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PubMed1999

A gastroenterological list for the millennium.

To determine the 10 most significant advances in gastroenterology during this century as we approach the millennium, the authors polled 50 distinguished active clinicians and leading researchers in the field, including workers in liver disease and the pathology of the gut and its associated glands. Forty-five persons (90%) responded and listed 58 different items. These were then organized into four groups: group A, with 10 categories that received between 42 and 11 votes; group B, with 10 categories that received between 10 and 3 votes; group C, with 3 items receiving 2 votes each; and group D, with the remaining 14 items receiving 1 vote each. The respondents did not indicate their choices in rank order. The top 10 leading choices (group A, containing between 42 and 11 votes) included Helicobacter pylori, fiberoptic endoscopy, gastrointestinal imaging by radiograph and computed tomographic scan, Australia antigen including vaccines for hepatitis A and B, the molecular basis of colon cancer, liver transplantation, laparoscopic-assisted surgery, therapy for peptic ulcer disease including H2-receptor antagonists and proton pump inhibitors, the discovery of gastrointestinal hormones beginning with secretin, and lastly the discovery of the role for gluten in celiac disease.

Data Collection↗
PubMed1988

Hormonal regulation of gastric acid in peptic ulcer disease.

Although the pathogenetic role of gastrin in gastric acid hypersecretion and peptic ulcer is well established in a number of uncommon disorders, such as Zollinger-Ellison syndrome, antral G-cell hyperfunction, and retained, excluded antrum after subtotal gastrectomy, the significance of hormonal abnormalities in normogastrinaemic peptic ulcer is less obvious. Most studies have pointed to an impaired feedback mechanism between gastric acid and antral gastrin secretion in duodenal ulcer disease, possibly due to antral somatostatin deficiency. Furthermore, antisecretory drugs may induce abnormalities of gastrointestinal hormones. Potent antisecretory drugs, such as omeprazole, increase serum and antral gastrin and reduce antral somatostatin, whereas certain prostaglandin E2 analogues inhibit serum gastrin secretion after feeding.

Animals↗
PubMed1978

Effect of glucagon and pentagastrin on gastric mucosal potential difference in man.

Glucagon given as an intravenous injection of 2 mg (0.57 mmol) or as constant intravenous infusion of 1.64 microgram/kg/h (0.47 nmol/kg/h) significantly increased gastric mucosal potential difference (PD) in man. Pentagastrin infusion of 2 microgram/kg/h (2.8 nmol/kg/h) dramatically reduced gastric PD in man. The effect of each of these hormones on PD was reversed by the administration of the other. Changes in PD induced by one hormone were not associated with reductions in blood levels of the other. There was an approximate correlation between changes in PD and pH of gastric aspirates, however, the patterns of PD and pH changes were at times dissimilar. This study indicates that administration of gastrointestinal hormones significantly alters gastric mucosal PD in man.

Adult↗
PubMed1983

Pituitary hormone release in response to food ingestion: evidence for neuroendocrine signals from gut to brain.

The synchrony of PRL and cortisol release with feeding is now well established. To delineate further the neuroendocrine mechanisms involved, meal-related pituitary and adrenal cortical activities were investigated in seven normal men in a series of experiments conducted in random sequence at 1-week intervals. Ingestion of a standardized mixed meal elicited a consistent acute release of PRL and cortisol at noon (1200 h), but not at breakfast (0800 h). No measurable changes in other pituitary hormones were observed. The relative magnitudes of PRL and cortisol release in response to lunch were not significantly influenced by a preceding breakfast. These responses appear unrelated to the cephalic or oral phases of food ingestion. However, the composition of the meals was found to be important. Whereas carbohydrate meals had no discernible effects, high protein meals induced a large increase in both PRL and cortisol; high fat meals caused selective release of PRL. Ingestion of L-tyrosine and L-tryptophan induced remarkable increments in serum concentrations of both PRL and cortisol, suggesting that these essential amino acids may be active components of the high protein meal. Choline had no effect. Meal-mediated PRL and cortisol release was unaffected by prior receptor blockade of the opioidergic and cholinergic systems with naloxone and atropine, respectively. These observations indicate that the protein component of the meal was responsible for the midday surges of PRL and cortisol and that the cephalic-vagal pathway was not required in food-entrained pituitary hormone release. Further, our data suggest that the neurotransmitter substrates in the protein meal may serve to link the gut and brain by modifying central catecholamine and serotonin biosynthesis, and thereby influence the hypothalamic factors controlling pituitary PRL and ACTH secretion. The possibility that gastrointestinal hormones may also influence the hypothalamic-pituitary system remains to be explored.

