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A double-blind-trial was performed to prove the effect of antacids containing Mg (OH)2, Al (OH)3 and CaCO3 on peptone-stimulated gastric secretion (intragastric titration). A high efficacy of antacids given after meals was demonstrated. After application of antacids no significant rise in serum gastrin levels during intragastric titration was found. Serum calcium and magnesium levels remained unchanged. Peptone-stimulated gastric secretion was not influenced by application of different antacids within a period of 2 hours.
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AIM: To examine the effects of beer, ethanol, peptone meal and combinations of either peptone meal and beer or peptone meal and ethanol on gastric acid secretion in vagally denervated pouch dogs. METHODS AND RESULTS: The oral administration of either 200 mL of beer, 5% ethanol or 10% peptone meal significantly stimulated gastric acid secretion for 60-90 min in these dogs. With 5% ethanol the plasma gastrin concentration was not affected for 90 min. Combinations of 10% peptone and beer (peptone-beer) or 10% peptone and 5% ethanol (peptone-ethanol) potentiated the acid secretion and increased the plasma gastrin level. While a selective cholecystokinin-B/gastrin receptor antagonist, S-0509, had no effect on ethanol-stimulated acid secretion, the compound markedly inhibited both peptone-beer-stimulated and peptone-ethanol-stimulated gastric acid secretion. Famotidine and atropine significantly inhibited gastric acid secretion stimulated by 5% ethanol, peptone-beer and peptone-ethanol. CONCLUSIONS: The mechanisms by which peptone-beer and peptone-ethanol stimulate gastric acid secretion may be mediated not only by increased plasma gastrin, but also by the action of histamine and acetylcholine coupled with the increased plasma gastrin. Ethanol-stimulated secretion appears to be unrelated to circulating gastrin, yet may be related to the acid regulatory mechanism involving histamine and acetylcholine.
To assess the role of endogenous cholecystokinin in the control of gastric emptying of peptone solutions and Intralipid suspensions, we examined the ability of a dose range of the CCK-A antagonist, devazepide to accelerate the gastric emptying of various caloric concentrations of peptone and Intralipid in rats. In the absence of devazepide, both peptone and Intralipid emptying slowed with increasing concentration. Devazepide's effect on peptone gastric emptying diminished with increasing peptone concentration. The threshold dose for accelerating the emptying of 0.2 kcal/ml peptone was lower than the threshold dose for affecting 0.5 kcal/ml peptone and devazepide had no effect on the gastric emptying of 1.0 kcal/ml peptone. In contrast, devazepide affected Intralipid gastric emptying at all three Intralipid concentrations and the threshold dose decreased with increasing Intralipid concentration. However, the magnitude of the effect of devazepide on peptone or Intralipid gastric emptying was partial and did not increase as a function of concentration. These data demonstrate a role for endogenous CCK in the emptying of peptone and Intralipid but suggest that endogenous CCK does not account for the increased slowing of gastric emptying evident with increased caloric concentration.
BACKGROUND: Moderate acidification of the gastric lumen inhibits peptone-induced gastrin release. The aim of the present study was to investigate if the gastric acid neutralization products CO2 (from secreted HCO3) and NO (from reduced salivary nitrite) could act as intermediate messengers between luminal acidity and the inhibition of peptone-induced gastrin release. METHODS: Fourteen healthy volunteers (mean age, 27 years; range, 20-39 years; 3 women) participated in the study. Intragastric perfusion with saline or peptone was performed on the healthy volunteers. Venous blood samples were analyzed for serum gastrin concentrations. Intragastric NO was measured by chemiluminescence. RESULTS: Basal serum gastrin ranged between 11 and 23 pmol/l. Peptone in Sörensen's phosphated buffer (pH 6.9, PCO2 0 mmHg) increased serum gastrin by 83% +/- 23%, whereas acidified peptone (pH 2.0) did not stimulate gastrin release. Acidified peptone buffered with NaHCO3 to neutrality (pH 6.9, PCO2 approximately 600 mmHg) increased serum gastrin by 166% +/- 29%. Low intragastric NO levels were obtained by deviation of saliva. During such salivary depletion, acidified peptone (pH 2.0) stimulated gastrin release to a level of about 40% of the control response (pH 6.9). This peptone-induced gastrin response during salivary deviation was inhibited by addition of nitrite to the perfusate. CONCLUSIONS: Acid-induced inhibition of peptone-stimulated gastrin release is partly dependent on intraluminal NO formed in the reaction between salivary nitrite and gastric acid. In addition, the gastric acid neutralization product CO2 seems to potentiate the effect of peptone on gastrin release.
