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PubMed1989

Effects of pancreatic polypeptide on basal and meal stimulated secretion of gastrointestinal, pancreatic and adrenocortical hormones in the dog.

We have assessed the effects of intravenous infusion of bovine pancreatic polypeptide (PP) (1 microgram kg-1 h-1) on the basal and postprandial secretion of gastrointestinal, pancreatic and adrenocortical hormones in normal dogs. Bovine PP within the physiological range increased plasma cortisol levels transiently but significantly. PP elicited an inhibition of insulin response to a protein-rich meal, and tended to reduce the gastrin response. There were, however, no significant changes in basal or postprandial plasma concentrations of motilin and pancreatic glucagon during PP infusion. These results suggest that PP may have a role in controlling insulin secretion from the pancreas. The possible mechanisms are discussed mainly on the basis of vagal innervation.

Adrenal Cortex Hormones↗
PubMed1985

Effect of exogenous somatostatin infusion on gastrointestinal blood flow and hormones in the conscious dog.

The purpose of this study was to investigate the effects of intravenous somatostatin infusion on gastrointestinal blood flow and hormone release in conscious dogs. Gastric, duodenal, jejunal, and pancreatic blood flows, quantitated using radioactive microspheres, were significantly decreased during somatostatin infusion (200 and 500 ng/kg min), resulting in an overall 30% reduction in summed portal blood flow. Fasting blood levels of glucose fell an average of 10 mg/dl. Immunoreactive insulin, gastrin, glucagon, and pancreatic polypeptide were all profoundly suppressed by somatostatin infusion. Our studies provide one possible explanation for somatostatin's apparent effectiveness in the control of upper gastrointestinal hemorrhage.

Animals↗
PubMed1987

[Role of changes in the hormonal system of the gastrointestinal tract after vagotomy].

The level of gastrin, serotonin, insulin and cortisol in the blood was raised after different types of vagotomy. Raised hormone secretion depends on the time following operation, the severity of a pathological process, to a lesser degree, on the type of surgical intervention and nature of postvagotomic disturbance. Shifts in the hormonal apparatus are caused by operation and associated with it functional-morphological changes of the digestive organs, the preservation of preoperative changes and developing compensatory-adaptive reactions. An excess of intestinal hormone secretion in the postoperative period can be responsible for the development of pathological disorders, in particular the dumping syndrome.

Adult↗
PubMed2003

Raf-1 activation suppresses neuroendocrine marker and hormone levels in human gastrointestinal carcinoid cells.

Gastrointestinal carcinoid cells secrete multiple neuroendocrine markers and hormones including 5-HT and chromogranin A. The intracellular signaling pathways that regulate production of bioactive molecules are not completely understood. Our aim was to determine whether activation of the raf-1/MEK/MAPK signal transduction pathway in carcinoid cells could modulate production of neuroendocrine markers and hormones. Human pancreatic carcinoid cells (BON) were stably transduced with an estrogen-inducible raf-1 construct creating BON-raf cells. Activation of raf-1 in BON-raf cells led to a marked induction of phosphorylated MEK and ERK1/2 within 48 h. Importantly, raf-1 activation resulted in morphological changes accompanied by a marked decrease in neuroendocrine secretory granules by electronmicroscopy. Moreover, induction of raf-1 in BON-raf cells led to significant reductions in 5-HT, chromogranin A, and synaptophysin levels. Furthermore, treatment of BON-raf cells with MEK inhibitors PD-98059 and U-0126 blocked raf-1-mediated morphological changes and hormone suppression but not ERK1/2 phosphorylation. These results show that raf-1 induction suppresses neuroendocrine marker and hormone production in human gastrointestinal carcinoid cells via a pathway dependent on MEK activation.

Biomarkers, Tumor↗
PubMed1995

Gastric motility in rats with varying ovarian hormone status.

