scholarly journals Inhibition of Sham Feeding-Stimulated Human Gastric Acid Secretion by Glucagon-Like Peptide-2

1999 ◽  
Vol 84 (7) ◽  
pp. 2513-2517 ◽  
Author(s):  
Morten Wøjdemann ◽  
Andre Wettergren ◽  
Bolette Hartmann ◽  
Linda Hilsted ◽  
Jens J. Holst
Keyword(s):  
Gastric Secretion ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Plasma Concentrations ◽  
Saline Infusion ◽  
Sham Feeding ◽  
Distal Small Intestine ◽  
Glucagon Like Peptide

Glucagon-like peptide (GLP)-2 is formed from proglucagon in the intestinal L cells and is secreted postprandially in parallel with the insulinotropic hormone GLP-1, the latter of which, in addition, acts to inhibit gastric secretion and motility by inhibiting central parasympathetic outflow. We now studied the effect of GLP-2 on gastric secretion stimulated by sham feeding to test the hypothesis that also GLP-2 acts as an enterogastrone. Eight healthy volunteers were studied twice on separate days. They were sham fed with and without GLP-2 infused iv at a rate of 0.8 pmol/kg·min. Gastric contents were aspirated continuously by a nasogastric tube for determination of acid secretion, volume, and osmolarity. Sham feeding increased gastric acid secretion nearly 5-fold. Infusion of GLP-2 reduced incremental acid secretion by 65 ± 6%, compared with saline infusion (Δ8.75 ± 0.37 vs. Δ3.04± 0.47 mmol × 60 min; P < 0.01). Plasma concentrations of GLP-2 rose from a basal mean of 3.3 ± 0.9 to a mean of 115 ± 8 pmol/L (range, 57–149 pmol/L) during infusion of GLP-2 and remained at basal level during saline infusion. Plasma concentrations of GLP-1, gastrin, cholecystokinin, and secretin remained low and unchanged on both study days. We conclude that GLP-2 is a powerful inhibitor of gastric acid secretion in man. Further investigations will show to what extent GLP-2 contributes to the inhibitory effects on gastric secretion exerted by hormones from the distal small intestine, under physiological circumstances.

Glucagon-like peptide-1 (7–36)-NH2: a physiological inhibitor of gastric acid secretion in man

1990 ◽  
Vol 126 (1) ◽  
pp. 169-173 ◽  
Author(s):  
D. J. O'Halloran ◽  
G. C. Nikou ◽  
B. Kreymann ◽  
M. A. Ghatei ◽  
S. R. Bloom
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Endocrine Cells ◽  
Acid Output ◽  
Plasma Concentrations ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Volume Output ◽  
Mixed Component

ABSTRACT Glucagon-like peptide (GLP)-1 (7–36)-NH2 is a peptide found in the mucosal endocrine cells of the intestine, and plasma levels of GLP-1 (7–36)-NH2 immunoreactivity show a rise after the ingestion of a fat or mixed-component meal. We investigated the effects of physiological infusion of GLP-1 (7–36)-NH2 on a submaximal gastric acid secretion in healthy volunteers at a rate known to mimic the observed postprandial rise in plasma concentrations. Corrected gastric acid output decreased to less than 50% and volume output to 33% of stimulated values. After the infusion, the secretion of gastric acid recovered immediately to preinhibition values. These results suggest a novel role for GLP-1 (7–36)-NH2 as a physiological inhibitor of gastric acid secretion in man. Journal of Endocrinology (1990) 126, 169–173

Sham Feeding Induced Gastric Acid Secretion in Patients with Caustic Induced Esophageal Stricture

Dysphagia ◽  
2021 ◽  
Author(s):  
Jimil Shah ◽  
Nikhil Bush ◽  
T. Mahesh ◽  
C. K. Nain ◽  
Rakesh Kochhar
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Esophageal Stricture ◽  
Sham Feeding

scholarly journals Acupuncture inhibits vagal gastric acid secretion stimulated by sham feeding in healthy subjects.

