[The effects of cholecystokinin on dynamics of the bile ducts, with special reference to the behavior of the sphincters of the gallbladder and common bile duct].
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Bile Ducts↗
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[Cholecystokinin in the x-ray examination of the bile ducts].
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Bile Ducts↗
[Cholecystokinin in the clinical practice of duodenobiliary intubation & cholecystography].
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Bile Ducts↗
Anti-inflammatory effect of the ghrelin agonist growth hormone-releasing peptide-2 (GHRP-2) in arthritic rats.
Chronic arthritis induces hypermetabolism and cachexia. Ghrelin is a gastrointestinal hormone that has been proposed as a treatment to prevent cachexia. The aim of this work was to examine the effect of administration of the ghrelin agonist growth hormone-releasing peptide-2 (GHRP-2) to arthritic rats. Male Wistar rats were injected with Freund's adjuvant, and 15 days later arthritic and control rats were daily injected with GHRP-2 (100 microg/kg) or with saline for 8 days. Arthritis induced an increase in serum ghrelin (P < 0.01) and a decrease in serum concentrations of leptin (P < 0.01), whereas GHRP-2 administration increased serum concentrations of leptin. GHRP-2 increased food intake in control rats but not in arthritic rats. However, in arthritic rats GHRP-2 administration ameliorated the external symptoms of arthritis, as it decreased the arthritis score (10.4 +/- 0.8 vs. 13.42 +/- 0.47, P < 0.01) and the paw volume. In addition, circulating IL-6 and nitrites/nitrates were increased by arthritis, and GHRP-2 treatment decreased the serum IL-6 levels (P < 0.01). To elucidate whether GHRP-2 is able to modulate IL-6 release directly on immune cells, peritoneal macrophage cultures were incubated with GHRP-2 or ghrelin, the endogenous ligand of the growth hormone (GH) secretagogue receptor. Both GHRP-2 (10(-7) M) and ghrelin (10(-7) M) prevented endotoxin-induced IL-6 and decreased nitrite/nitrate release from peritoneal macrophages in vitro. These data suggest that GHRP-2 administration has an anti-inflammatory effect in arthritic rats that seems to be mediated by ghrelin receptors directly on immune cells.
Adrenocorticotropic Hormone↗
The effect of duodenojejunal alimentation on gastric pH and hormones in intensive care unit patients.
We evaluated effects of duodenojejunal (DJ) feeding on gastric pH and selected gastrointestinal hormones in 13 randomly selected patients in an intensive care unit (ICU). To obtain baseline values for gastric pH, a nasogastric (NG) tube was placed in each patient and gastric pH was measured every 30 minutes for 2 hours. To obtain control values, a Dobbhoff tube was placed fluoroscopically and 0.45 percent saline solution (NaCl), 75 ml, was infused for 1 hour and gastric pH was measured again; the previously placed NG tube was left in position. Then, by randomization, either 0.45 percent NaCl (pH = 5) was continued (n = 6) or a high-nitrogen, isotonic, enteral feeding solution (Osmolite HN, pH = 6.4) (n = 7) was infused, both at 75 ml/h. Gastric pH was noted hourly for 96 hours; antacid (Maalox TC, 15-ml aliquots) was given by NG tube when the pH was 4 or less. After 96 hours, the infusion was stopped and gastric pH was noted for 4 additional hours. Before and during initial saline solution infusion; after 24, 48, 72, and 96 hours of continuous infusion; and 4 hours after stopping the infusion, peripheral venous blood was obtained for measurement of plasma gastric inhibitory polypeptide (GIP) and serum gastrin. Data were analyzed by ANOVA (RMD), Fishers' exact test, and the unpaired t-test. Groups did not differ demographically. Throughout the infusion, gastric pH tended to be higher with the enteral feeding solution than with saline solution, but this was significant only at 24 hours. Less antacid was required with the enteral feeding solution at 24 and 48 hours than with saline solution. Plasma GIP levels were significantly higher with the enteral feeding solution than with saline solution during most of the infusion. Serum gastrin levels did not differ between the groups. In this cohort, infusion of the enteral feeding solution tended to maintain a gastric pH of more than 4 and was associated with increased plasma GIP levels, which may inhibit gastric acid secretion. Early enteral feeding may benefit certain ICU patients.
Antacids↗
The diagnosis of pancreatic disease.
