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140 records · Page 8Linked to original sources
PubMed1984

The role of substance P in the control of gastric acid secretion.

Experiments were performed to determine whether substance P plays a physiologic role as an enterogastrone. Basal substance P levels averaged 6.4 +/- 0.2 pg/ml in dogs prepared with gastric and duodenal fistulas. Infusion of substance P at 5 ng/kg/min increased circulating hormone concentrations by more than 1 pg/ml and inhibited pentagastrin-stimulated (4 micrograms/kg/hr) gastric acid secretion by 44% (from 10.9 +/- 1.8 to 6.1 +/- 1.6 mEq/30 min); a similar dose of substance P (7 ng/kg/min) did not alter gastrin levels from the basal level of 19.8 +/- 1.2 fmol/ml. Duodenal acidification (with 0.1N HCl at 5 ml/min for 10 minutes) similarly inhibited pentagastrin-stimulated gastric fistula output (from 8.2 +/- 0.9 to an average of 5.0 +/- 0.9 mEq/30 min for the 30 minutes after irrigation) but did not alter circulating substance P levels. Thus, although physiologic concentrations of substance P inhibit gastric fistula output, this peptide does not seem to be involved in the endogenous acid-mediated duodenal control of acid secretion.

Animals↗
PubMed1978

[Metabolism of endogeneous gastrin (author's transl)].

The localization of production of gastrin is rather well known, the localization of metabolic breakdown however is still being discussed. Liver, kidneys, musculature and small intestine are being taken into consideration. Experiments were performed demonstrating a definite increase of serum gastrin after removal of the small intestine; the duodenum was not removed in these experiments, since enterogastrone is formed mainly in this organ. These results would suggest, that gastrin is metabolized in the small intestine. In order to further prove this point, truncal vagotomy was performed in rabbits, producing elevated serum gastrin levels. In other series subtotal removal of the small intestine was combined with truncal vagotomy. Serum gastrin levels were definitely higher after this latter procedure than after truncal vagotomy alone. These findings seem to support the hypothesis, that endogeneous gastrin is metabolized in the small intestine.

Animals↗
PubMed1983

Effects of antibodies to gastric inhibitory peptide on gastric acid secretion and gastrin release in the dog.

Previous studies have questioned the physiological role of gastric inhibitory peptide in inhibiting gastric acid secretion. The present study was designed to examine and compare peptone meal-stimulated gastric acid secretion in dogs after intravenous infusion of rabbit serum containing antibodies to gastric inhibitory peptide or normal rabbit serum (as control). Five dogs were prepared with gastric fistulas. Basal acid output was collected for 90 min through the gastric fistula. After 30 min of basal acid output collection, either rabbit serum containing antibodies to gastric inhibitory peptide or normal control rabbit serum (0.1 ml/kg) was infused intravenously over 1 min. After the basal acid output collection, a 10% peptone meal was infused into the stomach. Gastric acid output was measured by intragastric titration (pH 5.0) for 60 min. Peripheral venous plasma was collected for measurement of gastrin and gastric inhibitory peptide and for binding of endogenous plasma gastric inhibitory peptide by administered antibodies to gastric inhibitory peptide before and at 2, 5, 10, 15, 30, 60, 90, and 120 min after the meal. After intravenous administration of antibodies to gastric inhibitory peptide, 98% +/- 3% (SEM) of endogenous plasma gastric inhibitory peptide was bound by administered antibodies to gastric inhibitory peptide. No binding of endogenous plasma gastric inhibitory peptide was detected after infusion of normal rabbit serum. In dogs receiving intravenous antibodies to gastric inhibitory peptide, both peptone-stimulated gastric acid output and integrated gastrin release responses were increased when compared with dogs receiving normal rabbit serum. With infusion of antibodies to gastric inhibitory peptide, there was a high degree of correlation between the increase in gastric acid output and the increase in integrated gastrin response (r = 0.900, p less than 0.04) that followed the peptone meal. This study, using antibodies to bind endogenous gastric inhibitory peptide, demonstrates the capacity of circulating gastric inhibitory peptide to inhibit meal-stimulated gastric acid secretion. Furthermore, these results support the conclusion that this enterogastrone effect of gastric inhibitory peptide is due, at least in part, to inhibition of gastrin release.