Gut ◽  
1994 ◽  
Vol 35 (8) ◽  
pp. 1026-1029 ◽  
Author(s):  
G Lux ◽  
J Hagel ◽  
P Backer ◽  
G Backer ◽  
R Vogl ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Healthy Subjects ◽  
Sham Feeding

Effect of thyroid on gastric secretion and metabolism

1961 ◽  
Vol 201 (3) ◽  
pp. 567-570 ◽  
Author(s):  
E. S. Nasset ◽  
Dale P. J. Goldsmith
Keyword(s):  
Oxygen Consumption ◽  
Gastric Mucosa ◽  
Gastric Secretion ◽  
Thyroid Hormones ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Early Summer ◽  
Tissue Concentrations ◽  
Oxygen Ratio

The effect of administration of thyroid products on gastric acid secretion and metabolism was studied in dogs with gastric pouches and in gastric mucosa from rats and frogs. Whole thyroid, thyroxin, triiodothyronine, and iodinated casein generally reduced secretion in thyroidectomized dogs and in dogs with intact thyroids. The thyroid substances elevated BMR above euthyroid levels in normal dogs but not always in thyroidectomized dogs. In dogs with intact thyroids 2,4-dinitrophenol raised oxygen consumption but did not affect secretion. Whole thyroid elevated BMR in rats and frogs but did not change resting mucosal oxygen consumption. During spring and early summer thyroid feeding reduced histamine-stimulated acid secretion and mucosal oxygen consumption during secretion in frogs, but the acid-to-oxygen ratio was unaffected. These findings suggest that elevated tissue concentrations of thyroid hormones reduce the ability of the gastric mucosa to mobilize secretory energy in response to a stimulus. This effect of the thyroid hormones is apparently not directly correlated with their calorigenic properties.

scholarly journals The Effect of Sham Feeding on Neurocardiac Regulation in Healthy Human Volunteers

2007 ◽  
Vol 21 (11) ◽  
pp. 721-726 ◽  
Author(s):  
Markad V Kamath ◽  
Robert Spaziani ◽  
Sangeeta Ullal ◽  
Gervais Tougas ◽  
Juan C Guzman ◽  
...  
Keyword(s):  
Heart Rate ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Power Spectra ◽  
Area Ratio ◽  
Vagal Activity ◽  
Healthy Human ◽  
Sham Feeding ◽  
Efferent Pathways

BACKGROUND: Distension and electrical stimuli in the esophagus alter heart rate variability (HRV) consistent with activation of vagal afferent and efferent pathways. Sham feeding stimulates gastric acid secretion by means of vagal efferent pathways. It is not known, however, whether activation of vagal efferent pathways is organ- or stimulus-specific.OBJECTIVE: To test the hypothesis that sham feeding increases the high frequency (HF) component of HRV, indicating increased neurocardiac vagal activity in association with the known, vagally mediated, increase in gastric acid secretion.METHODS: Continuous electrocardiography recordings were obtained in 12 healthy, semirecumbent subjects during consecutive 45 min baseline, 20 min sham feeding (standard hamburger meal) and 45 min recovery periods. The R-R intervals and beat-to-beat heart rate signal were determined from digitized electrocardiography recordings; power spectra were computed from the heart rate signal to determine sympathetic (low frequency [LF]) and vagal (HF) components of HRV.RESULTS: Heart rate increased during sham feeding (median 70.8 beats/min, 95% CI 66.0 to 77.6; P<0.001), compared with baseline (63.6, 95% CI 60.8 to 70.0) and returned to baseline levels within 45 min. Sham feeding increased the LF to HF area ratio (median: 1.55, 95% C.I 1.28 to 1.77; P<0.021, compared with baseline (1.29, 95% CI 1.05 to 1.46); this increase in LF to HF area ratio was associated with a decrease in the HF component of HRV.CONCLUSIONS: Sham feeding produces a reversible increase in heart rate that is attributable to a decrease in neurocardiac parasympathetic activity despite its known ability to increase vagally mediated gastric acid secretion. These findings suggest that concurrent changes in cardiac and gastric function are modulated independently by vagal efferent fibres and that vagally mediated changes in organ function are stimulus- and organ-specific.

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