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.

Nitric oxide inhibits gastric acid secretion by increasing intraparietal cell levels of cGMP in isolated human gastric glands

2005 ◽  
Vol 289 (6) ◽  
pp. G1061-G1066 ◽  
Author(s):  
Anna Berg ◽  
Stefan Redéen ◽  
Magnus Grenegård ◽  
Ann-Charlott Ericson ◽  
Sven Erik Sjöstrand
Keyword(s):  
Nitric Oxide ◽  
Gastric Mucosa ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Enzymatic Digestion ◽  
Human Gastric Mucosa ◽  
Gastric Glands ◽  
Oxyntic Mucosa ◽  
No Donor

We have previously identified cells containing the enzyme nitric oxide (NO) synthase (NOS) in the human gastric mucosa. Moreover, we have demonstrated that endogenous and exogenous NO has been shown to decrease histamine-stimulated acid secretion in isolated human gastric glands. The present investigation aimed to further determine whether this action of NO was mediated by the activation of guanylyl cyclase (GC) and subsequent production of cGMP. Isolated gastric glands were obtained after enzymatic digestion of biopsies taken from the oxyntic mucosa of healthy volunteers. Acid secretion was assessed by measuring [14C]aminopyrine accumulation, and the concentration of cGMP was determined by radioimmunoassay. In addition, immunohistochemistry was used to examine the localization of cGMP in mucosal preparations after stimulation with the NO donor S-nitroso- N-acetylpenicillamine (SNAP). SNAP (0.1 mM) was shown to decrease acid secretion stimulated by histamine (50 μM); this effect was accompanied by an increase in cGMP production, which was histologically localized to parietal cells. The membrane-permeable cGMP analog dibuturyl-cGMP (db-cGMP; 0.1–1 mM) dose dependently inhibited acid secretion. Additionally, the effect of SNAP was prevented by preincubating the glands with the GC inhibitor 4 H-8-bromo-1,2,4-oxadiazolo[3,4-d]benz[b][1,4]oxazin-1-one (10 μM). We therefore suggest that NO in the human gastric mucosa is of physiological importance in regulating acid secretion. Furthermore, the results show that NO-induced inhibition of gastric acid secretion is a cGMP-dependent mechanism in the parietal cell involving the activation of GC.

Gastric acid secretion and parietal cell mass: effects of thyroidectomy and thyroxine

1989 ◽  
Vol 256 (6) ◽  
pp. G975-G978 ◽  
Author(s):  
K. O. Adeniyi ◽  
M. O. Olowookorun
Keyword(s):  
Gastric Mucosa ◽  
Thyroid Hormones ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Parietal Cell ◽  
Cell Function ◽  
Cell Mass ◽  
Chronic Administration ◽  
Basal Acid

The role of thyroid hormones on parietal cell function and number was studied in the rat. Chronic administration of thyroxine (6-8 micrograms/100 g body wt/day) for 35 days significantly increased parietal cell mass (from 21.18 +/- 0.13 x 10(6) to 26.71 +/- 0.14 x 10(6] as well as basal acid secretion (from 3.69 +/- 0.08 to 4.99 +/- 0.16 mueq/10 min) and histamine-stimulated acid secretion (from 2.45 +/- 0.12 to 3.69 +/- 0.21 mueq/10 min). Thyroidectomy decreased the number of parietal cells in the gastric mucosa (to 10.48 +/- 0.09 x 10(6] and basal acid secretion (to 3.09 +/- 0.08 mueq/10 min). Histamine (0.2 mg) injection into the thyroidectomized rats increased acid secretion by only 1.41 +/- 0.06 mueq/10 min as against 2.45 +/- 0.12 mueq/10 min obtained for control rats. The results suggest that thyroid hormones regulate basal and secretagogue-stimulated acid secretion via their effects on parietal cell mass.

