cholecystokinin and Diarrhea

Information concerning GEP hormones has progressively advanced since the initial discovery of a GEP hormone, secretin, in 1902. Studies in this area flourished with the advent of radioimmunoassay, and have provided an understanding of the secretion, regulation, metabolic actions, and role in certain diseases of major GEP hormones. Measurement of GEP hormones has achieved importance in clinical medicine and allowed understanding of the pathophysiology of several clinical disorders. The decade to come should witness additional advances in this rapidly expanding field.

Topics: Chemical Phenomena; Chemistry; Cholecystokinin; Diabetes Mellitus; Diarrhea; Endocrine System Diseases; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Hypoglycemia; Motilin; Neoplasms; Neurotensin; Pancreatic Polypeptide; Peptic Ulcer; Secretin; Skin Diseases; Somatostatin; Substance P; Vasoactive Intestinal Peptide

Topics: Adult; Cholecystokinin; Colon; Colonic Diseases; Constipation; Diarrhea; Eating; Electromyography; Female; Gastrointestinal Motility; Humans; Male; Mental Disorders; Parasympatholytics; Pressure

Topics: Adenoma, Islet Cell; Carcinoid Tumor; Cholecystokinin; Diarrhea; Gastrins; Gastrointestinal Hormones; Gastrointestinal Neoplasms; Glucagon; Hormones, Ectopic; Humans; Insulin; Insulin Secretion; Neurosecretory Systems; Pancreatic Hormones; Paraneoplastic Endocrine Syndromes; Prostaglandins; Serotonin; Syndrome; Vasoactive Intestinal Peptide; Werner Syndrome; Zollinger-Ellison Syndrome

Topics: Bradykinin; Cecum; Cholecystokinin; Colitis, Ulcerative; Colon; Colonic Diseases, Functional; Constipation; Diarrhea; Diverticulum, Colon; Gastrins; Gastrointestinal Motility; Humans; Muscle Contraction; Parasympathomimetics; Prostaglandins; Radiography; Rectum; Serotonin

Tumoral secretions and pathophysiology of diarrhea were studied in 1 patient with pancreatic cholera. High concentrations of vasoactive intestinal peptide were found in both systemic blood and tumoral extracts, together with increased plasma levels of calcitonin and protaglandins E and Falpha. Gastric inhibitory peptide and gastrointestinal and pancreatic hormones were absent from the tumor, except for small amounts of glucagon, and their blood levels were normal. Decreased basal but normal pentagastrin-stimulated gastric acid secretion, normal basal and secretin-stimulated pancreatic secretion, increased volume of gallbladder bile with high bicarbonate, and low bile salt concentrations were observed, but the electrolyte content and flow rate of fluid passing the duodenojejunal junction were within normal limits. Small intestine was found to be the origin of the water and electrolyte fasting losses. Jejunum was the site of bicarbonate secretion. Jejunal glucose and leucine-stimulated water and sodium transports were also strikingly decreased, whereas the absorption rates of the sugar and amino acid were normal. Colon reabsorbed high amounts of water and sodium but increased potassium losses. Biological effects of vasoactive intestinal peptide may explain most of the patient's upper digestive secretion abnormalities and small intestinal function impairments, whereas secondary aldosteronism might explain the modified colonic function.

Topics: Adult; Bile; Blood Vessels; Calcitonin; Cholecystokinin; Cholera; Colon; Depression, Chemical; Diarrhea; Duodenum; Feces; Female; Gastric Mucosa; Gastrins; Glucagon; Humans; Ileostomy; Insulin; Insulin Secretion; Intestinal Secretions; Intestine, Small; Pancreas; Pancreatic Diseases; Pancreatic Neoplasms; Peptides; Prostaglandins E; Prostaglandins F; Secretin; Stomach

Topics: Achlorhydria; Acute Kidney Injury; Adenoma, Islet Cell; Adult; Cholecystokinin; Dehydration; Diarrhea; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Hypercalcemia; Hypokalemia; Kidney Diseases; Male; Pancreatic Neoplasms; Protein Precursors; Secretin; Syndrome; Zollinger-Ellison Syndrome

