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Circulatory effects of gastrointestinal hormones and related peptides are surveyed. Only experiments using low peptide dosages, non-extensive surgery and intravenous infusions give relevant data in this field. Glucagon, secretin, vasoactive intestinal peptide, gastrin, cholecystokinin, Substance P and Somatostatin are vasoactive within the splanchnic area, each fraction in a specific pattern.
The effects of pharmacological concentrations of several gastrointestinal hormones on the rate of sucker activity and the frequency and the amplitude of spontaneous longitudinal muscle contractions have been examined in adult Fasciola hepatica. Caerulein and serum decrease the rate of oral sucker activity; motilin decreases and CCK-PZ increases ventral sucker activity when compared to controls. Caerulein, serum and motilin significantly inhibit the frequency of contractions while bile, caerulein and motilin decrease the amplitude of contractions. These results suggest that F. hepatica can recognize and respond to certain gastrointestinal hormones and there may be adaptive value in these behavioural responses.
The chemistry, localisation, release and effects of gastrointestinal hormones and some related peptides are surveyed. Their main presumed physiologic actions are: gastric acid and pepsin secretion are stimulated by gastrin and to a less degree by secretin. Acid secretion is inhibited by bulbo-enterogastrone and GIP. Biliary water and electrolytes are augmented by gastrin, CCK-PZ, secretin and VIP and inhibited by Substance P. Pancreatic bicarbonate and enzyme secretions are stimulated by secretin and CCK-PZ, especially in combination. Lower oesophageal and antral motility and tonus are elevated following gastrin and motilin; the gallbladder and small intestine empty following CCK. Gastrin regulates gastrointestinal, and CCK pancreatic, tissue growth. Somatostatin inhibits all gut hormones. All peptides are vasoactive within the splanchnic area, each one in a specific manner.
Using adult mongrel dogs, remnant gastric motility in relation to the changes of gastrointestinal hormone (gastrin and motilin) levels were measured under conscious states before and after distal partial gastrectomy in the Billroth I (BI) or II (BII) reconstruction and proximal partial gastrectomy with or without pyloroplasty. Remnant gastric motility was studied during the digestive and interdigestive states by chronically implanted strain gage transducer (S.G.T.) along the gastrointestinal tract. Gastrointestinal hormone levels were determined by radioimmunoassay. Results were summarized as follows: 1. Remnant gastric motility after BI was different from BII, that is, digestive patterns after BII were more shorter than BI, as a result, gastric emptying times were shortened. 2. Gastrin release by the meal intake in the dogs with BI was greater than that in BII. On the other hand, motilin release in the dogs with BII was higher level than that in BI during the digestive and interdigestive states. Gastrointestinal hormone levels after BI were approximately as same responses as controls. These findings suggested that BI reconstruction for distal partial gastrectomy was more physiological surgical procedure than BII reconstruction. 3. Remnant gastric motility during the digestive state after proximal gastrectomy showed the excitatory pattern and gastric emptying time was remarkably shortened than in controls. 4. In gastrin and motilin levels stimulated by the meal in the dogs with proximal gastrectomy, the peak of gastrin and the depression of motilin were observed more early in relation to remnant gastric emptying time. These findings suggested that the pyloroplasty for the proximal gastrectomy was necessary to prevent an increased motility of the remnant stomach during the digestive states.
Effects of gastrointestinal hormones on the electrical and mechanical activities of the smooth muscle of the cat small intestine were examined. Both spontaneous electrical and mechanical activities of the intestinal smooth muscle were inhibited by tetragastrin, pentagastrin and pancreozymin. The spike activity and the phasic contraction of the smooth muscle were depressed by these hormones while the slow waves were maintaned. On the other hand, secretin showed an excitatory action on the mechanical activity of the isolated preparation of smooth muscle. Spike activity disappeared and the level of tone was increased gradually. The inhibitory and excitatory actions of each hormone on the mechanical activity were not abolished by the application of atropine and tetrodotoxin. Furthermore, the inhibitory effects of pentagastin and pancreozymin on the smooth muscle were not antagonized with phenoxybenzamine or propranolol. These results suggest that the inhibitory actions of pentagastrin and pancreozymin on the smooth muscle were not mediated by alpha or beta receptors and not due to the stimulation of an inhibitory nervous system in the gut. Antagonistic relations between secretin and pentagastrin and also between secretin and pancreozymin were observ ed. The mechanisms of the actions of gastrointestinal hormones are discussed.
