Plasma catecholamine and serum gastrin concentrations during sham feeding

Plasma adrenaline, plasma noradrenaline and serum gastrin concentrations were measured before and after sham feeding in eight patients with duodenal ulcer and in four normal subjects. No significant change in the concentrations was observed after sham feeding. In three patients with duodenal ulcer an insulin test resulted in a 25-fold rise in plasma adrenaline. The ulcer patients showed significantly higher levels of plasma adrenaline and plasma noradrenaline than the normal subjects both before and after sham feeding, and this difference was probably not caused only by age difference in the two groups. It is concluded that sympathetic nervous activity and serum gastrin concentrations are not influenced by sham feeding in contrast to the influence of insulin hypoglycemia.     

Relationship of postprandial motilin, gastrin, and pancreatic polypeptide release to intestinal motility during vagal interruption.

Experiments were performed to determine how postprandial motilin, gastrin, and pancreatic polypeptide plasma concentrations measured during vagal blockade relate to coincident small intestinal motility patterns. Feeding produced a postprandial pattern of intestinal motility coincident with a sustained increase in gastrin and pancreatic polypeptide and a decline in motilin plasma concentrations. Vagal blockade replaced the fed pattern with one similar to migrating motor complex (MMC) activity. Highest motilin plasma concentrations were observed during phase III of this MMC-like activity, as occurs in the fasted state. Vagal blockade reduced but did not abolish the postprandial increase in plasma gastrin and pancreatic polypeptide concentrations. Termination of vagal cooling produced a decline in motilin and an elevation in gastrin and pancreatic polypeptide concentrations, coincident with the return of the fed pattern. In conclusion, during vagal blockade in the fed state (i) motilin, but not gastrin or pancreatic polypeptide plasma concentrations, fluctuate with the MMC-like activity, and any measurement of motilin concentration under these circumstances must be interpreted on the basis of gut motility patterns, and (ii) gastrin and pancreatic polypeptide concentrations are marginally elevated, but these changes are not enough to disrupt the MMC or have any motor effect. Lastly, the fed pattern and the postprandial changes in motilin, gastrin, and pancreatic polypeptide concentrations are in part dependent upon intact vagal pathways.     

FMRF-amide immunoreactivity in the mammalian gastroenteropancreatic neuroendocrine system

The presence of FMRF-amide, a cardioactive tetrapeptide, was studied by immunocytochemistry in human and rat gastric antrum and pancreas, and in the ovine, bovine, canine and rabbit pancreas. In human and rat gastric antrum, numerous cells contained FMRF-amide immunoreactive material. By staining of serial sections and by double staining, colocalization of immunoreactivity for gastrin and FMRF-amide was observed in part of the gastrin cells. In the pancreas of these and the other species, immunoreactivity for FMRF-amide was located both in acinar and islet endocrine cells. Colocalization of FMRF-amide and pancreatic polypeptide was found in a proportion of pancreatic polypeptide cells in the pancreas. FMRF-amide immunoreactivity never colocalized with the other neurohormonal peptides which occur in the gastric antrum and the pancreas. Our observations show that neuroendocrine cells occur in the gastric antrum and pancreas which are exclusively immunoreactive or gastrin and for pancreatic polypeptide respectively. In addition cells occur which show immunoreactivity for FMRF-amide as well as for gastrin in the gastric antrum and with antiserum to FMRF-amide as well as for pancreatic polypeptide in the pancreas. It is concluded that FMRF-amide antibodies probably recognize a substance in G and PP cells which is not identical but may be structurally related to gastrin and pancreatic polypeptide.     