In rats, protein hydrolysates (peptones) stimulate cholecystokinin (CCK) release both in vivo and in a model of isolated vascularly perfused duodeno-jejunum. However, the mechanisms involved in peptone-induced stimulation of CCK cells are not well understood. In particular, the possibility that peptones may directly interact with CCK-producing cells to stimulate CCK release and gene transcription has not yet been examined. To test this hypothesis, we used the enteroendocrine cell line STC-1. Incubation of STC-1 cells for 2 h with albumin egg hydrolysate over the concentration range 0.01-1% (wt/ vol) caused a dose-dependent release of CCK, with a maximal increase at 1420% of the control value. In contrast, BSA (1%, wt/vol) or a mixture of amino acids (1%, wt/vol) induced a modest rise in CCK secretion. A dose-dependent, hydrolysate-specific, increase in the CCK steady state RNA level was also observed. It was detectable by 2-4 h of peptone treatment and sustained until 24-48 h. Peptones did not increase the CCK RNA level in the colonic CCK-producing cell line GLUTag or in nonintestinal CCK-expressing cell lines, namely the pancreatic cell line RINm5F and the medullar thyroid carcinoma cell line CA77. The peptone-induced increase in the CCK RNA level resulted from enhanced gene transcription, because labeled CCK transcripts from nuclear run-on incubations increased 3-fold when cells were incubated with peptones, whereas the level of beta-actin transcripts was not modified. Finally, peptones dose-dependently stimulated the transcriptional activity of an 800-bp fragment of CCK gene promoter transfected in STC-1 cells. These studies indicate that peptones specifically stimulate CCK secretion and gene transcription in the intestinal cell line STC-1, and that cis-acting elements conferring peptone inducibility are located in the first 800 bp of the 5'-flanking region of the CCK gene.
H. pylori infection is associated with acid-peptic disease, although its role in the pathogenesis is unclear. The purpose of this study was to determine if chronic infection in asymptomatic subjects impairs the inhibition of meal-stimulated gastrin and acid secretion that is observed normally at low intragastric pH. Presence of infection was determined by both C-14 urea breath test and serology. Acid secretion was measured under basal conditions and in response to peptone meal stimulation and pentagastrin. Plasma gastrin concentrations were determined by radioimmunoassay under basal conditions and during peptone meal stimulation. Intragastric titration with 1% peptone during the first hour, and 8% peptone during the second hour, was performed at both pH 7.0 and 2.5 on different days to compare the inhibition of gastrin and acid secretion. Compared to noninfected subjects, asymptomatic individuals infected with H. pylori had significantly increased: (1) basal gastrin values (P < 0.005); (2) 8% peptone-stimulated gastrin responses at both pH 7.0 and 2.5 (P < 0.05); and (3) 8% peptone-stimulated acid output at pH 2.5 (P = 0.01). During the second hour of peptone-stimulation, subjects infected with H. pylori had significantly decreased inhibition of gastrin (52% vs 95%) (P = 0.002) and acid (30% vs 81%) (P = 0.01) secretion from pH 7.0 to 2.5. Thus, chronic infection with H. pylori results in impaired inhibition of gastrin and acid secretion at low intragastric pH during the second hour of peptone meal stimulation. These defects may be unrelated to the pathogenesis of acid-peptic disease, since they occur in asymptomatic subjects infected with H. pylori.
Peptone perfusion of the excluded duodenum in dogs is associated with an increase in lower esophageal sphincter pressure (LESP). This study investigates the role of cholinergic, adrenergic, and hormonal mediators in the response of the LES to intraduodenal peptone infusion. Adult dogs underwent duodenal exclusion via a Roux-en-Y pylorojejunostomy with formation of a mucocutaneous fistula. Manometric measurements of LESP and radioimmunoassay determinations of gastrin and pancreatic polypeptide (PP) blood levels were made at rest and at 15-min intervals following peptone infusion of the excluded duodenum. In control experiments, peptone infusion resulted in an increase in mean LESP at all time intervals (P less than 0.05). PP blood levels increased significantly, while gastrin levels remained unchanged. Both truncal vagotomy and pretreatment with atropine blocked the changes in LESP. PP release in response to peptone was accentuated in vagotomized dogs, while atropine suppressed the release of PP following peptone infusion. Treatment with 6-hydroxydopamine did not affect the increase in either LESP or PP blood levels observed in controls. Intravenous somatostatin suppressed the release of PP following intraduodenal peptone, but did not block the lower esophageal sphincter response. This data indicates that the increase in LESP seen following intraduodenal peptone infusion is centrally mediated and dependent on vagal innervation and cholinergic neurotransmission.
It is clear that the intestinal hormone cholecystokinin (CCK) inhibits gastric emptying, but doubts remain about the physiological significance of this action. Evaluation of the apparently conflicting data is complicated by the fact that little is known of the duration of action of CCK-releasing meals in delaying emptying. We have studied this issue by following the emptying of the second of two successive liquid test meals instilled into the stomach in conscious gastric fistula rats. Prior administration of peptone, but not saline, delayed the emptying of subsequently administered saline and delayed still further the emptying of subsequently administered peptone. The action of isotonic peptone lasted about 10 min from the initial instillation into the stomach. Radioimmunoassay of plasma CCK indicated a significant increase 5 min after intragastric peptone, and a still further rise occurred 5 min after administration of the second of two consecutive peptone meals; 21 min after the first meal, plasma CCK had returned to basal levels. Intravenous infusion of CCK in a dose that matched the inhibition of gastric emptying caused by peptone gave plasma concentrations about 35% higher than those seen 5 min after the second of two consecutive peptone meals. It is concluded that a liquid test meal of peptone delays gastric emptying in part through release of CCK and that the response lasts 10 min or less. The relatively short duration of action of endogenous CCK released by a single protein-rich meal in the rat should be kept in mind in interpreting the significance of studies on the physiology of CCK.