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Effects of an artificial mental stress on colonic motility, autonomic nervous system, and gastrointestinal hormones were examined in patients with irritable bowel syndrome (IBS). The subjects were 20 patients with typical IBS and 12 controls. A transducer was inserted to the sigmoid colon from the anus for measuring colonic intraluminal pressure, and mirror drawing test was loaded as psychological stress. At the same time, coefficient of variation of R-R interval on ECG (CV-RR) was measured and the levels of plasma catecholamines, gastrin, glucagon, and motilin were assessed. Colonic motility showed a significant increase in the IBS patients during the stress compared with that in controls (p less than 0.01). Motilin also increased significantly in the IBS patients after the stress (p less than 0.01). CV-RR and motilin revealed positive relationship with colonic motility alteration in the IBS patients although no significant change was detected in controls. These phenomena are thought to be due to autonomic nervous dysfunction and/or gastrointestinal hormonal derrangments induced by psychological stress. It is suggested that organ specificity of the alimentary tract for the stress exists in this disease.
This article discusses experiments demonstrating that the gastrointestinal hormones, gastrin, secretin, and CCK (cholecystokinin), stimulate the growth of the exocrine pancreas. Exogenous gastrin, secretin, and CCK increase pancreatic weight DNA, RNA and protein content of the rat pancreas. Antrectomy, which removes most endogenous gastrin, decreases pancreatic growth. The effects of antrectomy are prevented by exogenous gastrin. Infusion of HCl into the duodenum to release secretin and infusion of amino acids into the duodenum to release CCK also stimulate pancreatic growth. These results provide evidence that the regulation of pancreatic growth is an important action of the gastrointestinal hormones.
The effect of alpha-2 adrenoreceptor agonists, cholinergic drugs, autacoids and some gastrointestinal hormones upon the evocation of rumination in sheep when injected by close-arterial injection into the forestomach was examined. Apart from adrenaline, noradrenaline, dopamine and xylazine only one alpha-2 agonist (BHT933) evoked rumination effectively. Acetylcholine, neostigmine, the gastrointestinal hormones and the autacoids examined did not evoke rumination consistently. Tyramine did not usually evoke rumination and guanethidine injected before adrenaline did not prevent the latter from evoking rumination. The evocation of rumination by catecholamines does not appear to involve sympathetic, cholinergic or non-sympathetic non-cholinergic neurones in the enteric nervous system to activate the nervous sensory receptors involved in the reflex evocation of rumination.
This study was undertaken to elucidate the impact of hypercortisolism in meal-related gastrointestinal hormone secretion and appetite in female endurance athletes. Thirteen elite runners and seven sedentary women participated on two occasions, either receiving intravenous injection of 250 micrograms synthetic adrenocorticotropic hormone (ACTH) 1-24 or saline. Blood samples were collected before and after the injection, and then in connection with a standardized meal. Serum concentrations of cortisol, cholecystokinin (CCK), gastrin, insulin and glucose were analyzed. Self-ratings of appetite were assessed by visual analog scales. Elevated basal levels of cortisol and glucose were found in the athletes. ACTH-induced cortisol response was comparable between groups, but a negative correlation between basal cortisol levels and the ACTH-induced response was found. In sedentary women, ACTH challenge enhanced meal-related CCK and gastrin responses, whereas athletes showed a blunted response of these hormones combined with decreased satiety and reduced levels of insulin. Blunted meal-related response of gastrointestinal hormones and decreased satiety in female runners after ACTH stimulation compared to sedentary women are probably due to difference in the effect of cortisol, which could be explained by cortisol insensitivity as a result of basal hypercortisolism in the athletes. Decreased CCK response and satiety in female athletes may reflect increased nutritional requirements.
Because the gastrointestinal hormones are known to dilate the splanchnic vasculature, their effects on transport of water and solutes during peritoneal dialysis were studied in an experimental model, the rabbit. In unanesthetized rabbits, dialysate volume was calculated by isotope dilution, and clearances were estimated by dialysate/plasma concentration ratio factored by minute volume. With isotonic dialysis solution, the mean increment in dialysate volume per minute of intraperitoneal dwell was 0.19 ml/kg/min, and mean clearances of creatinine and urea were 0.71 and 0.90 ml/kg/min, respectively. When administered intravenously, secretin significantly augmented osmotically induced water flux, but not when given intraperitoneally. Neither glucagon nor cholecystokinin affected dialysate volume. Intravenously, but not intraperitoneally, glucagon increased peritoneal clearances of creatinine and urea to more than 150% of control values. Neither cholecystokinin nor secretin augmented significantly peritoneal mass transport when given by either route. The data suggest that the site of acton is the endothelial surface of the membrane, that the mechanisms of augmenting transport involve increased permeability and/or surface area, and that agents which combine an increase in mass transport and capillary filtration coefficient may be clinically useful.