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Gastrointestinal Hormones↗
Effects of gastrointestinal polypeptides on hormone content of endocrine pancreas in the rat.
Although trophic actions of gastrointestinal peptides on exocrine pancreas have been shown, little is known regarding their effects in endocrine pancreas. Therefore, we measured the contents of somatostatin-like immunoreactivity (SLI), insulin and glucagon, in pancreatic extracts from rats that had been treated three times a day for 10 days with saline; 1 microgram/kg caerulein; 5, 25, and 100 microgram/kg secretin; 1 microgram/kg caerulein plus 5, 25, and 100 microgram/kg secretin; 25 microgram/kg pancreatic polypeptide; 15 microgram/kg glicentin; or 15 microgram/kg gastric-inhibitory polypeptide. Pancreatic SLI content was significantly increased in rats treated with glicentin and caerulein plus secretin at the two higher doses. No difference was noted between the control and the caerulein plus 100 microgram/kg secretin groups in delta-cell number per islet when examined by the immunoperoxidase technique. These data suggest that because of their effect on SLI content gastrointestinal polypeptides may modulate pancreatic endocrine function.
Animals↗
Vitamin E and the Y4 agonist BA-129 decrease prostate cancer growth and production of vascular endothelial growth factor.
BACKGROUND: A biologically active form of vitamin E, alpha-tocopherol succinate (ATS), has been shown to induce apoptosis of hormone-refractory prostate cancer in vitro and inhibit cell growth in vivo. The gastrointestinal hormone peptide YY (PYY) has growth inhibitory activity against multiple cancer cell lines and is synergistic with ATS against breast and pancreatic cancer growth. BA-129, a specific Y4 receptor agonist, has growth inhibitory effects on pancreatic cancer in vitro. We investigated the effects of BA-129 and ATS on prostate cancer growth and evaluated their effects on vascular endothelial growth factor (VEGF) production. METHODS: A hormone-refractory human prostate cancer cell line, PC-3, was treated with ATS alone at 10 pg/ml, PYY or BA-129 alone at doses of 75 and 500 pmol/ml, or a combination of the two agents. Cell growth was measured by MTT assay and hemocytometry using trypan blue. Quantitative measurement of VEGF was performed by ELISA. Statistical analysis was achieved by ANOVA. RESULTS: ATS exhibited significant (P < 0.05) growth inhibitory effects in prostate cancer cells. PYY also inhibited growth (P < 0.05). ATS treatment reduced VEGF production (P < 0.05). PYY treatment increased VEGF. When ATS was given in combination with BA-129, VEGF production was further reduced (P < 0.05). CONCLUSIONS: Both PYY and ATS inhibit growth in hormone-refractory prostate cancer, with augmentation when used in combination. VEGF production is inhibited by vitamin E, but increased by PYY. ATS abolishes the augmented VEGF response to PYY. Our data suggest that PYY is involved in the regulation of VEGF production and prostate cancer growth.
Antineoplastic Agents↗
[Ogilvie's syndrome].
"Ogilvie's syndrome" or the idiopathic dilatation of the colon is an infrequent pathology whose underlying physiopathology is not yet well known. On the basis of their experience and having reviewed the literature, the authors affirm that this syndrome is caused by the inhibition of gastrointestinal hormones which, under the control of the neurohypophysis, contribute to colon motility. This supposition is backed up by the fact that medical treatment with somatostatin or octreotide leads to the resolution of the disorder.
Adolescent↗
Circulating ghrelin levels in patients with pancreatic and gastrointestinal neuroendocrine tumors: identification of one pancreatic ghrelinoma.
Ghrelin is a novel gastrointestinal hormone involved in several metabolic functions. Although the expression of ghrelin has been demonstrated in most gastrointestinal carcinoids and pancreatic tumors, the circulating levels of this peptide have been marginally assessed in patients with these disorders. We measured plasma ghrelin levels in 16 patients with gastrointestinal carcinoid (10 with midgut and 6 with gastric carcinoid), 24 patients with pancreatic tumor (8 with gastrinoma, 2 with insulinoma, 2 with vipoma, 1 with glucagonoma, and 11 with nonfunctioning tumor), and 35 healthy controls. Plasma ghrelin levels recorded in patients with gastroenteropancreatic tumors were similar to controls (mean +/- SE, 182.7 +/- 66.5 pM in patients vs. 329 +/- 32 pM in controls, P = not significant), and no significant difference between gastrointestinal and pancreatic, functioning and nonfunctioning, and metastatic and nonmetastatic tumors was observed. One patient with metastatic nonfunctioning pancreatic tumor had circulating ghrelin levels of 12,000 pM that were slightly reduced during chemotherapy and interferon therapy. Immunohistochemistry performed on peritoneal lesions showed an intense, focal cytoplasmic positivity for ghrelin. Despite the 50-fold increase in ghrelin concentrations, the patient had normal serum GH and IGF-I levels. In conclusion, the study showed that carcinoids and pancreatic tumors rarely cause ghrelin hypersecretion. However, in this series, 1 pancreatic ghrelinoma not associated with clinical features of acromegaly was identified.