Adult↗
PubMed1977

Prophylactic effect of somatostatin on stress ulcer formation in rats.

The aim of the present study was to investigate the effect of somatostatin (growth-hormone release-inhibiting hormone) on ulcer formation during immobilisation stress. This was done in male Albino-rats to study the effect of somatostatin on number and size of ulcers, to calculate ulcer index, to measure pH-value of gastric juice as well as plasma levels of gastrointestinal hormones. Rats treated with somatostatin before and during stress exposition had only the third part of the ulcers compared with the untreated animals. Total ulceration area was less than the tenth of the untreated rats. Normal corticoid plasma levels during stress exposition were found in the lower range of normal values in somatostatin treated rats. Decrease of plasma gastrin during stress exposition exceeded the gastrin decrease of somatostatin treated rats. Rise of plasma glucagon was completely inhibited during somatostatin application. Results of serum glucose paralleled those seen in glucagon.

Animals↗
PubMed2001

Ghrelin-producing endocrine tumors of the stomach and intestine.

Ghrelin is a novel gastrointestinal hormone produced by about 20% of the rat and human gastric neuroendocrine cell population, which possesses strong GH-releasing activity, but also plays other central and peripheral roles, including influence on food intake, gastric motility, and acid secretion. The aim of the present study was to determine whether gastrointestinal endocrine hyperplastic and neoplastic lesions produce ghrelin, at both protein (immunohistochemistry) and mRNA (in situ hybridization and/or RT-PCR) levels, and express the GH secretagogue receptor mRNA by RT-PCR. Sixteen gastric and 20 intestinal carcinoids as well as normal gastrointestinal mucosa and atrophic gastritis-associated neuroendocrine cell hyperplasia were studied. The majority (12 of 16, 75%) of gastric carcinoids and only 5 of 18 (27%) of intestinal endocrine tumors were immunoreactive for ghrelin. In situ hybridization confirmed the immunohistochemical data, but also showed ghrelin mRNA in 1 gastric and 8 intestinal additional tumors. RT-PCR showed ghrelin mRNA in 14 of 14 cases, indicating a low level of ghrelin gene expression in all gastrointestinal endocrine tumors tested. Gastric neuroendocrine hyperplastic cells were also strongly positive for ghrelin. GH secretagogue receptor mRNA was absent in 3 gastric, but present in 7 of 11 intestinal carcinoids studied by RT-PCR. These findings demonstrate that most gastric carcinoids (and related neuroendocrine cell hyperplasias) and some intestinal carcinoids produce ghrelin. These hyperplastic/neoplastic conditions could represent the clinical model to clarify the existence and impact of ghrelin hypersecretion on endocrine and nonendocrine functions.

Adult↗
PubMed1991

Effects of gastrointestinal peptides on azoxymethane-treated colonic mucosa in vitro.