BACKGROUND: Accumulating evidence suggests that certain dietary polyphenols have biological effects in the small intestine that alter the pattern of glucose uptake. Their effects, however, on glucose tolerance in humans are unknown. OBJECTIVE: The objective was to investigate whether chlorogenic acids in coffee modulate glucose uptake and gastrointestinal hormone and insulin secretion in humans. DESIGN: In a 3-way, randomized, crossover study, 9 healthy fasted volunteers consumed 25 g glucose in either 400 mL water (control) or 400 mL caffeinated or decaffeinated coffee (equivalent to 2.5 mmol chlorogenic acid/L). Blood samples were taken frequently over the following 3 h. RESULTS: Glucose and insulin concentrations tended to be higher in the first 30 min after caffeinated coffee consumption than after consumption of decaffeinated coffee or the control (P < 0.05 for total and incremental area under the curve for glucose and insulin). Glucose-dependent insulinotropic polypeptide secretion decreased throughout the experimental period (P < 0.005), and glucagon-like peptide 1 secretion increased 0-120 min postprandially (P < 0.01) after decaffeinated coffee consumption compared with the control. Glucose and insulin profiles were consistent with the known metabolic effects of caffeine. However, the gastrointestinal hormone profiles were consistent with delayed intestinal glucose absorption. CONCLUSIONS: Differences in plasma glucose, insulin, and gastrointestinal hormone profiles further confirm the potent biological action of caffeine and suggest that chlorogenic acid might have an antagonistic effect on glucose transport. Therefore, a novel function of some dietary phenols in humans may be to attenuate intestinal glucose absorption rates and shift the site of glucose absorption to more distal parts of the intestine.
Calcitonin gene-related peptide (CGRP) is a recently discovered widespread regulatory peptide which is encoded in the same gene as calcitonin. We assessed the effect of systemic infusion of synthetic rat CGRP at low dose (range 0.32-2.56 pmol/kg per min) on submaximal pentagastrin-stimulated gastric secretion and on gastrointestinal hormones. To assess its pharmacokinetic parameters in man the MCR and plasma half-life were estimated by the continuous infusion method. Gastric acid output and pepsin secretion were significantly reduced by CGRP (-29% of basal, P less than 0.01 and -40% of basal, P less than 0.005, respectively). There was a significant fall in basal levels of gastrin (-39%, P less than 0.001); gastric inhibitory peptide (-44.7%, P less than 0.001); enteroglucagon (-25%, P less than 0.001) and neurotensin (-33%, P less than 0.05). There was no significant change in plasma levels of insulin, motilin, pancreatic polypeptide or glucose. Suppression of gastric secretion and the fall in gastrointestinal hormones was prolonged and basal levels were not re-established after stopping the CGRP infusion. The disappearance curve of immunoreactive CGRP from the plasma was bi-exponential. The plasma half-life of immunoreactive CGRP was calculated as 6.9 +/- 0.9 min for the fast decay and 26.4 +/- 4.7 min for the slow decay. The calculated MCR was 11.3 +/- 1.2 ml/kg per min. Except for flushing of the face no untoward effects were observed. The results of this study suggest the possibility that CGRP could play a role in the regulation of gastric secretion and gastrointestinal hormone release.
The pancreatic duct cell adenocarcinoma induced by di-isopropanol nitrosamine in Syrian golden hamsters could be easily and repeatedly into the subcutaneous tissues or the pancreas of the homologous animals. We examined the anti-tumor effects of the administration of FT-207 and the coadministration of FT-207 and uracil on the pancreatic cancer transplanted into the subcutaneous tissues and the pancreas. The inhibitory effect on the tumor growth observed in the group treated with FT-207 and uracil was more striking than that in the group treated with only FT-207. Such enhanced anti-tumor effect observed in the coadministration group seemed to be due to the increased 5-FU concentration in the tumor tissues. Some gastrointestinal hormones (cholecystokinin, caerulein, secretin and tetragastrin) injected intraperitoneally promoted the growth of subcutaneously transplanted tumor. These gastrointestinal hormones except tetragastrin also increased the weight of the pancreas. In an analysis of RNA and DNA contents and RNA/DNA ratio in tumor tissues, the promotion of the tumor growth seemed to stem from hyperplasia and/or hypertrophy of the cancer cells. Therefore, it is suggested that some gastrointestinal hormones have trophic actions on the pancreatic duct cell adenocarcinoma as well as normal pancreas.