Adolescent↗
The role of gut-glucagon-like immunoreactants in the control of gastrointestinal epithelial cell renewal.
In vitro and in vivo studies have provided considerable information on the possible physiologic function of circulating gastrointestinal hormones as well as locally acting regulatory peptides in the multifactorial control of adaptive gastrointestinal epithelial cell proliferation and cell renewal. It has been suggested by circumstantial evidences that enteroglucagon (EG; G-GLI I) may act as a trophic factor on the intestinal mucosa which may account for adaptive changes of the small intestine following various stimuli. However, we have shown that there are experimental conditions (germ-free rats after conventionalisation; jejunal self-filling blind loops) in which intestinal hyperplasia does not correspond to an increase in the concentrations of enteroglucagon in plasma or intestinal mucosa. Furthermore, despite a continuous immunoneutralisation of circulating endogenous enteroglucagon by monoclonal antibodies there was an adaptive, hyperplastic response of the ileal remnants after a 70% proximal small bowel resection which was of the same magnitude as in the control group but was even greater considering the increased number of mitoses per crypt. In order to gain additional insight into the putative role of enteroglucagon as an enterotrophic regulatory peptide, an in vitro model was used to investigate the effect of highly purified rat G-GLI I on the proliferative response of primary small intestinal epithelial cells of fetal rats. Whereas there was a well known growth-promoting action of EGF, the proliferation of rat fetal intestinal epithelial cells was inhibited by the addition of purified G-GLI I. These results indicate that enteroglucagon does not act as an enterotrophic factor but provide the first direct evidence consistent with an antitrophic role of enteroglucagon in the small intestine.
Adaptation, Physiological↗
[Endoscopy, a hobby for specialists--or more?].
In the years between 1958 and 1970, diagnostic endoscopy made decisive advances. In this period, the ground was prepared for operative endoscopy. This applies not only to the technical, but also to the psychological aspects. The fact that formerly hidden structures could now be directly inspected and ""grasped'', spurned the endoscopist to intensive activity. Polypectomy, papillotomy with the removal of gallstones and, increasingly, photocoagulation for the arrest of bleeding, have made in many cases classical surgical operations superfluous. In close cooperation and rapport with the surgeons, the indications for, but also the limitations of, the new procedure are being established. In addition to the more practical aspects, modern endoscopy has also created a bridge to better understanding of biochemical processes in the gastrointestinal tract. The possibility of being able to investigate the effects of newly discovered, analysed and synthesized gastrointestinal hormones has been considerably improved. Endoscopy, formerly considered, more or less, a hobby for a few specialists, has become a sort of intermediary system which is capable of providing excellent diagnostic information, of making possible elegant therapeutic measures and of producing new biochemical information. In this creative function, it is surpassed by virtually no other method. A pre-condition for this development was, however, that the endoscopist was not content to remain merely an observer of interesting views, but was, rather, an active physician, to whom the advantages to the patient of early detection of disease and suitable therapeutic measures were equally important as the useful information obtained on biochemical relationships.
Cholelithiasis↗
Catabolic outcome from non-gastrointestinal malignancy-related malabsorption leading to malnutrition and weight loss.