An organ-culture system has been used to investigate the effect of certain gastrointestinal peptides on the morphology and cell proliferation of explants of azoxymethane (AOM)-treated colonic mucosa. Our aim was to ascertain whether such factors play a direct part in the maintenance of hyperplastic changes in the large intestine. Explants of AOM-treated colonic mucosa from 15 animals were maintained in a serum-free medium in the presence of either gastrin-17 (250 pg/ml and 250 ng/ml), peptide YY (80 pmol/l and 160 pmol/l) epidermal growth factor (EGF) (10 ng/ml and 100 ng/ml) or the C-terminal fragment of glucagon-37 (30 pmol/l) for a period of up to 7 days. Other explants (controls) received fresh medium only each day. After 1, 2, 3, 5 and 7 days of culture both experimental and control explants received vincristine (4 micrograms/ml) for 3 h prior to fixation. The proportion of vincristine-arrested metaphases within the explants was determined together with crypt length. Neither gastrin nor peptide YY was found to influence cell division at either concentration. Despite an initial inhibitory effect, both concentrations of EGF exerted a trophic effect which increased with time. The glucagon-37 fragment caused an immediate increase in proliferation which then declined as time progressed. None of these factors, however, were able to maintain the hyperplastic changes seen in the pre-culture samples of AOM-treated mucosae.

Animals↗
PubMed1993

The effect of non-starch polysaccharide supplementation on circulating bile acids, hormone and metabolite levels following a fat meal in human subjects.

The effects of guar gum, sugar-beet fibre (SBF) and wheat bran supplementation of a high-fat test meal were compared with an NSP-free control meal and a meal containing an equivalent amount of the ion-exchange resin cholestyramine in healthy non-obese human volunteers. Their effects on gastric emptying, postprandial circulating bile acids, triacylglycerols and gastrointestinal hormone levels were studied. The in vitro binding of NSP and cholestyramine to [1-14C]glycocholic acid was measured and compared with their in vivo effect. Guar gum and cholestyramine supplementation significantly lowered circulating postprandial bile acid, triacylglycerol and gastric inhibitory polypeptide concentrations, but sugar-beet fibre and wheat bran were without effect. Liquid gastric emptying, as assessed by circulating paracetamol levels, was slightly accelerated in the guar gum-supplemented meal. Glycocholic acid bound strongly to the insoluble fraction of cholestyramine and the soluble fraction of guar gum. The insoluble fractions of SBF and wheat bran bound only small quantities of glycocholate; no bile acid binding was detected in the soluble fractions of these NSP. The study demonstrates that measurement of postprandial bile acids enables an indirect measurement to be made of bile acid binding to NSP in vivo. The results support the hypothesis that the hypocholesterolaemic action of guar gum is largely mediated via interruption of the enterohepatic bile acid circulation, but indicate that the hypocholesterolaemic action of SBF is mediated by another mechanism.

Adult↗
PubMed2000

Effects of very long chain versus long chain triglycerides on gastrointestinal motility and hormone release in humans.

Fish oil (a very long chain triglycerides, VLCT) has received much attention because of its favorable metabolic properties; however, its effect on gastrointestinal function has not been studied. We investigated the effects of intraduodenally administered VLCT on gut-hormone release [cholecystokinin (CCK), neurotensin, peptide YY (PYY)], gallbladder emptying, antroduodenal motility, and small bowel transit time (SBTT) in comparison to intraduodenal administration of saline and long chain triglycerides (LCT, corn oil) in nine healthy volunteers. Gallbladder contraction duration was significantly shorter after VLCT than after LCT (138 +/- 16 min vs 233 +/- 38 min, P < 0.05). Both fats induced a fed motility pattern, while SBTT was not significantly altered. CCK secretion was significantly reduced after VLCT compared to LCT (36 +/- 12 pM x 120 min vs 78 +/- 15 pM x 120 min, P < 0.05), whereas PYY and neurotensin release were not significantly different. In conclusion, effects of triglycerides on CCK and gallbladder motility appear to be chain-length dependent, in contrast to the effects on distal gut-hormone release and intestinal motility and transit, which appear to be chain-length independent.

Adolescent↗
PubMedDate not supplied

Silver stains in the study of endocrine cells of the gut and pancreas.

The usefulness of argentaffin (Masson) and argyrophil (Davenport, Sevier-Munger and Grimelius) staining methods for identification of endocrine cell types in the gastrointestinal tract and pancreas is discussed and comments are made on the techniques themselves. The applicability of silver impregnation methods in the histopathological investigations of endocrine tumours in the above-mentioned organs is outlined, and the chemical background of the silver reactions is briefly reviewed.