The effects of gastrointestinal hormones on gastric carcinomas were examined in vitro and in vivo. In five of seventeen cases of human gastric carcinomas, the uptake of 14C-leucine into the tumor tissue in organ culture was enhanced by 10 micrograms/ml of gastrin. Also, in four of thirteen cases of human gastric carcinomas, the production of 14C-labelled proteins in medium was increased by gastrin. All the cases in which protein synthesis was enhanced by gastrin were histologically poorly differentiated adenocarcinomas. The effects of gastrin and secretin on the growth of gastric carcinoma, which was serially transplanted in athymic mice, were examined. The doubling time of the tumor was 7.1 days. The doubling time was shortened to 4.1 days by daily administration of 250 micrograms/kg of gastrin. This topic effect of gastrin on gastric carcinoma was inhibited by 100 U/kg of secretin. These results showed that the growth and protein synthesis of gastrointestinal tumor may be regulated by gastrointestinal hormones.
The effects of the gastrointestinal hormones secretin and cholecystokinin (CCK) were investigated on rat portal-vein mechanical activity. Doses of 0.03-0.60 units/ml Boots secretin; 0.18-0.60 units/ml pure, natural secretin; and 0.12-0.60 units/ml CCK elicited dose-dependent decreases in amplitude and simultaneous increases in frequency of spontaneous contractions that were unaffected by alpha-or beta-adrenergic or cholinergic blocdade. These effects were mimicked by isoproterenol, theophylline, and cyclic AMP, and all agents tested were also effective in reducing K-or norepinephrine-induced tension. Additionally, subthreshold doses of CCK and secretin elicited responses when given in combination, and the effects of the hormomes at all doses were potentiated by theophyline, indicating an interaction berween these hormones on rat portal vein thatmay involve cyclic AMP. It is suggested that part of the mechanism of hormone-induced mesenteric vasodilatation may involve a direct relaxing effect of the hormones on vascularsmooth muscle.
Several gastrointestinal (GI) hormones, such as gastrin, cholecystokinin, and bombesin, have been reported to affect the development of pancreatic cancer. The receptors for these hormones are found in normal and neoplastic pancreatic cells. Activation of these receptors enhances pancreatic carcinogenesis and promotes the growth of established pancreatic carcinoma either in vitro or in vivo. On the other hand, some studies have shown that these GI hormones may have no effect or may play an inhibitory role in the development of pancreatic cancer. The reasons for the apparent discrepancies in the published literature are discussed in this review. In recent years, increasing emphasis has been placed on the effects of GI hormones on cancer invasion and metastasis. As the transition from noninvasion to the invasive state is the crucial event in cancer development, further investigation of the way in which GI hormones affect the invasion and metastasis of pancreatic cancer may be important for the development of new therapeutic approaches with eventual clinical utility.
Experiments were performed on adult beagle dogs to investigate the nutritional state and the release of gastrointestinal hormones after pancreatoduodenectomy. A new variation of reconstruction of the alimentary tract was devised and compared with the classical Child's method. In our method, the remaining stomach was anastomosed to the oral stump of the jejunum in an end-to-end fashion. A short mid-intestinal segment was interposed between the pancreatic and bile ducts and the upper jejunum. During the observation period of six months after surgery, the loss of body weight was significantly smaller in the new method, and the frequency of both morbidity and mortality was lower. Although perforated stomal ulcer was observed in one dog after the Child's method, no peptic ulcer was detectable after our method. The integrated increase of plasma triglyceride in response to ingested butter was slightly greater in our method than in the Child's. At six weeks after surgery, plasma concentrations of both cholecystokinin and secretin, not only during fasting but after intake of butter, were augmented in both groups, particularly in the group receiving the new method. These results indicate that retaining the remaining upper small intestine as the food pathway is effective in maintaining good nutritional state, and in facilitating the release of gastrointestinal hormones.