Topics: Bile; Binding Sites; Celiac Disease; Cholecystokinin; Cholestyramine Resin; Diarrhea; Diet Therapy; Digestion; Fatty Acids, Nonesterified; Humans; Hydrolysis; Malabsorption Syndromes; Neomycin; Phospholipids; Secretin; Triglycerides

it was aimed to investigate the efficacy and safety of cupping moxibustion in patients with functional diarrhea. 51 patients diagnosed with functional diarrhea from January 2021 to December 2021 were selected as the objects, and they were randomly divided into the control group (oral montmorillonite powder) and the experiment group (oral montmorillonite powder combined with cupping moxibustion). The number of diarrheas, Bristol stool, traditional Chinese medicine (TCM) syndromes, clinical efficacy indexes, self-rating anxiety scale (SAS) score, the MOS item short from health survey (SF-36) scale score, peripheral blood cell levels of CD4+, CD8+, and Th17, gastrin (GAS), motilin (MTL), and cholecystokinin (CCK) levels was assessed before and after treatment. The adverse events were also recorded. Compared with those before treatment, all indexes of both groups were significantly improved (P<0.05). Compared with those of the control group, the number of diarrheas, Bristol stool, TCM syndrome score, SAS score, and CD8+ cell levels was significantly decreased after treatment in the experiment group (P<0.05). The clinical cure rate (48.0% vs. 73.1%), SF-36 score, GAS, MTL, CCK contents, and CD4+, and Th17 cell levels were significantly increased (P<0.05). No significant difference was in the incidence of adverse events between the two groups (P>0.05). It could be suggested that cupping moxibustion could be applied in the treatment of functional diarrhea, improving the clinical symptoms, relieving anxiety, enhancing gastrointestinal and immune functions, and promoting the quality of life of patients significantly.

Topics: Bentonite; Cholecystokinin; Diarrhea; Gastrins; Humans; Immunity; Motilin; Moxibustion; Powders; Quality of Life

A randomized, double-blind, placebo-controlled, cross-over, dose-escalating, single-center study was conducted to evaluate the safety, tolerability, and pharmacokinetic (PK) profile of multiple once-daily (qd) subcutaneous (sc) doses of pasireotide in healthy male subjects. Subjects received pasireotide 50, 200, or 600 μg sc qd for 14 days and placebo in separate sequences. Thirty-three subjects were randomized. The most frequently reported drug-related adverse events were injection-site reactions (n = 18), diarrhea (n = 14) and nausea (n = 10), which were mostly mild or moderate in intensity. Pasireotide 600 μg sc was associated with pre- and post-prandial elevations in glucose levels relative to placebo; however, this effect was less pronounced on day 14 compared with day 1. PK steady state appeared to be achieved after 3 days of dosing and PK exposures had a moderate accumulation of 20-40 % across doses. Pasireotide demonstrated fast absorption (T(max,ss): 0.25-0.5 h), low clearance (CL/F(ss): 8.10-9.03 L/h), long effective half-life (T(½,eff): ~12 h, on average between 9.7 and 13.1 h for 50, 200, and 600 μg sc qd), and large volume of distribution (V(z)/F(ss): 251-1,091 L) at steady state. Dose proportionality was confirmed for C(max,ss); other PK parameters (C(max), AUC(0-24 h) and AUC(tau)) were approximately dose proportional. Growth hormone inhibition was observed with pasireotide 200 and 600 μg sc qd. Gallbladder volume increased post-prandially with pasireotide 200 and 600 μg sc qd, which appeared to correlate with reduced levels of cholecystokinin at these doses. Pasireotide was generally well tolerated up to the tested dose of 600 μg qd, with a linear and time-independent PK profile after sc qd dosing in healthy subjects.

Topics: Adult; Antineoplastic Agents, Hormonal; Cholecystokinin; Cross-Over Studies; Diarrhea; Dose-Response Relationship, Drug; Double-Blind Method; Gallbladder; Half-Life; Human Growth Hormone; Humans; Hyperglycemia; Injections, Subcutaneous; Male; Metabolic Clearance Rate; Nausea; Organ Size; Somatostatin; Tachyphylaxis; Young Adult

