastric acid, and insulin secretion, using conscious dogs prepared with gastric and pancreatic fistulas. Intravenous administration of PYY-(1-36), PYY-(3-36), or PYY-(4-36) (400 pmol.kg-1 x h-1) inhibited cholecystokinin-8-stimulated (25 pmol.kg-1 x h-1) pancreatic exocrine secretion (P < 0.05); however, PYY-(1-10), PYY-(1-20), PYY-(6-36), PYY-(10-36), PYY-(13-36), PYY-(24-36), and PYY-(27-36) did not inhibit pancreatic exocrine secretion. Intravenous administration of PYY-(1-36), PYY-(3-36), or PYY-(4-36) (200, 400, 800 pmol.kg-1 x h-1) inhibited pentagastrin (0.5 microgram.kg-1 x h-1)-stimulated gastric acid secretion (P < 0.05), as well as 2-deoxy-D-glucose-stimulated insulin release (75 mg/kg) in a dose-related manner. PYY-(6-36), PYY-(13-36), and [Leu31, Pro34] neuropeptide Y did not inhibit either gastric acid secretion or insulin release. In the gastric acid and insulin secretion bioassays, PYY-(1-36) was significantly more potent than PYY-(3-36) and PYY-(4-36); however, in the pancreatic exocrine secretion bioassay, the inhibitory effects of PYY-(3-36) and PYY-(1-36) did not differ significantly. PYY-(4-36) was less potent than PYY-(1-36) on pancreatic exocrine secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Stimulation of neurons in rat ARC inhibits gastric acid secretion via hypothalamic CRF1/2- and NPY-Y1 receptors

2003 ◽  
Vol 285 (6) ◽  
pp. G1075-G1083 ◽  
Author(s):  
Johannes J. Tebbe ◽  
Silke Mronga ◽  
Martin K.-H. Schäfer ◽  
Jens Rüter ◽  
Peter Kobelt ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Receptor Antagonist ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Excitatory Amino Acid ◽  
Inhibitory Effect ◽  
Receptor Subtypes ◽  
Npy Receptor ◽  
Y1 Receptors ◽  
Open Question

Neuropeptide Y (NPY) neuronal projections from the arcuate nucleus (ARC) have been proposed to target corticotropin-releasing factor (CRF)-positive neurons in the paraventricular nucleus (PVN) as part of the ARC-PVN axis. The existence of a positive feedback loop involving CRF receptors in the PVN has been suggested. Exogenous NPY and CRF in the PVN have been shown to inhibit gastric acid secretion. Recently, we have demonstrated that activation of ARC neurons inhibits gastric acid secretion via vagal pathways. To what extent NPY- and CRF-mediated mechanisms in the PVN contribute to the CNS modulation of gastric acid secretion is still an open question. In the present study, we performed consecutive bilateral microinjections of antagonists to NPY receptor subtypes Y1 and Y2 and to CRF1/2 receptors in the PVN and of the excitatory amino acid kainate in the ARC to assess the role of NPY- and CRF-mediated mechanisms in the kainate-induced effects on gastric acid secretion. Gastric acid secretion was measured at the basal condition and during pentagastrin (16 μg/kg body wt) stimulation. Microinjection of vehicle in the PVN and kainate in the ARC decreased gastric acid secretion. Microinjection of the specific NPY-Y1 receptor antagonist BIBP-3226 (200 pmol) and the nonspecific CRF1/2 antagonist astressin (30 pmol) in the PVN abolished the inhibitory effect of neuronal activation in the ARC by kainate on gastric acid secretion. The CRF antagonist astressin was more effective. Pretreatment with the NPY-Y2 receptor antagonist BIIE-0246 (120 pmol) in the PVN had no significant effect. Our results indicate that activation of neurons in the ARC inhibits gastric acid secretion via CRF1/2 and NPY-Y1 receptor-mediated pathways in the PVN.

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