FMRF-amide immunoreactivity in the mammalian gastroenteropancreatic neuroendocrine system

Summary The presence of FMRF-amide, a cardioactiv tetrapeptide, was studied by immunocytochemistry in human and rat gastric antrum and pancreas, and in the ovine, bovine, canine and rabbit pancreas. In human and rat gastric antrum, numerous cells contained FMRF-amide immunoreactive material. By staining of serial sections and by double staining, colocalization of immunoreactivity for gastrin and FMRF-amide was observed in part of the gastrin cells. In the pancreas of these and the other species, immunoreactivity for FMRF-amide was located both in acinar and islet endocrine cells. Colocalization of FMRF-amide and pancreatic polypeptide was found in a proportion of pancreatic polypeptide cells in the pancreas. FMRF-amide immunoreactivity never colocalized with the other neurohormonal peptides which occur in the gastric antrum and the pancreas.Our observations show that neuroendocrine cells occur in the gastric antrum and pancreas which are exclusively immunoreactive or gastrin and for pancreatic polypeptide respectively. In addition cells occur which show immunoreactivity for FMRF-amide as well as for gastrin in the gastric antrum and with antiserum to FMRF-amide as well as for pancreatic polypeptide in the pancreas. It is concluded that FMRF-amide antibodies probably recognize a substance in G and PP cells which is not identical but may be structurally related to gastrin and pancreatic polypeptide.In honour of Prof. P. van Duijn     

Variations of plasma immunoreactive motilin, pancreatic polypeptide, gastrin and somatostatin along the duodenal motility cycle in the pig

The peripheral plasma concentrations of immunoreactive motilin, pancreatic polypeptide (PP), somatostatin and gastrin were measured in 7 pigs fasted to 24 h and subsequently fed a standard meal. Plasma motilin peaked during the last part of phase II activity of the migrating myoelectric complex (MMC) sequence (25.2 +/- 2.3 pM), the lowest value being recorded during phase I (10.6 +/- 1.5 pM) after a 24 h fast. Plasma motilin remained at a low level during the digestive pattern of duodenal activity, no fluctuation occurring when the first postprandial MMC recurred. At variance analysis, gastrin and PP were not released phasically with MMC in the fasting state, while at autocovariance both peptides tended to fluctuate during the MMC sequence with positive and negative peaks at regular intervals along MMC cycles. No variation of plasma somatostatin was observed in the fasting animals. These findings argue against a major role of circulating PP, gastrin and somatostatin-like components in the control of fasted and post absorptive duodenal motility in pigs while the role of motilin remains equivocal.     

The role of luminal gastrin in the regulation of pancreatic juice secretion in preruminant calves

The effect of luminal gastrin on the secretion of pancreatic juice was studied in seven conscious preruminant calves employing luminal infusions of gastrin and cholecystokinin (CCK)-9 and pharmacological CCK1 and CCK2 receptor blocks with antagonists. The study was performed in the preprandial and prandial states. Pharmacological blocking of the CCK2 receptor, like that of the CCK1 receptor, resulted in reduction of pancreatic postprandial secretion and increased the duration of the prandial pattern of duodenal electrical activity. Exogenous luminal gastrin, like luminal CCK-9, enhanced the secretion of pancreatic juice proteins, though the overall effect of gastrin was weaker than that of CCK-9. The effect was inhibited by infusion of CCK2 but also by CCK1 receptor antagonist. In conclusion, duodenal luminal gastrin can stimulate exocrine pancreatic secretion by a mechanism that depends on CCK2 receptors in calves. Involvement of the CCK1 receptor in this mechanism needs further investigation. Prandial pancreatic secretory and duodenal motility cycles can be regulated by endogenous gastrin release.     

Value of CA 19-9 assay in serum and duodenal juice in the differential diagnosis of pancreatic disease

Levels of CA 19-9 in the serum and duodenal juice of nine patients with pancreatic adenocarcinoma (PC), ten patients with chronic calcifying pancreatitis (CCP) and ten healthy volunteers (C) were determined by immunoassay. Duodenal juice was obtained by duodenal intubation during the secretin caerulein test. Elevated CA 19-9 levels in the serum were significantly more frequent in PC than in CCP patients, but two PC patients gave levels only slightly above the cut-off value of 37 U/ml. CA 19-9 levels in duodenal juice were significantly higher in PC than in CCP patient, but there was some overlap between them; no overlapping was seen between PC or CCP group and controls. Two PC patients with duodenal juice CA 19-9 levels overlapping those of CCP were the same who showed only a slight rise in serum CA 19-9 levels. The CA 19-9 to total protein ratio in duodenal juice did not permit better discrimination between PC and CCP. We conclude that CA 19-9 assay in duodenal juice can differentiate healthy subjects from patients with pancreatic diseases, but it cannot improve the differential diagnosis between CCP and PC patients with a slight rise of CA 19-9 levels in serum.     