To characterize cholagenic diarrhea as a nosological entity with its specific features of etiology, pathogenesis, clinical picture and treatment.. A total of 167 patients with chronic diarrhea (CD) participated in the trial. Of them, 25 patients have undergone resection of the small intestine, 98--cholecystectomy for cholelithiasis, 44 had concurrent hypokinesia of the gall bladder caused by celiac disease (n = 30) or biliary dyskinesia (n = 14). The examination included estimation of cholic acid in the duodenal content (40% glucose solution or cholecystokinin were used as stimulators); 24-h fecal mass; fecal mass for 24 hours, fat, potassium and sodium content in the feces; electromotor activity (EMA) of the gall bladder, small intestine and colon.. Duodenal intubation with 40% glucose in patients with extensive resection of the small intes- tine detected a fall in cholic acid content in vesical bile to 408 +/- 58.39 mg compared to normal (910 +/- 97.29 mg%). In intravenous administration of cholecystokinin cholic acid concentration rose insignificantly (547.0 +/- 94.7 mg%) and was accompanied with bile loss with feces, polyfecalia, steatorrhea and high sodium concentration in feces. In celiac disease patients bile with high cholic acid concentration was secreted only in administration of cholecystokinin (1673 +/- 175.9 mg/%, normal 1701 +/- 140.6 mg/%). In patients after cholecystectomy colon EMA was primarily slow-wave and middle-amplitude, typical for hypermotor dyskinesia.. CD develops after extensive resection and in inflammatory ileac diseases, suppression of contractile function of the gall bladder and after cholecystectomy. CD after cholecystectomy can be considered as a variant of postcholecystectomy syndrome. The treatment of CD should include drugs binding excessive bile acids in the colon, in hypokinesia of the gall bladder the treatment should include stimulators of its contractile function.

Topics: Adolescent; Adult; Cholagogues and Choleretics; Cholecystokinin; Chronic Disease; Diagnosis, Differential; Diarrhea; Digestive System Surgical Procedures; Female; Humans; Ileal Diseases; Ileum; Injections, Intravenous; Male; Middle Aged; Postoperative Complications; Prognosis

Visceral hypersensitivity is a feature of the irritable bowel syndrome (IBS). Postprandial symptoms are common in these patients. The effects of nutrients on colonic perception in IBS are incompletely understood.. We studied 13 healthy subjects and 16 patients with IBS-eight had diarrhoea predominant (IBS-D) and eight constipation predominant (IBS-C) IBS.. Colonic perception thresholds to balloon distension and viscerosomatic referral pattern were assessed before and after duodenal infusion of lipid or saline, respectively. At the end of the infusions, plasma levels of gastrointestinal peptides were determined.. Lipids lowered the thresholds for first sensation, gas, discomfort, and pain in the IBS group but only for gas in the control group. The percent reduction in thresholds for gas and pain after lipids was greater in the IBS and IBS-D groups but not in the IBS-C group compared with controls. IBS patients had an increased area of referred discomfort and pain after lipids compared with before infusion whereas the referral area remained unchanged in controls. No group differences in colonic tone or compliance were observed. In both groups higher levels of cholecystokinin, pancreatic polypeptide, peptide YY, vasoactive intestinal polypeptide, and neuropeptide Y were seen after lipids. Motilin levels were higher in patients and differences in the subgroups were observed. Levels of corticotrophin releasing factor were lower in the constipated group than in the diarrhoea group.. Postprandial symptoms in IBS patients may be explained in part by a nutrient dependent exaggerated sensory component of the gastrocolonic response.

Topics: Adult; Analysis of Variance; Case-Control Studies; Catheterization; Cholecystokinin; Colon; Colonic Diseases, Functional; Constipation; Diarrhea; Dietary Fats; Female; Humans; Male; Middle Aged; Motilin; Neuropeptide Y; Pain Threshold; Pancreatic Polypeptide; Peptide YY; Postprandial Period; Pressure; Statistics, Nonparametric; Stomach; Vasoactive Intestinal Peptide

We investigated the effect of acarbose, an alpha-glucosidase and pancreatic alpha-amylase inhibitor, on gastric emptying of solid meals of varying nutrient composition and plasma responses of gut hormones. Gastric emptying was determined with scintigraphy in healthy subjects, and all studies were performed with and without 100 mg of acarbose, in random order, at least 1 wk apart. Acarbose did not alter the emptying of a carbohydrate-free meal, but it delayed emptying of a mixed meal and a carbohydrate-free meal given 2 h after sucrose ingestion. In meal groups with carbohydrates, acarbose attenuated responses of plasma insulin and glucose-dependent insulinotropic polypeptide (GIP) while augmenting responses of CCK, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY). With mixed meal + acarbose, area under the curve (AUC) of gastric emptying was positively correlated with integrated plasma response of GLP-1 (r = 0.68, P < 0.02). With the carbohydrate-free meal after sucrose and acarbose ingestion, AUC of gastric emptying was negatively correlated with integrated plasma response of GIP, implying that prior alteration of carbohydrate absorption modifies gastric emptying of a meal. The results demonstrate that acarbose delays gastric emptying of solid meals and augments release of CCK, GLP-1, and PYY mainly by retarding/inhibiting carbohydrate absorption. Augmented GLP-1 release by acarbose appears to play a major role in the inhibition of gastric emptying of a mixed meal, whereas CCK and PYY may have contributory roles.