Recent advances in the physiology of gastrin

1968 ◽  
Vol 170 (1018) ◽  
pp. 81-88 ◽  
Keyword(s):  
Gastric Secretion ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Chemical Mechanism ◽  
Antral Mucosa ◽  
Aqueous Extracts ◽  
Gastric Digestion ◽  
Hormonal Mechanism ◽  
Vagal Reflex

On 18 May 1905 there was presented at a meeting of this Society a paper in the name of John Sydney Edkins entitled ‘On the chemical mechanism of gastric secretion’ (Edkins 1905). It described experiments in which simple aqueous extracts of antral and fundic mucosa were tested for their power to stimulate gastric secretion when injected as single intravenous doses into anaesthetized cats. Antral extracts excited a secretion of acid and pepsin; fundic extracts did not. Edkins concluded that certain cells in the antral mucosa contained a principle which he named ‘gastrin’; this, he considered, entered the circulation during gastric digestion and stimulated the fundic glands to further activity following on the initial vagal reflex excited by the eating of the meal. These experiments, later recounted in detail (Edkins 1906) initiated more than 40 years of controversy as to the existence of a gastric antral hormone. When attempts were made to confirm and extend Edkins’s observations it was soon discovered that a stimulant of gastric acid secretion could be found not only in antral mucosa but also in many other tissues; and when eventually this ubiquitous agent was identified as histamine (Barger & Dale 1910; Dale & Laidlaw 1910; Popielski 1919) it was widely concluded that the activity of Edkins’s antral extract was due to the presence in it of this substance. The situation was further confused by the failure of apparently well-designed attempts to prove by physio­logical experiment that an antral hormonal mechanism existed, whatever the nature of the hormone. For example, Ivy & Whitlow (1922) and Priestley & Mann (1932) provided dogs with fundic and antral pouches and irrigated the latter with solutions regarded at the time as likely to cause a release of the hormone; but no response from the fundic pouch could be detected, and many years elapsed before the probable reason for such failure became appreciated.

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.

Peptide histidine valine-42 stimulates gastric acid secretion in man

1989 ◽  
Vol 9 (3) ◽  
pp. 369-374 ◽  
Author(s):  
G. C. Nikou ◽  
Y. Yiangou ◽  
B. J. Chrysanthou ◽  
J. Domin ◽  
S. R. Bloom
Keyword(s):  
Gastric Secretion ◽  
Acid Secretion ◽  
Healthy Volunteers ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Local Control ◽  
Significant Stimulation ◽  
New Finding ◽  
Stimulation Of

The effect of peptide histidine valine-42 (PHV-42) on gastric acid secretion was studied in man. PHV-42 was infused into 5 healthy volunteers at a dose of 10 pmol/kg/min. This dose caused a significant stimulation of basal gastric acid and potassium output. there were no significant changes in circulating gastrin throughout the infusion. In 2 subjects with a background of submaximal pentagastrin stimulation, PHV-42 infusion at the same dose did not alter acid secretion in either subject. The previous observation that PHV-42 is found particularly in the stomach and the new finding that it stimulates basal gastric secretion suggest the possibility that PHV-42 could have a role in local control of acid secretion.

Role of blood flow in gastric acid secretion

1988 ◽  
Vol 254 (3) ◽  
pp. G281-G293 ◽  
Author(s):  
L. Holm ◽  
M. A. Perry
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Hydrogen Gas ◽  
Inert Gases ◽  
Simple Relationship ◽  
Consistent Finding ◽  
Doppler Flowmetry

The relationship between gastric acid secretion and blood flow has been investigated with a variety of different blood flow techniques including aminopyrine clearance, hydrogen gas clearance, intravital microscopy, laser-Doppler flowmetry, radioactive microspheres, and the elimination of inert gases. The most commonly used technique, aminopyrine clearance, predicts that increasing acid secretion is accompanied by a parallel increase in blood flow. However, the efficiency of clearance of aminopyrine is low in the nonsecreting stomach and increases as secretion rate increases. This precludes the use of aminopyrine clearance as a reliable measure of gastric mucosal blood flow at all but the highest steady-state level of acid secretion and casts doubt on the findings with this technique. Other methods for measuring blood flow indicate that there is no simple relationship between secretion and flow, with some studies finding that secretion and flow change in parallel and others finding that secretion varies quite independently of flow to the mucosa. One consistent finding is a strong correlation between stimulated acid secretion and gastric oxygen consumption. Both acid secretion and oxygen consumption fall if celiac blood flow is reduced below a critical value, which in the anesthetized dog stomach is approximately 30-40 ml.min-1.100 g-1. Driving blood flow above this value does not increase oxygen consumption and acid secretion, i.e., they reach a plateau. The shape of this relationship with its flow-dependent and flow-independent portions is used to explain the apparently contradictory findings in the literature regarding gastric acid secretion and blood flow.

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