苓桂术甘汤对老年脾胃气虚型功能型消化不良患者胃蛋白酶原、胃泌素及血液流变学的影响

摘要 目的：研究苓桂术甘汤对老年脾胃气虚型功能型消化不良患者的临床治疗效果,并探讨治疗对患者胃蛋白酶原、胃泌素和血液流变学的影响。方法：选取2020年1月到2021年10月在我院接受治疗的老年脾胃气虚型功能型消化不良患者120例,按治疗方式分为对照组以及研究组,对照组患者给予常规药物治疗,研究组患者在对照组基础上加用苓桂术甘汤进行治疗,比较两组患者临床治疗疗效和治疗前后生活质量评分、中医症候积分、血清胃蛋白酶I和II、血清胃泌素-17、血液流变学。结果：（1）研究组患者临床治疗总有效率显著高于对照组（93.33 % vs 75.00 %,P<0.05）;（2）治疗后,两组患者的生活质量评分升高,而中医症候积分降低,且研究组优于对照组（P<0.05）;（3）两组患者治疗后血胃蛋白酶I和II、血清胃泌素-17均显著降低,并且治疗后研究组低于对照组（P<0.05）;（4）两组患者治疗后血液流变学指标（高切全血黏度、低切全血黏度和血浆黏度）均显著降低,并且研究组降低程度显著高于对照组（P<0.05）。结论：加用苓桂术甘汤治疗老年脾胃气虚型功能型消化不良可显著提高临床治疗疗效,改善患者生活质量,降低患者血清胃蛋白酶原、胃泌素以及血流变学指标表达。     

Do motilin and pancreatic polypeptide regulate duodenal bile acid delivery?

The plasma levels of the enteric hormones, motilin and pancreatic polypeptide, cycle in association with fasting intestinal motility and are altered by feeding. Intravenous administration of motilin causes gallbladder contraction and increased sphincter of Oddi phasic motor activity, whereas pancreatic polypeptide causes gallbladder relaxation. To determine if endogenous plasma levels of motilin and pancreatic polypeptide control sphincter of Oddi and gallbladder motility, and regulate duodenal bile acid delivery, we measured during fasting and after feeding the correlation between (a) changes in plasma motilin or pancreatic polypeptide, and (b) the duodenal delivery of a steady-state hepatic output of radiolabelled bile acid. Four dogs were prepared with duodenal cannulas. Duodenal motility was recorded manometrically. Plasma levels of pancreatic polypeptide and motilin were determined during a full cycle of the migrating myoelectric complex for 20 min before and 40 min after ingestion of a standard meal. To assess the effect of the sphincter of Oddi and the gallbladder together, or the gallbladder alone on duodenal bile acid delivery, the dogs received a continuous i.v. infusion of [14C]taurocholic acid (TCA); duodenal delivery of TCA was quantitated with the sphincter of Oddi intact using duodenal marker perfusion, or with the sphincter of Oddi cannulated and zero outflow resistance. In the interdigestive period with the sphincter of Oddi intact, only 0.1 (r2) of the variance of duodenal bile acid delivery can be predicted from the variance of motilin, and the correlation of plasma pancreatic polypeptide with duodenal TCA delivery is opposite that expected if pancreatic polypeptide caused gallbladder relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of vagotomy on the duodenal mechanisms regulating gastric secretion

Gastric acid secretion, gastrin and secretin serum levels after duodenal acidification were studied in 6 dogs, before and after a troncular vagotomy was performed in each one. After duodenal acidification in normal dogs, a 45.2% inhibition of gastric acid secretion with parallel 55-84% increases in the serum secretin levels, without changes in the serum gastrin levels, was noted. When a troncular vagotomy was performed in the same dogs, duodenal acidification produced a 20% (non significant) inhibition of gastric acid secretion with parallel 34-72% increases in the serum secretin levels and without changes in the serum gastrin levels. It is concluded that vagus nerve is necessary to assess a physiological inhibition of gastric secretion after duodenal acidification and it is suggested that humoral and nervous factors are implicated and coexist in these mechanisms.     