Topics: Acarbose; Administration, Oral; Adult; Area Under Curve; Blood Glucose; Cholecystokinin; Diarrhea; Dietary Carbohydrates; Energy Intake; Enzyme Inhibitors; Flatulence; Gastric Emptying; Gastric Inhibitory Polypeptide; Glucagon; Glucagon-Like Peptide 1; Humans; Insulin; Male; Peptide Fragments; Peptide YY; Protein Precursors; Sucrose

Severe congenital diarrhea occurs in approximately half of patients with Aristaless-Related Homeobox (ARX) null mutations. The cause of this diarrhea is unknown. In a mouse model of intestinal Arx deficiency, the prevalence of a subset of enteroendocrine cells is altered, leading to diarrhea. Because polyalanine expansions within the ARX protein are the most common mutations found in ARX-related disorders, we sought to characterize the enteroendocrine population in human tissue of an ARX mutation and in a mouse model of the corresponding polyalanine expansion (Arx).. Immunohistochemistry and quantitative real-time polymerase chain reaction were the primary modalities used to characterize the enteroendocrine populations. Daily weights were determined for the growth curves, and Oil-Red-O staining on stool and tissue identified neutral fats.. An expansion of 7 alanines in the first polyalanine tract of both human ARX and mouse Arx altered enteroendocrine differentiation. In human tissue, cholecystokinin, glucagon-like peptide 1, and somatostatin populations were reduced, whereas the chromogranin A population was unchanged. In the mouse model, cholecystokinin and glucagon-like peptide 1 populations were also lost, although the somatostatin-expressing population was increased. The ARX protein was present in human tissue, whereas the Arx protein was degraded in the mouse intestine.. ARX/Arx is required for the specification of a subset of enteroendocrine cells in both humans and mice. Owing to protein degradation, the Arx mouse recapitulates findings of the intestinal Arx null model, but is not able to further the study of the differential effects of the ARX protein on its transcriptional targets in the intestine.

Topics: Adolescent; Animals; Cell Differentiation; Cholecystokinin; Chromogranin A; Diarrhea; Disease Models, Animal; Duodenal Diseases; Duodenum; Enteroendocrine Cells; Failure to Thrive; Female; Glucagon-Like Peptide 1; Homeodomain Proteins; Humans; Intestinal Pseudo-Obstruction; Male; Mice; Mice, Inbred C57BL; Mutagenesis, Insertional; Peptides; Somatostatin; Steatorrhea; Transcription Factors

Enteroendocrine cells secrete over a dozen different hormones responsible for coordinating digestion, absorption, metabolism, and gut motility. Loss of enteroendocrine cells is a known cause of severe congenital diarrhea. Furthermore, enteroendocrine cells regulate glucose metabolism, with the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) playing critical roles in stimulating insulin release by pancreatic β-cells. Islet1 (Isl1) is a LIM-homeodomain transcription factor expressed specifically in an array of intestinal endocrine cells, including incretin-expressing cells. To examine the impact of intestinal Isl1 on glycemic control, we set out to explore the role of intestinal Isl1 in hormone cell specification and organismal physiology. Mice with intestinal epithelial-specific ablation of Isl1 were obtained by crossing Villin-Cre transgenic animals with mice harboring a Isl1(loxP) allele (Isl1(int) model). Gene ablation of Isl1 in the intestine results in loss of GLP-1, GIP, cholecystokinin (CCK), and somatostatin-expressing cells and an increase in 5-HT (serotonin)-producing cells, while the chromogranin A population was unchanged. This dramatic change in hormonal milieu results in animals with lipid malabsorption and females smaller than their littermate controls. Interestingly, when challenged with oral, not intraperitoneal glucose, the Isl-1 intestinal-deficient animals (Isl1(int)) display impaired glucose tolerance, indicating loss of the incretin effect. Thus the Isl1(int) model confirms that intestinal biology is essential for organism physiology in glycemic control and susceptibility to diabetes.