Gastrointestinal (GI) symptoms suggestive of altered motility vary with menstrual cycle phase and menopause, but the effects of ovarian hormones on gastric motility have not been described. Basal and stimulated gastric motility were studied in male and female rats that were ovariectomized and implanted with continuous-release progesterone and/or estrogen pellets. Following 26 days of hormone treatment, rats were implanted with a gastric tension transducer. Contractile activity was recorded, then thyrotropin-releasing hormone (TRH) or saline was injected intracisternally and motility was monitored. An index was calculated based on frequency and amplitude; response to TRH was expressed as percentage of the basal index. Basal contraction frequency was highest in the estrogen and estrogen+progesterone groups. Hormone treatment significantly affected the TRH-stimulated motility index; TRH induced increased motility in all groups, with larger, more sustained responses in vehicle, progesterone, and male groups. Results demonstrate the ovarian hormone modulation of basal and stimulated gastric motility. Such modulation may contribute to changes in GI symptoms with altering ovarian hormone state.

Animals↗
PubMed2000

Gastrointestinal effects of growth hormone.

GH receptor immunoreactivity is found throughout the gastrointestinal tract. GH has proliferative effects upon intestinal epithelium, and influences enteroendocrine cell secretion, calcium absorption, and intestinal amino acid and ion transport. The proliferative effects of GH may be reflected in the increased incidence of neoplastic colonic polyps in individuals with long-term GH excess reported by some investigators. GH also increases hepatic cytochrome P450 expression, potentially altering drug and steroid hormone metabolism. Current clinical research efforts include the use of exogenous GH as a stimulant of gut growth and adaptation in patients who have undergone massive intestinal resection. Exogenous GH is also being studied in animal models of critical illness where it appears to increase intestinal glutamine uptake, which may prevent deterioration of the intestinal mucosal barrier.

Animals↗
PubMed2004

Food intake and ageing--the role of the gut.

Healthy ageing is associated with decreased appetite and energy intake and this is generally associated with weight loss after about 70 years of age. The mechanisms responsible for this 'physiological' anorexia are not well understood, but it may predispose to the development of protein-energy malnutrition in older people, which is associated with increased morbidity and mortality. Many sensory and social factors, including olfactory changes and economic status, contribute to under-nutrition in older people; however, normal ageing is associated with a number of significant changes in gastrointestinal function. The control of appetite is complex but it is clear that gastrointestinal signals are important in the regulation of appetite and food intake. This review examines the role of small intestinal hormones and gastrointestinal motor function in the observed changes to appetite and food intake in older people.

Aging↗
PubMed1988

Suppression of postprandial glucose, insulin, C-peptide, and glucose-dependent insulinotropic peptide (GIP) in man by oral administration of a prostaglandin analogue (enprostil).

Enprostil, a long-acting, orally active dehydroprostaglandin E2 with cytoprotective and gastric antisecretory properties, is a potent inhibitor of meal-stimulated gastrin release. Recent data have suggested suppression of additional other gastrointestinal peptide hormones following single doses of enprostil. The current investigation was conducted to further clarify the effects of enprostil administration on gastrointestinal hormones and glucose metabolism under physiologic conditions and to determine whether these effects were present following multiple doses of the agent. Enprostil 70 mcg/d and its placebo were each administered for 7 1/2 days to eight normal male subjects in a study of crossover design, each treatment period lasting 7 1/2 days and separated by a 7 day washout period. Subjects received a test meal on days 1 and 8 and an oral glucose challenge on day 3 of each treatment period following enprostil or its placebo. Following the test meal, there was a delay and suppression of the maximum measured serum glucose levels. Mean overall peak glucose concentrations were lower during the enprostil phase compared to placebo (112 vs. 121 mg/dd, P = 0.025) with a trend toward delay in the time to achievement of peak glucose concentrations. Mean overall peak levels for insulin, C-peptide, and glucose-dependent insulinotropic peptide (GIP) were significantly suppressed by 36%, 16% and 60%, respectively by enprostil when compared to placebo. The overall integrated postprandial responses for insulin, C-peptide, and GIP were significantly reduced by 42%, 39% and 90%, respectively while that for glucose above baseline was reduced by 44% (P = 0.098). Similar effects were present following the oral glucose challenge.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed2001

Immunoprecipitation and liquid chromatographic-mass spectrometric determination of the peptide glucose-dependent insulinotropic polypeptides GIP1-42 and GIP3-42 from human plasma samples. New sensitive method to analyze physiological concentrations of peptide hormones.