Effects of fasting and refeeding on antral, duodenal, and serum gastrin levels and on colonic thymidine kinase activity in rats

Antral, duodenal, and serum gastrin levels and colonic thymidine kinase activity were determined in 1- to 4-day-fasted rats and after refeeding of 4-day-fasted rats for 3-24 h. The effect of pentagastrin on colonic thymidine kinase activity was also determined. Total deprivation of food caused a drastic reduction in gastrin concentrations in serum and tissues. After 4 days of fasting, serum gastrin levels in most animals fell below the present detection limit of the assay (10-15 pg/ml), and antral and duodenal gastrin levels decreased to 15 and 50% of the respective initial fed control. After 9 and 24 h of refeeding, gastrin concentration in serum and antrum had increased to about 35% of the initial fed level. On the other hand, refeeding for 3-24 h produced no significant change in duodenal gastrin concentration. Fasting for 1-4 days resulted in a 60-70% reduction in colonic thymidine kinase activity, compared to the initial fed control. Refeeding caused a prompt stimulation in the enzyme activity, which after 6 h was found to be 72% above the 4-day-fasted group. Daily injection of pentagastrin, at doses between 125 and 500 micrograms/kg, during a 4-day fasting period resulted in a significant stimulation in colonic thymidine kinase activity, compared to the saline-treated control. The maximal stimulation of an enzyme activity 90% higher than in the saline control was attained with a pentagastrin dose of 125 micrograms/kg. Higher doses decreased the maximal stimulatory effect of pentagastrin.(ABSTRACT TRUNCATED AT 250 WORDS)     

Plasma and tissue levels of digestive regulatory peptides during postnatal development and weaning in the calf.

Changes in the concentrations of cholecystokinin, gastric inhibitory peptide, gastrin, motilin, pancreatic polypeptide, secretin, somatostatin, and vasoactive intestinal peptide in calf plasma and antral, duodenal and/or pancreatic tissues were assessed by radioimmunoassay during postnatal development and after weaning in 50 male Holstein-Friesian calves (randomly distributed into 10 groups of 5 animals each). The calves in the first group were killed at birth while those in 6 other groups were colostrum-fed for 2 days and then milk-fed until 7, 28, 56, 70 or 119 days of age. Those in the remaining 3 groups were given the same diets until day 28, were then weaned between day 29-56, and slaughtered on days 56, 70 or 119. In milk-fed animals, changes in plasma and tissue concentrations of almost all digestive regulatory peptides were observed during the 1st month of postnatal life, especially at day 2. Weaning was accompanied by variations in the plasma concentrations of somatostatin, secretin, gastrin, pancreatic polypeptide and gastric inhibitory peptide but not by any apparent change in peptide tissue concentrations (except VIP in the duodenum). Thus, the variations in tissue concentrations are primarily age-related, while plasma concentrations were modified by age and weaning.     

The fasting and food-stimulated serum gastrin concentration in 151 duodenal ulcer patients compared to 41 healthy subjects

The basal and postprandial serum gastrin concentrations (SGC) were compared between 151 duodenal ulcer (DU) patients and 41 non-dyspeptic volunteers. All DU patients had an eventful history and were submitted to us for surgery. The basal SGC was significantly higher in DU patients (40 +/- 30 vs 17 +/- 8 pg/ml). The peak post-prandial SGC was also significantly higher (123 +/- 83 vs 52 +/- 28 pg/ml) and the integrated gastrin output twice as high as in healthy subjects (5311 +/- 3879 vs 2554 +/- 1995 pg/ml x min; P less than 0.01). A statistically significant linear correlation for fasting and maximal postprandial SGC was found. No statistically significant interrelation between gastrin and acid parameters existed. In the DU patients no differences in SGC were found according to age. Fifteen patients complained of nonalimentary vomiting as part of their ulcer symptoms. They had significantly higher SGC although no differences in acid secretion were found. No significant differences in gastrin or acids were related to ulcer complications.     