Animals↗
PubMed1977

[New views on gastrointestinal hormones].

In addition to established gastrointestinal hormones--secretin, cholecystokinin-pancreozymin (CCK-PZ), gastrin, and glucagon---some 30 polypeptides with gastrointestinal actions can be listed. New aspects of these substances include the following: Gastrin and vasoactive intestinal peptide (VIP) can be also encountered in the central nervous system and may act as transmitters. CCK-PZ-serum concentrations are found markedly elevated in patients with exocrine pancreatic insufficiency; this may provide the opportunity to establish a realtively simple screening test. Moreover, there is evidence that serum-CCK-PZ levels serve as satiety signal. Secretin secretion is said to be enhanced in hunger and then to act as a lipolytic hormone. In addition to enteroglucagon, a gastrintestinal peptide identical to pancreatic glucagon has been detected. Gastric inhibitory polypeptide (GIP) inhibits gastric secretion and motility (enterogastrone activity) and together with glucose it stimulates insulin release (incretin activity). Motilin increases lower esophageal sphincter pressure, enhances gastric pepsin secretion and slows down gastric evacuation. Serum levels of pancreatic polypeptide may be found elevated as a diagnostic index in patients with endocrine peptide tumors of the pancreas. Recently, the potential importance of local (paracrine) actions of gastrointestinal polypeptides has been amphasized. Predominantly paracrine activity is exhibited by some prototype hormones, e.g. somatostatin, substance P, bombesian, and the non-polypeptide compounds, prostaglandins.

Bombesin↗
PubMed1998

Human immunodeficiency virus-related wasting: malabsorption syndromes.

Diarrhea and malabsorption are common findings in patients with the acquired immunodeficiency syndrome (AIDS). The pathogenesis and consequences of malabsorption in human immunodeficiency virus (HIV) infection are similar to those found in non-HIV-related conditions, and are related to both direct intestinal damage and alterations in the coordination of the body's response to feeding. The pathogenesis of malabsorption is multifactorial and includes primary enterocyte injury with partial villus atrophy and crypt hyperplasia, ileal dysfunction with bile salt wasting and fat malabsorption, and exudative enteropathy. Clinical studies show that intestinal cryptosporidiosis leads to excess fecal losses of about 20% for protein and fat. The consequences of malabsorption include decreased appetite; "enterogastrone" effects including dry mouth, decreased gastric acid secretion, decreased rate of gastric emptying, and slowed intestinal transit; anemia resulting from iron, folate, or vitamin B12 malabsorption; and metabolic effects including osteomalacia, gallstones, renal stones, and hypocholesterolemia. Few studies of nutritional therapy have been applied specifically to AIDS patients with malabsorption. Total parenteral nutrition promotes weight gain, although the response to this therapy depends on the underlying clinical problem, with body cell mass repletion noted in patients with malabsorption but predominantly fat gain in patients with systemic infections. Nutritional stabilization also was noted in response to oral administration of a semielemental diet.

HIV Infections↗
PubMed1998

[Clinical significance of glucose-dependent insulinotropic polypeptide (GIP)].

Findings on the effects of GIP indicate that its incretory effect on stimulation of insulin secretion under conditions of hyperglycaemia is more important than the formerly known effect of enterogastrone. Numerous experimental trials provide evidence that GIP can participate in the regulation of the postprandial glucose and lipid metabolism and circulation in the splancnic area. The physiological action of GIP has however still obscure consequences in pathological conditions. Because GIP secretion by the mucosa of the small intestine is conditioned by nutrient absorption and its incretory effect on the functional capacity of the B-cells of the pancreas, it is assumed that it is of clinical importance in diseases of the digestive tract and in metabolic disorders. The author presents a review of recent findings on GIP and its action in diabetes, obesity, chronic pancreatic disease and other pathological conditions. In view of the controversial reports the clinical importance of GIP is not quite clear so far.

Animals↗