Topics: Age Factors; Animals; Animals, Newborn; Biomarkers; Blood Glucose; Cholecystokinin; Chromogranin A; Diarrhea; Dietary Fats; Enteroendocrine Cells; Female; Gastric Inhibitory Polypeptide; Gastrins; Genotype; Ghrelin; Glucagon-Like Peptide 1; Glucose Metabolism Disorders; Glucose Tolerance Test; Integrases; Intestinal Absorption; Intestinal Mucosa; Intestine, Small; LIM-Homeodomain Proteins; Malabsorption Syndromes; Male; Mice, Inbred C57BL; Mice, Knockout; Microfilament Proteins; Phenotype; Serotonin; Somatostatin; Transcription Factors; Weight Gain

Medium-chain triglycerides are known to induce diarrhea, possibly resulting from accelerated intestinal transit. We performed antroduodenal manometry and lactulose hydrogen breath testing simultaneously in eight healthy subjects in order to determine the effects of intraduodenally administered medium-chain triglycerides (MCT) and long-chain triglycerides (LCT) on gastrointestinal motility and small bowel transit time. LCT (15 mmol/hr) induced a fed motor pattern. In contrast, during MCT, in both equimolar (15 mmol/hr; MCT-1) and equicaloric (30 mmol/hr; MCT-2) amounts comparable to LCT, interdigestive motility was preserved but with a significantly (P < 0.05) shorter MMC cycle length (MCT-1, 65 +/- 7 min; MCT-2, 53 +/- 6 min) compared to control (saline infusion; 127 +/- 14 min). Duodenocecal transit time (DCTT) was significantly (P < 0.05) accelerated during administration of MCT (MCT-1, 56 +/- 6 min; MCT-2, 69 +/- 9 min) and was not affected by LCT (105 +/- 13 min) when compared to control (101 +/- 9 min).. MCT, in contrast to LCT, preserve interdigestive motility with a shorter MMC cycle length and accelerate DCTT.

Topics: Abdominal Pain; Adult; Cecum; Cholecystokinin; Diarrhea; Duodenum; Female; Gastrointestinal Motility; Gastrointestinal Transit; Humans; Male; Manometry; Sodium Chloride; Triglycerides

Peptide YY is an ileocolonic peptide known to inhibit postprandial and cholecystokinin-induced pancreatic exocrine secretion. It has also been shown to increase intestinal water and electrolyte absorption. These findings implicate PYY as being potentially useful for controlling watery diarrhea. Although its inhibitory effect on stimulated pancreatic secretion has been well established, PYY effects on interdigestive, unstimulated pancreatic secretion is not known. This study was designed to evaluate the effect of PYY on basal pancreatic exocrine secretion in a conscious rat. Male Sprague-Dawley rats were prepared with catheters for internal biliary bypass, pancreatic juice collection, and intraduodenal reinfusion of pancreatic juice. Jugular and carotid catheters were inserted for drug infusions and blood sampling. After overnight recovery, fasting rats were infused over 6 hours with saline or PYY (400 or 800 pmol/kg/hr). Pancreatic juice was measured and sampled at 60-minute intervals for volume and its protein and bicarbonate content. The remainder was reinfused into the duodenum. Before and after the experiment, pancreatic juice was automatically reinfused by a photocell-controlled peristaltic pump system. Intraductal pancreatic secretion was not affected by PYY at a dose of 400 pmol/kg/hr. PYY at a dose of 800 pmol/kg/hr significantly reduced the volume of pancreatic secretion and its protein and bicarbonate content. Pancreatic secretory response normalized within 24 hours. In conclusion, unstimulated pancreatic exocrine secretion can be inhibited by exogenous PYY in the rat.