The effects of antagonists of receptors for gastrin, cholecystokinin and bombesin on growth of gastroduodenal mucosa and pancreas.

The effects of gastrin, cholecystokinin (CCK) and bombesin on the DNA synthesis, as a biochemical indicator of trophic action in the gastroduodenal mucosa and the pancreas have been examined in rats fasted for 48 h and in rats refed for 16 h with or without administration of specific receptor antagonists for bombesin, gastrin and CCK. Bombesin and gastrin administered three times daily for 48 h in fasted rats significantly increased the rate of DNA synthesis as measured by the incorporation of [3H] thymidine into DNA in each tissue tested. CCK significantly increased DNA synthesis in the duodenal mucosa and pancreatic tissue, but not in the gastric mucosa. The stimulation of DNA synthesis induced by bombesin in the gastroduodenal mucosa and pancreas was abolished by bombesin/GRP receptor antagonist, RC-3095. RC-3095 did not affect DNA synthesis stimulated by gastrin and CCK in these tissues. L-365,260, a receptor antagonist for gastrin suppressed the DNA synthesis induced by gastrin but not by CCK or bombesin in the gastrointestinal mucosa and pancreas. L-364,718 a specific antagonist for CCK receptors was effective only against CCK stimulated duodenal mucosa and pancreatic growth. Refeeding of 48 h fasting rats strongly enhanced the DNA synthesis in all tissues tested, and this effect was significantly reduced in the gastroduodenal mucosa by blocking only gastrin receptors (with L-365,260) and that in the duodenal mucosa and the pancreas by antagonizing of CCK receptors (with L-364,718). Antagonism of bombesin receptors (with RC-3095) did not significantly affect the stimulation of DNA synthesis induced by refeeding in all tissues tested. This study indicates that the stimulation of DNA synthesis can be achieved by exogenous gastrin, CCK and bombesin acting through separate receptor but that only gastrin and CCK play the major role in the postprandial stimulation of the growth of gastroduodenal mucosa and pancreatic tissue.     

Three digestive tract endocrine peptides and the circannual cycle of body weight in Spermophilus lateralis

• 1.1. Thirty-one male golden-mantled ground squirrels were divided into four physiological groups: low wt summer, medium wt summer, high wt summer and hibernation period. A second group of 10 females was divided into two groups: hibernation period at low T_b and hibernation period during a periodic arousal.
• 2.2. Blood serum, pancreas and antral stomach region were collected from each animal.
• 3.3. The serum was analysed by radioimmunoassay for pancreatic polypeptide immunoreactivity, the pancreas for pancreatic polypeptide and somatostatin immunoreactivity and the antral region of the stomach for gastrin immunoreactivity.
• 4.4. Significant between-stage differences (P < 0.05) were found in serum pancreatic polypeptide concentration and in pancreatic somatostatin content.

     

NH2-terminal of gastrin-17 in duodenal ulcer disease: identification of progastrin-17

Serum gastrin concentrations were measured using antisera with specificity for the carboxyl and amino terminus of gastrin-17 in 50 healthy subjects and 18 patients with active duodenal ulcer disease (DU). The amino terminal of gastrin-17 immunoreactivity was significantly higher in DU patients than in healthy subjects. NH2-terminus of gastrin-17 immunopurified material from serum of DU patients was subjected to Sephadex G50 column chromatography and eluates were monitored by an additional antiserum EG10 that recognizes COOH-terminally extended gastrin. Besides the NH2 terminal tridecapeptide of gastrin-17, COOH-terminally extended progastrin was found. This may reflect abnormal processing of gastrin in patients with active duodenal ulcer disease.     