Adenoma, Islet Cell↗
PubMed1997

Differential effects of subcutaneous GLP-1 on gastric emptying, antroduodenal motility, and pancreatic function in men.

In this study of eight healthy male volunteers, we investigated the effects of graded doses of subcutaneous glucagon like peptide-1(7-36)amide (GLP-1) on: 1) the gastric emptying pattern of a mixed liquid meal (300 kcal); 2) pancreatic enzyme secretion; 3) antroduodenal motility; and 4) the glycemic response as well as releases of insulin, C-peptide, and glucagon. GLP-1, 0.125 nmol/kg, or 0.25 nmol/kg, or placebo was injected subcutaneously 5 min before meal ingestion. Subcutaneous GLP-1 dose-dependently prolonged the lag period (i.e., the time to reach maximal velocity of gastric emptying) by 46.2% (low dose) and 93.7% (high dose) (p < .05) but left unaltered maximal emptying velocity, total emptying time, and exponential emptying rate. With and without GLP-1, a fed motor pattern was induced by the meal and was terminated by an antral phase III when 98% of the meal had emptied. In parallel to the prolonged lag period, GLP-1 dose-dependently inhibited antral and duodenal motility and coordinated antroduodenal contractions by > 50% (low dose) and > 70% (high dose) (p < .05). GLP-1 initially reduced and thereafter transiently stimulated pancreatic enzyme secretion. This pattern correlated with the prolonged lag period and mirrored the delayed gastric emptying. GLP-1 retarded and diminished the postprandial glucose peak and reduced the total plasma glucose response by 46.6% (low dose) and by 59.4% (high dose) (p < .05). Both doses of GLP-1 delayed the postprandial insulin peak, enhanced total insulin release, and diminished postprandial responses of glucagon and pancreatic polypeptide. The duration of the lag period strongly correlated with the timing of postprandial glucose and insulin peaks (p < .001). The initial delay of gastric emptying, the enhancement of postprandial insulin release, and the inhibition of postprandial glucagon release were independent determinants (p < .01-.05) of the postprandial glucose response after subcutaneous administration of GLP-1.

Adult↗
PubMed2001

Adaptive physiological processes in the host during gastrointestinal parasitism.

Parasite infection of the gastrointestinal tract with helminths or protozoa induces detrimental effects on host tissues and host physiology, which have been extensively studied and reviewed. However, parasitism of the digestive system is also associated with adaptive, compensatory phenomena based on changes in host physiology or structures and which tend to counterbalance the negative consequences. The objective of this review is to describe these adaptive processes and their possible underlying mechanisms. Different processes which tend to attenuate the effect of either the loss of appetite, the intestinal malabsorption or the increased tissue losses have been assessed. These processes have been reported both for helminth and protozoan infections, where they present similar characteristics. The mechanisms involved in the adaptation to parasitism remain largely unidentified. The role of feedback mechanisms based on host regulation, possibly through gastrointestinal hormones, has been raised. On the other hand, some data support the proposal that parasites themselves may initiate some of the adaptive processes and consequently favour their own survival. These adaptive phenomena appear to be an essential component in the dynamic balance between host and parasites. Also, parasite infections represent unique models to study the adaptation of the gastrointestinal tract to aggressors.

Adaptation, Physiological↗
PubMed1993

[Multiple endocrine neoplasia type 1. Digestive hormones in the screening].

Detection of subjects from a multiple endocrine neoplasia type 1 family must rest on clinical, biochemical and radiological data, since study of the genome is unable to detect these subjects. In the new family described here, 6 out of the 14 subjects explored were affected. One had a confirmed pancreatic endocrine tumour and in 3 others a pancreatic endocrine tumour was highly probable, since insulin and glucagon levels, as well as ultrasonic exploration of the pancreas were pathological. Measurements of gastrointestinal hormones gave normal results in all cases. We conclude that to detect this endocrine neoplasia in subjects at risk it seems necessary to measure plasma insulin levels and perform an abdominal ultrasonography.

Adolescent↗