PURPOSE OF REVIEW: Malnutrition of cancer patients is a significant cause of mortality and morbidity. RECENT FINDINGS: The contributory factors in cancers anatomically involving the gastrointestinal tract are self-evident. However, how non-gastrointestinal malignancies affect gastrointestinal structure and function is not clear. The aim of this paper is to review the relationship between non-gastrointestinal malignancies and malabsorption, which leads to malnutrition, weight loss and increased mortality. In non-gastrointestinal cancer patients, intestinal morphological atrophy occurs, whereas in the jejunum absorption is impaired. Cytokines including IL-1 and TNF-alpha primarily induce delayed gastric emptying and also act directly on intestinal mucosa to induce malabsorption. These cytokines also directly act on several gastrointestinal hormones including cholecystokinin, neuropeptides including corticotropin-releasing factor, and via the vagus to decrease gastrointestinal motility. SUMMARY: The combination of small intestine atrophy and delayed gastrointestinal motility are some of the reasons for malabsorption in cancer patients with non-gastrointestinal malignancies that contribute to the catabolic process.
Cytokines↗
Ovine model for clear-cut study on the role of cholecystokinin in antral, small intestinal and gallbladder motility.
Cholecystokinin (CCK) is one of the major gastrointestinal hormones involved in the control of digestive tract and gallbladder motility. Its action involves several mechanisms. The ovine model was developed in order to further explore the role of CCK in gastric, small intestinal and gallbladder motility under various experimental conditions. Five Merino sheep were used with bipolar electrodes implanted to their antrum, entire small intestine and gallbladder as well as strain gauge force transducers were attached to the duodenum and gallbladder fundus, near the electrodes. In the course of chronic experiments, the myoelectric and motor activity were recorded by means of the adapted electroencephalograph. Among the variety of CCK-octapeptide or cerulein doses, three doses of each CCK peptide were selected and then applied for various time periods. Finally, the effects of the hormones administered within 30 s during phase 2 of the same or different migrating myoelectric complexes (MMCs) on gastrointestinal and gallbladder myoelectric and motor activity were studied in fasted and non-fasted animals. Injection of the highest dose inhibited rumination in four of the five sheep and inhibited phase 3 MMC in the antroduodenal region. Hormone administration inhibited dose-dependently antral myoelectric activity. The effects of moderate dose of both CCK peptides on myoelectric activity of the duodeno-jejunum was usually opposite (i.e. stimulatory) than that of the ileum. Gallbladder response to CCK peptides exhibited mostly the tonic character, and in some experiments, the slow wave frequency and amplitude were altered. It is concluded that CCK acts on several targets and different mechanisms underlie its multiple actions on gastrointestinal and gallbladder motility in sheep.
Action Potentials↗
The effects of somatostatin and octreotide on the human sphincter of Oddi.
OBJECTIVE: Somatostatin acts at different sites in the human gastrointestinal tract and generally inhibits the release and effects of many gastrointestinal hormones and neuropeptides. Together with its long-acting analogue octreotide, somatostatin is widely used in the treatment of hormone-producing tumours, variceal bleeding, etc., but multi-centre trials have failed to prove a beneficial effect in the treatment of acute pancreatitis or in the prevention of post-ERCP pancreatitis (pancreatitis following endoscopic retrograde cholangiopancreatography). The aim of the present work was to study the effects of somatostatin and octreotide on the human sphincter of Oddi by means of quantitative hepatobiliary scintigraphy (QHBS). METHOD: Fifteen cholecystectomized patients were enrolled in the study, six in the somatostatin group and nine in the octreotide group. QHBS was performed initially with a standard protocol (baseline data), then repeated after 0.1 mg octreotide or a 250 microg bolus + 250 microg/h somatostatin administration. In the 60th min of QHBS, 0.5 mg glyceryl trinitrate (GTN) was administered sublingually. RESULTS: QHBS demonstrated that both somatostatin and octreotide caused a marked impairment in the bile flow: the half-time of excretion (T1/2) over the common bile duct was significantly prolonged compared with baseline data (somatostatin group: common bile duct T1/2 180 min versus 59.7+/-31 min; octreotide group: common bile duct T1/2 140.9+/-60.5 min versus 30.7+/-11.7 min). Glyceryl trinitrate administration accelerated the transpapillary bile flow, with significant decreases in the elevated T1/2 in both groups. CONCLUSION: Increased transpapillary flow induced by glyceryl trinitrate may be beneficial in the treatment of acute or post-ERCP pancreatitis.
Bile↗
Intestinal phase of human antro-pyloro-duodenal motility: cholinergic and CCK-mediated regulation.