Serum concentration of pancreatic polypeptide in normal subjects and in peptic ulcer patients

The present study evaluates the serum concentration of pancreatic polypeptide (PP) in normal male and female subjects of different ages (ranging from 20 to 69) and also in patients with peptic ulcers. The PP level rose with age and was higher in the male subjects (from the age of 30). Serum levels of the peptide in patients with gastric or duodenal ulcers were not significantly different from the normal subjects (age and sex matched with the diseased groups).     

A qualitative comparison of canine plasma gastroenteropancreatic hormone responses to bombesin and the porcine gastrin-releasing peptide (GRP)

The effect on plasma gastroenteropancreatic hormone levels on infusing the porcine gastrin-releasing peptide and bombesin into dogs demonstrated no qualitative difference in the spectrum of activity of the two peptides. Sustained elevations in plasma immunoreactive gastrin, pancreatic polypeptide, enteroglucagon, gastric inhibitory polypeptide, pancreatic glucagon and transient elevations in plasma insulin were seen during infusions of both peptides. The similar spectrum of activities and the structural homology between the two peptides suggests that the porcine gastrin releasing peptide is the porcine counterpart of the amphibian peptide bombesin.     

The effect of antagonist of receptors for gastrin, cholecystokinin and bombesin on growth of gastroduodenal mucosa and pancreas.

The effects of gastrin, cholecystokinin (CCK) and bombesin on the DNA synthesis, as a biochemical indicator of trophic action in the gastroduodenal mucosa and the pancreas, have been examined in rats fasted for 48 h and in rats refed for 16 h with or without administration of specific receptor antagonists for bombesin, gastrin and CCK. Bombesin and gastrin administered three times daily for 48 h in fasted rats significantly increased the rate of DNA synthesis as measured by the incorporation of [3H] thymidine into DNA in each tissue tested. CCK significantly increased DNA synthesis in the duodenal mucosa and pancreatic tissue, but not in the gastric mucosa. The stimulation of DNA synthesis induced by bombesin in the gastroduodenal mucosa and pancreas was abolished by bombesin/GRP receptor antagonist, RC-3095. RC-3095 did not affect DNA synthesis stimulated by gastrin and CCK in these tissues. L-365,260, a receptor antagonist for gastrin suppressed the DNA synthesis induced by gastrin but not by CCK or bombesin in the gastrointestinal mucosa and pancreas. L-364,718, a specific antagonist for CCK receptors was effective only against CCK stimulated duodenal mucosa and pancreatic growth. Refeeding of 48 h fasting rats strongly enhanced the DNA synthesis in all tissues tested, and this effect was significantly reduced in the gastroduodenal mucosa by blocking only gastrin receptors (with L-365, 260) and that in the duodenal mucosa and the pancreas by antagonizing of CCK receptors (with L-364,718). Antagonism of bombesin receptors (with RC-3095) did not significantly affect the stimulation of DNA synthesis induced by refeeding in all tissues tested. This study indicates that the stimulation of DNA synthesis can be achieved by exogenous gastrin, CCK and bombesin acting through separate receptors, but that only gastrin and CCK play the major role in the postprandial stimulation of the growth of gastroduodenal mucosa and pancreatic tissue.     

Role of gastrin in duodenal mechanisms of inhibition of gastric secretion in the dog and man

Gastrin serum levels after acidification of the second portion of the duodenum were studied, in dogs and humans, while simultaneously measuring secretin levels and gastric acid secretion. After duodenal acidification in dogs, a 50% inhibition of gastric acid secretion with parallel 100% increases in the serum secretin levels was noted whereas gastrin serum levels did not change (after duodenal acidification). In humans, a 25% inhibition of gastric acid secretion with parallel 50% (not significative) increases in the secretin serum levels was noted. In the entire group gastrin levels did not change, but in 35.2% of the subjects a little increment without statistical significance was noted. It is concluded that the inhibition mechanism of gastric acid secretion after duodenal acidification is more important in dog than in man, and that, probably, gastrin does not play an important role in this mechanism.