Topics: Amylases; Animals; Bicarbonates; Body Water; Cholecystokinin; Diarrhea; Digestion; Electrolytes; Gastrointestinal Hormones; Infusion Pumps; Injections, Intravenous; Intestinal Mucosa; Intestines; Male; Pancreatic Juice; Pancreatin; Peptide YY; Peptides; Proteins; Rats; Rats, Sprague-Dawley

Future treatments of functional intestinal disorders (FID) are essentially dependent on the possible pathophysiologic hypotheses. Schematically, symptoms experienced by patients with FID can be attributed to intestinal (small or large intestine) motor disturbances or to visceral sensitivity derangement, which, in turn, may be primary or secondary to an anomalous response to alimentation, liberation of hormones or neuromediators, or to a "stress" situation. New therapeutic agents can be directed against the symptoms experienced by patients (? action on pain or intestinal transit disorders) or against the initial pathophysiologic mechanisms. In the treatment of functional diarrhea, several substances have been proposed recently. Encephalines are peptides with extremely short duration of action which are degraded by two membranous enzymes, encephalinase and carboxypeptidase. Recently, it has been shown that acetorphan, an inhibitor of encephalinase, is efficacious in acute diarrhea. Alpha-2-antagonists are substances which are capable of slowing intestinal transit time and increasing intestinal absorption. Their antidiarrheic action is moderate, and they do not act on abdominal pain. Molecules that do not traverse the neuromeningeal barrier but that act selectively on the digestive tract and are better tolerated are expected. In patients complaining of severe idiopathic constipation substances capable of stimulating colonic motility are useful: substance P or neurotensin analogues might prove interesting. Antagonists of opium receptors such as Naloxone have proved efficacious in the treatment of certain cases of chronic idiopathic intestinal pseudo-obstructions or severe constipation. The development of orally active substances or with hepatic elimination are a prerequisite. Therapy based on well characterized pathophysiologic abnormalities would be welcome.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Abdominal Pain; Antidiarrheals; Benzodiazepines; Cholecystokinin; Colonic Diseases, Functional; Constipation; Diarrhea; Female; Humans; Male; Proglumide

Exocrine pancreatic insufficiency has been observed in some diabetics with peripheral neuropathy and diarrhea. Several mechanisms may be responsible for this insufficiency: (1) pancreatic atrophy, (2) disruption of the cholinergic enteropancreatic reflexes, or (3) elevated serum levels of peptides such as glucagon and pancreatic polypeptide which are known to inhibit pancreatic exocrine secretion. To clarify the mechanism(s) involved in this exocrine pancreatic impairment, we studied 10 diabetics with diarrhea and peripheral neuropathy. Their results were compared to those of eight normal volunteers. Each subject underwent a standardized pancreatic function study which assessed nonstimulated secretion, the response to intrajejunal infusion of a mixture of amino acids, and the output following intravenous administration of secretin and cholecystokinin (CCK). In separate studies, the effect of a background infusion of bethanechol and secretin on the pancreatic response to CCK was assessed in six patients and six normal controls. Compared to normals, all diabetics exhibited a significant reduction in both enzyme and bicarbonate secretion to all stimuli. This reduction was not corrected by administering bethanechol. Plasma glucagon and pancreatic polypeptide levels in diabetics were not significantly higher than those in controls. We conclude that diabetics with diarrhea and peripheral neuropathy exhibit impairment of their exocrine pancreatic secretion and possible mechanisms for this are discussed.

Topics: Adult; Amino Acids; Bethanechol; Bethanechol Compounds; Cholecystokinin; Chronic Disease; Diabetes Mellitus, Type 2; Diabetic Neuropathies; Diarrhea; Dose-Response Relationship, Drug; Humans; Intubation, Gastrointestinal; Male; Middle Aged; Pancreas; Secretin

Toddler diarrhoea is the commonest cause of chronic diarrhoea without failure to thrive in childhood, but its pathogenesis remains obscure. We have studied upper small intestinal motility in three groups of children (control group 1 - children with no intestinal pathology undergoing duodenal intubation, n = 6; control group 2 - children with gastrointestinal pathology other than toddler diarrhoea, n = 11; control group 3 - children with toddler diarrhoea, n = 8). We studied fasting motor patterns and the response of the migrating motor complex to intravenous cholecystokinin and an intraduodenal bolus of 5% dextrose. The characteristics of the migrating motor complex in the three groups did not differ but their response to dextrose did. Intraduodenal dextrose disrupted the migrating motor complex in four out of four children in group 1; seven out of nine children in group 2; and nil of eight children with toddler diarrhoea in group 3. We suggest that this failure of intestinal motor response may play a major role in the pathogenesis of the diarrhoea in this condition.

