Increase In Plasma Gastrin Concentration Research Articles

The effect of antenatal corticosteroids on gut peptides of preterm infants—a matched group comparison: Corticosteroids and gut development

Background: Postnatal glucocorticosteroid administration has trophic effects on the gastrointestinal tract of preterm infants. The aim of the present study was to investigate whether antenatal glucocorticosteroids affect the secretion of gastrointestinal peptides that are involved in the regulation of secretion, motility and mucosal protection of the gastrointestinal tract. Methods: Plasma levels of gastrin, motilin and vasoactive intestinal peptide (VIP) were estimated in 28 preterm infants with a mean birth weight of 1280 g, and mean gestational age of 30.5 weeks, whose mothers had received a full course of antenatal glucocorticosteroids (GC group) and in 17 preterm infants with mean birth weight of 1200 g, mean gestational age of 30.2 weeks, whose mothers had not received corticosteroids (control group). GI peptides were estimated on two occasions: (a) Immediately after birth and (b) following the initiation of enteral feeding. Results: Gastrin levels in the GC group were significantly higher both immediately after birth (early measurement) and also after receiving enteral feeding (late measurement) ( p<0.001, p<0.05, respectively) but the increase in plasma gastrin concentration was identical in both groups (32 vs. 33 pg/ml). Motilin levels in the GC group were also significantly higher as compared to the control group but only in the late measurement ( p<0.001). Gastrin and motilin levels in both groups were significantly higher in the late measurement as compared to the early measurement (GC group: p<0.001, p<0.001, respectively; Controls: p<0.001, p<0.01, respectively). There was no significant difference in VIP levels between the two groups both in the early and the late measurements. Conclusion: Antenatal glucocorticoids (GCs) stimulate gastrin secretion in the fetus but not in the neonate. Contrary to this, corticosteroid effect on motilin is seen only postnatally following the introduction of enteral feeding. Glucocorticosteroids appear to have no effect on VIP levels. Plasma gastrin and motilin levels increase significantly following the introduction of enteral feeding regardless of the use of steroids.

Effects of Differently Composed Feeds and Physical Stress on Plasma Gastrin Concentration in Horses

Plasma gastrin concentrations were determined in 6 Standardbreds (4 geldings and 2 mares) after 3 different meals consisting of unlimited amounts of hay (8-9 kg per horse), a restricted amount of hay (0.6 kg/100 kg body-weight) and grain (0.2 kg/100 kg body-weight) in combination or of grain alone (0.2 kg/100 kg body-weight). In another series of experiments the possible role of gastrin as a stress hormone was investigated. Plasma gastrin and cortisol concentrations were determined during fasting and compared with concentrations during hay feeding. In addition, gastrin and cortisol concentrations were determined before, during and after 2 kinds of physical exercise on a treadmill. Meal stimulation significantly increased the plasma gastrin concentration, irrespective of the meal composition. An immediate and large increase in plasma gastrin concentration was found when voluminous meals were given, whereas a small meal evoked a later onset of gastrin release, suggesting that gastric distention plays an important role in inducing gastrin release during a meal. Meals consisting of grain seem to evoke a slower onset and then a more prolonged gastrin response than a hay meal, possibly due to different emptying rates of the stomach. Nervous excitation may play a minor role in the activation of gastrin release in horses. No experimental support was obtained for the idea that gastrin acts as a stress hormone in the horse.

The effect of gastrin-releasing peptide on gastrin and somatostatin messenger RNAs in humans infected with Helicobacter pylori

BACKGROUND & AIMS: Gastrin-releasing peptide stimulates gastrin secretion but also inhibits its release via somatostatin. Exogenous gastrin-releasing peptide stimulates a greater increase in plasma gastrin concentrations in patients infected with Helicobacter pylori than in uninfected controls. Because this infection suppressed gastric mucosal somatostatin, we studied whether the increased gastrin response was a result of an abnormal response of the somatostatin cell. METHODS: Patients without dyspeptic ulcers received an infusion of either gastrin-releasing peptide or saline on separate occasions. Acid secretion was measured, and gastric biopsy specimens were taken for gastrin and somatostatin messenger RNA (mRNA) analysis and H. pylori diagnosis. RESULTS: In response to gastrin-releasing peptide, the increase in plasma gastrin concentrations in the infected patients was significantly higher than in the uninfected. Antral gastrin mRNA also increased significantly in the infected group but decreased significantly in the uninfected group. Basal somatostatin was lower in the infected group; gastrin-releasing peptide produced a significant increase in antral somatostatin mRNA concentration in infected, but not uninfected, patients. CONCLUSIONS: The somatostatin cell responds to gastrin-releasing peptide in H. pylori infection. Gastrin-releasing peptide normally inhibits gastrin mRNA expression, but inhibition is deficient in H. pylori infection, possibly because of low stimulated somatostatin levels. (Gastroenterology 1997 Jun;112(6):1940-7)

24-Hour intragastric acidity and plasma gastrin after omeprazole treatment and after proximal gastric vagotomy in duodenal ulcer patients

The relationship between suppressed gastric acidity and the increase in plasma gastrin levels after pharmacological and surgical treatment of peptic ulcer disease were compared in this study. Eight patients with chronic duodenal ulcer and referred for proximal gastric vagotomy were studied. 24-hour intragastric acidity and plasma gastrin levels were investigated in the same patients on three consecutive occasions: preentry without any treatment; after 4 weeks of administration of 20 mg of omeprazole daily, and 4–6 months after proximal gastric vagotomy. Intragastric acidity was slightly more reduced by omeprazole (94%) than after proximal gastric vagotomy (78%), with no difference found during the day or night with either. Plasma gastrin levels increased slightly more after proximal gastric vagotomy [284% (median, 2120 pmol · h/L; range, 733–2831 pmol · h/L)] than after omeprazole administration [186% (median, 1586 pmol · h/L; range, 495–2573 pmol · h/L)]. There is strong evidence that the increased plasma gastrin concentration following omeprazole treatment is caused by the reduced intragastric acidity. The slight increase in plasma gastrin concentration following proximal gastric vagotomy despite a lesser reduction in intragastric acidity may be the result of additional effects on gastrin release by the vagotomy. Both treatments resulted in a modest increase in plasma levels of gastrin that were far below the gastrin levels observed in achlorhydric patients, e.g., patients with pernicious anemia.