In this study the muscarinic receptor antagonist atropine and the cholecystokinin (CCK)-A receptor antagonist loxiglumide were used to investigate the relative importance of cholinergic and CCK-mediated regulation of intestinal phase antro-pyloro-duodenal motility. Plasma levels of gastrointestinal hormones [pancreatic polypeptide (PP), gastrin, CCK] were concomitantly determined to estimate biological potency of the doses of the receptor antagonists. In eight healthy male volunteers, a 30-min basal interdigestive period was followed by duodenal perfusion of a mixed liquid meal for 150 min at 1.6 kcal min-1 against a background of saline or atropine (5 micrograms kg-1 h-1) or loxiglumide (10 mg kg-1 h-1). Antropyloro-duodenal motility was continuously monitored with a sleeve straddling the pylorus. Against a background of saline, duodenal nutrients persistently stimulated isolated pyloric pressure waves. After 60 min, the initially low antral and duodenal contraction rates increased. In the fed state, atropine reduced total number of antral contractions and integrated motility index by 73% (P < 0.01) and 76% (P < 0.005), total number of pyloric contractions and integrated motility index by 43% and 50% (P < 0.05) with inhibition increasing over time. It did not alter duodenal contraction frequency but diminished duodenal motility index by 39% (P < 0.05) owing to a reduction in amplitude and duration of contractions. Loxiglumide decreased total numbers of antral, pyloric and duodenal contractions by 44% (P < 0.05), 74% (P < 0.005) and 41% (P < 0.005) respectively. It reduced cumulative antral, pyloric and duodenal motility indexes by 60% (P < 0.01), 80% (P < 0.01) and 61% (P < 0.05) respectively. Atropine fully abolished PP release to duodenal nutrients whereas loxiglumide reduced it by 60% (P < 0.05). Both atropine and loxiglumide enhanced gastrin release whereas only loxiglumide markedly stimulated CCK release. We conclude that both cholinergic input and endogenous CCK are major stimulatory regulators of antro-pyloroduodenal motility in the intestinal phase. There appears to be a regional heterogeneity of cholinergic and CCK control. Cholinergic input predominates in the antrum. Both systems are equipotent at the pylorus. CCK predominates in the duodenum. We suggest that CCK primarily interacts with receptors on cholinergic neurons in the antropyloric region and primarily affects smooth muscle receptors in the duodenum.
Acetylcholine↗
"Virtual rat": a tool for understanding hormonal regulation of gastrointestinal function.
This manuscript describes a "dry laboratory" using the "virtual rat" to help students understand the hormonal regulation of gastrointestinal function. The laboratory was modeled after a recent exercise that used the virtual rat to teach basic endocrine physiology. The virtual rat concept avoids the many obstacles associated with animal experimentation (for example, lack of adequate animal facilities, expense, equipment, and limited teacher experience). Our goal was to create a fun and educational experience while avoiding the complications associated with laboratory experimentation. No additional materials are required to complete this exercise. After finishing this laboratory, the students should have a greater understanding and appreciation for experimental design and the collection, analysis, and interpretation of data.
Animals↗
The activity front of the migrating motor complex of the human stomach but not of the small intestine is motilin-dependent.
The role of motilin in the generation of the gastric component of phase 3 of the migrating myoelectric complex (MMC) was studied in human volunteers. Interdigestive motor activity was recorded manometrically in five normal subjects after a fast of at least 15 h. Intraluminal pressures were measured in the gastric antrum at 4 levels 3 cm apart and in the upper small bowel at 3 levels 25 cm apart. Blood samples were drawn every 10 min for radioimmunoassay of motilin and PP. After 2 spontaneously occurring activity fronts (AF) had been recorded, bovine PP was infused intravenously at a rate of 50 micrograms/h. Following the third AF a combination of PP (50 micrograms/h) and 13-norleucine-motilin (30 micrograms/h) was infused until after the next AF. It was found that 90% of the spontaneous AFs originated in the stomach. They were preceded by a motilin peak. During the PP infusion, plasma PP levels increased from 29 to 256 pmol/l, motilin decreased from 42 to 15 pmol/l, and all AFs originated in the small bowel. During the combined PP and motilin infusion, plasma motilin increased to 330 pmol/l, and all AFs again originated in the stomach. It is concluded that motilin has an important role in the regulation of the MMC activity front in the stomach, but not in the small intestine. Postprandial rises in plasma PP might be involved in lowering motilin levels after a meal, and indirectly, in the disruption of gastric MMCs during digestion.
Adult↗