Topics: Child; Child, Preschool; Cholecystokinin; Diarrhea; Duodenum; Female; Gastrointestinal Motility; Glucose; Humans; Infant; Intestine, Small; Jejunum; Male; Pressure

Topics: Animals; Cathartics; Cholecystokinin; Diarrhea; Guinea Pigs; Intestine, Small; Male; Mice

Topics: Achlorhydria; APUD Cells; Apudoma; Carcinoid Tumor; Carcinoma; Cholecystokinin; Diarrhea; Endocrine System Diseases; Humans; Hypokalemia; Malignant Carcinoid Syndrome; Neoplasms; Pancreatic Diseases; Paraganglioma; Paraneoplastic Endocrine Syndromes; Peptides; Prostaglandins E; Somatostatin; Syndrome; Thyroid Neoplasms; Vasoactive Intestinal Peptide

With the advent of radioimmunoassay and immunocytochemical methods, the peptides of the gastrointestinal tract have been identified and measured. Gastrinoma and insulinoma syndromes have been wall characterized. The pancreatic cholera syndrome and some of the evidence that the major manifestations of this disease may be mediated by vasoactive intestinal peptide have been re-examined. Pancreatic polypeptide seems to be an ideal peptide for study of vagal-cholinergic mechanisms that regulate hormone release; it also appears to be a tumor marker for several types of pancreatic endocrine tumors, particularly those of pancreatic cholera. Secretin and cholecystokinin are important regulators of pancreatic exocrine secretion and have been used to test pancreatic function, but there is little evidence that they account for clinical disease. Glucagon-secreting tumors produce a clinical syndrome of diabetes mellitus and distinctive skin lesions, which can be cured by tumor resection. Hormone-secreting tumors may provide insight into normal gut physiology.

Topics: Adenoma, Islet Cell; Animals; Apudoma; Cholecystokinin; Diarrhea; Dogs; Gastric Inhibitory Polypeptide; Gastrointestinal Hormones; Glucagon; Hormones; Humans; Intestines; Pancreas; Pancreatic Neoplasms; Pancreatic Polypeptide; Stomach; Stomach Neoplasms; Vasoactive Intestinal Peptide

The pathogenesis of Salmonella diarrhea is unclear. Bacterial invasion of the ileal and colonic mucosa resulting in an intense ileocolitis regularly occurs in concert with secretion of water and sodium in jejunum, ileum, and colon. To examine the role of altered permeability in Salmonella diarrhea we studied intestinal histology, water and electrolyte transport, clearance of intravenously injected [14C]erythritol and [3H]mannitol, and changes in transmural electrical potential difference in normal and Salmonella-infected rhesus monkeys. In normal animals, absorption of water and sodium occurred in jejunum, ileum, and colon and a gradient of diminishing permeability from jejunum to ileum to colon for both erythritol and mannitol was observed. Permeability as measured by determining permeability coefficients was not increased by Salmonella infection and in fact was significantly reduced for erythritol in the jejunum of infected animals. Perfusion with hypertonic erythritol and mannitol produced the same streaming potentials (deltaPD) in control and infected animals, indicating no differences in transmucosal permeability. As a positive control, perfusion with 25 mM ethylenediaminetetraacetic acid in normal animals increased permeability, resulting in increased plasma-to-lumen isotope flux and no deltaPD in response to hypertonic perfusates. These data show that despite severe alterations in intestinal histology, transmucosal permeability remains unchanged and thus is not a contributing factor in Salmonella diarrhea.

Topics: Animals; Body Water; Cell Membrane Permeability; Cholecystokinin; Diarrhea; Erythritol; Haplorhini; Intestinal Absorption; Intestinal Mucosa; Male; Mannitol; Membrane Potentials; Norepinephrine; Salmonella Infections; Salmonella typhimurium; Sodium

The availability of pure intestinal hormones and the development of radioimmunoassays for their measurement has expedited research into many aspects of gastrointestinal endocrinology. A complex balance evidently exists between the different intestinal hormones and also the rest of the endocrine system. Polyendocrinopathies have been described, and, so far, two diseases due to intestinal hormone excess (Zollinger-Ellison syndrome and the syndrome of watery diarrhea, hypokalemia and achlorhydria) elucidated. It seems likely that many more gastrointestinal endocrine diseases await discovery.