Plasma gastrin and secretin in neonates.

AbstractWith a view to investigating the dynamics of gastrointestinal hormones after birth, chronological changes in gastrin and secretin in the blood after birth were determined with radioimmunoassay. At delivery, the gastrin concentration in the umbilical cord plasma was 201 ±10 pg/ml (mean±SEM), significantly higher than that in the maternal vein. In the first 4–48 hours of life, it decreased to the adult level and rose again at 5 days of age. Next, the post‐prandial gastrin responses in both neonates and adults were examined. Percent increase in neonatal plasma gastrin concentration after feeding, as compared with the pre‐feeding level, was significantly higher than that observed in the adults. From these findings, we presumed that the “release setting” of gut endocrine cells differs between neonates and adults and also that enteral feeding might trigger the postnatal increase in the plasma gastrin concentration. The secretin concentration in the arterial cord plasma was 314 ±22 pg/ml. The secretin concentration in the blood also decreased in the first –8 hours of life, this decrease being similar to that of the gastrin level. However, a second rise in the level, as in the case of gastrin, was not observed at 5 days of age. In milk‐fed neonates, secretin did not show a postprandial response as did gastrin.

Beer and wine but not whisky and pure ethanol do stimulate release of gastrin in humans.

In humans, the action of ethanol on gastrin release is still unclear and that of alcoholic beverages greatly unknown. We studied the effect of a drink of various concentrations of pure ethanol and several commonly ingested alcoholic beverages on plasma levels of immunoreactive gastrin in 6 healthy human volunteers and compared the results to a protein-rich meal. A drink of distilled water (250 ml) and of pure ethanol (250 ml or 125 ml in the case of 40% v/v ethanol) in concentrations (4, 10, 20 and 40% v/v) normally present in beer, wine, liquor and whisky did not stimulate plasma gastrin levels above basal. Of the alcoholic beverages given only whisky (125 ml) did not stimulate gastrin release. Beer, red and white wine (250 ml each) caused a rapid increase in plasma gastrin concentrations with a peak at 15-20 min, basal levels being reached 60 min after starting the drink. The 60-min integrated plasma gastrin response to beer, red and white wine was about 50% of the gastrin response to the protein-rich (steak) meal (883 +/- 297 pmol X min X 1(-1); mean +/- SE). A drink of 250 ml of white wine together with the meal did not cause a significantly higher integrated gastrin response than the protein meal with 250 ml of distilled water. We conclude that commonly ingested alcoholic beverages such as beer, red and white wine, but not whisky, are potent stimulants of gastrin release in humans. The ethanol content of these beverages cannot be responsible for the increase in plasma gastrin levels, since oral ingestion of pure ethanol in equivalent concentrations and amounts did not elicit a rise in plasma gastrin levels. Some unknown ingredients present in beer and wine are most likely responsible for the gastrin release by both alcoholic beverages.

Increase in duodenal tissue gastrin in dogs following antrectomy with gastroduodenostomy and after total gastrectomy with oesophagoduodenostomy.

The gastrin concentration in plasma and duodenal tissue was determined in dogs following antrectomy and total gastrectomy as well as in unoperated control animals. The first week after both types of operations, during which time the dogs were parenterally fed the basal plasma gastrin concentration was markedly reduced, and then it slightly increased. The increase in plasma gastrin concentration from the second postoperative week until sacrifice was found to be statistically significant in one of six antrectomized dogs and in two of three dogs in which the whole stomach had been resected. In unoperated controls the gastrin concentration in the proximal third of the duodenum was found to be 6.8 +/- 0.8 pmol/g tissue wet weight (mean value +/- SE, n = 11). Following antrectomy a time dependent increase was seen, the corresponding values being 11.0 +/- 2.5 (n = 4), 36.4 +/- 15.7 (n = 6) and 136.1 +/- 44.2 (n = 6) pmol/g at 3, 9-10 and 14-16 weeks after operation, respectively. A similar increase was seen following total gastrectomy. 8 weeks after this type of operation the concentration was 22.2 +/- 12.5 (n = 3) pmol/g. The gastrin concentration of the middle and distal thirds of the duodenum was not changed by the operations. The results show that removal of the main source of gastrin, i.e. the pyloric antrum, induces an increase in the tissue level of gastrin in the upper portion of the duodenum.

Effect of urogastrone in the Zollinger-Ellison syndrome.

The effects of human urogastrone (0-25 mug. per kg. per hour intravenously) in four male patients with proven Zollinger-Ellison syndrome (z.e.s.) and in four healthy control subjects have been studied. After urogastrone in z.e.s. patients gastric acid volume and concentration decreased and basal acid output was reduced by 50-82%; the concentrations of intrinsic factor and pepsin in gastric juice increased by 60-300%; and peak plasma-gastrin concentration increased by 127-164% of basal concentration. A significant negative correlation between increase in plasma-gastrin concentration and decrease in acid output was observed (r=-0-72, P less than 0-01). Ulcer pain was relieved 30-60 minutes after the beginning of urogastrone infusion. These results suggest that urogastrone can inhibit the endogenously stimulated acid hypersecretion in z.e.s.