The gastrointestinal peptide glucose-dependent insulinotropic polypeptide (GIP1-42) is one of the incretin hormones regulating glucose-induced insulin secretion from the endocrine pancreas. GIP1-42 is a substrate of the circulating enzyme dipeptidyl peptidase IV, which removes the N-terminal peptide Tyr-Ala resulting in the inactive polypeptide GIP3-42. Hither to existing immunoassays do not enable a separate quantification of active and inactive forms, respectively. Therefore, we developed a highly specific and sensitive LC-MS assay for the identification and quantification of GIP1-42 and GIP3-42. Total GIP was immunoprecipitated from crude plasma samples using a C-terminally directed antibody. Thus, peptides were purified and concentrated prior to LC-MS analysis. The present immunoprecipitation-LC-MS assay enables the quantification of active and inactive GIP over a concentration range from 5 to 350 pmol/l in human plasma samples. Since this range covers the basal and postprandial levels of GIP the method is applicable to the determination of concentration changes and changes in the ratio of active and inactive forms of GIP in human plasma.

Chromatography, Liquid↗
PubMed1979

Peptide hormone-like immunoreactivity in the gastrointestinal tract and endocrine pancreas of eleven teleost species.

The distribution of peptide hormone-like immunostaining in the gastrointestinal tract of 11 teleost species was investigated by immunofluorescence. Cells immunoreactive for somatostatin were found in the glandular epithelium of the stomach of four species and in the epithelium of the pyloric appendage of one species. The mid-gut epithelium contained cells reactive with antibodies to glucagon (three species), gastrin (five species), pancreatic polypeptide (five species), and substance P (two species). Cells immunoreactive for met-enkephalin were found in the epithelium of both the mid-gut and the stomach of six species. In six species in which the endocrine pancreas was investigated, insulin-, glucagon-, and somatostatin-like immunoreactivity was observed. Pancreatic polypeptide was definitely localised by immunostaining in cells of the endocrine pancreas of only one out of three species examined. Vasocative intestinal polypeptide-, neurotensin-, bombesin-, and enkephalin-like immunoreactivity was identified in the gastrointestinal nerve fibres in various species. In view of the considerable species variation found, caution should be exercised in generalising about the peptides present in the gastrointestinal tract of fish.

Animals↗
PubMed2004

Gut-derived signaling molecules and vagal afferents in the control of glucose and energy homeostasis.

PURPOSE OF REVIEW: The control of glucose and energy homeostasis, including feeding behaviour, is tightly regulated by gut-derived peptidic and nonpeptidic endocrine mediators, autonomic nervous signals, as well as nutrients such as glucose. We will review recent findings on the role of the gastrointestinal tract innervation and of portal vein glucose sensors; we will review selected data on the action of gastrointestinally released hormones. RECENT FINDINGS: The involvement of mechanosensory vagal afferents in postprandial meal termination has been clarified using mouse models with selective impairments of genes required for development of mechanosensory fibres. These activate central glucogen-like peptide-1/glucogen-like peptide-2 containing ascending pathways linking the visceroceptive brainstem neurons to hypothalamic nuclei. Mucosal terminals comprise the chemosensory vagal afferents responsive to postprandially released gastrointestinal hormones. The mechanism by which the hepatoportal glucose sensor stimulates glucose utilization by muscles was demonstrated, using genetically modified mice, to be insulin-independent but to require GLUT4 and AMP-kinase. This sensor is a key site of glucogen-like peptide-1 action and plays a critical role in triggering first phase insulin secretion. PeptideYY and ghrelin target intracerebral receptors as they are bidirectionally transported across the blood brain barrier. The anorectic functions of peripherally released peptideYY may however be mediated both via vagal afferents and intracerebral Y2 receptors in the brainstem and arcuate nucleus. SUMMARY: These recent findings demonstrate that the use of improved anatomical and physiological techniques and animal models with targeted gene modifications lead to an improved understanding of the complex role of gastrointestinal signals in the control of energy homeostasis.

Afferent Pathways↗