Topics: Cholecystokinin; Diagnosis, Differential; Diarrhea; Digestive System; Endocrine Glands; Esophagogastric Junction; Gastrins; Gastrointestinal Hormones; Humans; Hypoglycemia; Intestinal Diseases; Intestine, Large; Pancreas; Peptic Ulcer; Prostaglandins; Pylorus; Secretin; Syndrome; Zollinger-Ellison Syndrome

Idiopathic late-onset immunoglobulin deficiency in a young man was associated with achlorhydria and a severe intestinal malabsorption syndrome that did not respond to conventional therapy. Combined therapy with high doses of prednisone and tetracycline hydrochloride resulted in weight gain, cessation of diarrhea, improved absorption of water, fat, and vitamin B12, and production of gastric acid after stimulation with histamine. Serum immunoglobulin levels, however, did not increase.

Topics: Achlorhydria; Adult; Age Factors; Body Weight; Celiac Disease; Cholecystokinin; Diarrhea; Drug Therapy, Combination; Humans; Immunoglobulin M; Immunologic Deficiency Syndromes; Malabsorption Syndromes; Male; Prednisone; Tetracycline; Vitamin B 12

Topics: Bile Acids and Salts; Cholecystokinin; Colonic Diseases, Functional; Diarrhea; Gastrins; Gastrointestinal Motility; Humans; Lactose Intolerance; Stress, Psychological

Topics: Celiac Disease; Cholecystokinin; Clinical Laboratory Techniques; Diarrhea; Feces; Gastric Juice; Gastric Mucosa; Hormones; Humans; Hydrogen-Ion Concentration; Intestine, Small; Jejunum; Pancreas; Peptic Ulcer; Secretin; Time Factors

Topics: Cholecystokinin; Diarrhea; Gastric Juice; Gastrins; Humans; Hyperplasia; Pancreatic Diseases; Peptides; Stomach

Topics: Bile Acids and Salts; Child; Child, Preschool; Cholecystokinin; Diarrhea; Humans; Infant; Injections, Intravenous; Intestine, Small; Intubation, Gastrointestinal; Malabsorption Syndromes; Methods; Pancreas

Topics: Achlorhydria; Adenoma, Islet Cell; Animals; Biological Transport, Active; Cell Membrane Permeability; Cholecystokinin; Diarrhea; Gallbladder; Gastrins; Gastrointestinal Hormones; Hypokalemia; Rabbits; Secretin; Tissue Extracts

Topics: Adult; Asthenia; Cholecystectomy; Cholecystography; Cholecystokinin; Cholelithiasis; Colon; Colon, Sigmoid; Constipation; Desensitization, Immunologic; Diarrhea; Dyspepsia; Female; Headache; Histamine H1 Antagonists; Humans; Hypersensitivity; Middle Aged; Pain; Postoperative Complications; Sleep Wake Disorders; Stomach

Topics: Achlorhydria; Adenoma, Islet Cell; Adult; Animals; Bile; Biological Assay; Cholecystokinin; Diarrhea; Dogs; Female; Gastric Acidity Determination; Glucagon; Histamine; Humans; Hypokalemia; Liver Neoplasms; Male; Middle Aged; Neoplasm Metastasis; Pancreatic Neoplasms; Secretin; Tissue Extracts

Topics: Amylases; Celiac Disease; Cholecystokinin; Diarrhea; Humans; Lipase; Pancreas; Pylorus; Secretin; Vagotomy

Topics: Amylases; Bicarbonates; Cholecystokinin; Cystic Fibrosis; Diarrhea; Gastrointestinal Hormones; Hemochromatosis; Humans; Liver Cirrhosis; Pancreas; Pancreatic Juice; Pancreatic Neoplasms; Pancreatitis; Physiology; Secretin

Topics: Amylases; Bicarbonates; Cholecystokinin; Cystic Fibrosis; Diarrhea; Gastrointestinal Hormones; Hemochromatosis; Humans; Liver Cirrhosis; Pancreas; Pancreatic Juice; Pancreatic Neoplasms; Pancreatitis; Pharmacology; Physiology; Secretin

Topics: Amylases; Bicarbonates; Cholecystokinin; Diarrhea; Gastrointestinal Hormones; Hemochromatosis; Humans; Liver Cirrhosis; Pancreas; Pancreatic Neoplasms; Pancreatitis; Pathology; Physiology; Secretin