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At least 1,315 records · Page 73Linked to original sources
PubMed1995

PYY and GLP-1 contribute to feedback inhibition from the canine ileum and colon.

To explore mechanisms whereby unabsorbed nutrients in the ileum inhibit the upper gut ("ileal brake"), we perfused the canine ileum or colon and monitored phase 3 in the duodenum. Fasting motility was recorded when the ileum or colon was perfused with 154 mM NaCl, a mixed isotonic nutrient solution (Ensure), or individual nutrients (maltose, casein hydrolysates, or sodium oleate). Blood samples were collected before and during the perfusions. The ileum was also perfused with 154 mM NaCl while peptide YY (PYY) was infused by vein. In both sets of experiments, plasma levels of PYY, neurotensin, and glucagon-like peptide-1 (GLP-1) were measured. Ileal or colonic perfusion of Ensure delayed phase 3 [migrating motor complexes (MMC)] in the duodenum, inhibited ileal motility, and increased plasma levels of PYY and GLP-1. Ileal casein and oleate and colonic casein also delayed the duodenal MMC. The MMC cycle length and plasma levels of PYY were closely correlated. Intravenous PYY prolonged the MMC cycle; an intravenous dose of 100 pmol.kg-1.h-1 of PYY mimicked the effects of ileal Ensure. These results support the hypothesis that PYY, and possibly GLP-1, participate in the ileal brake. This negative feedback loop also affects the distal small bowel. The proximal colon also triggers the feedback inhibition of gut motility (colonic brake).

Animal Nutritional Physiological Phenomena↗
PubMed1998

Antistress Pattern Induced by Oxytocin.

Repeated oxytocin injections cause lowered blood pressure, decreased cortisol levels, increased withdrawal latency, increased release of vagally controlled gastrointestinal hormones, and increased weight gain. Together, these effects form an antistress pattern. Nonnoxious sensory stimuli release oxytocin and induce an effect spectrum similar to the one caused by oxytocin injections.

Journal Article↗
PubMed2006

Curcumin inhibits neurotensin-mediated interleukin-8 production and migration of HCT116 human colon cancer cells.

PURPOSE: Neurotensin, a gut tridecapeptide, acts as a potent cellular mitogen for various colorectal and pancreatic cancers that possess high-affinity neurotensin receptors. Cytokine/chemokine proteins are increasingly recognized as important local factors that play a role in the metastasis and invasion of multiple cancers. The purpose of this study was to (a) determine the effect of neurotensin on cytokine/chemokine gene expression and cell migration in human cancer cells and (b) assess the effect of curcumin, a natural dietary product, on neurotensin-mediated processes. EXPERIMENTAL DESIGN: The human colorectal cancer, HCT116, was treated with neurotensin, with or without curcumin, and interleukin (IL)-8 expression and protein secretion was measured. Signaling pathways, which contribute to the effects of neurotensin, were assessed. Finally, the effect of curcumin on neurotensin-mediated HCT116 cell migration was analyzed. RESULTS: We show that neurotensin, acting through the native high-affinity neurotensin receptor, induced IL-8 expression in human colorectal cancer cells in a time- and dose-dependent fashion. This stimulation involves Ca2+-dependent protein kinase C, extracellular signal-regulated kinase-dependent activator protein-1, and extracellular signal-regulated kinase-independent nuclear factor-kappaB pathways. Curcumin inhibited neurotensin-mediated activator protein-1 and nuclear factor-kappaB activation and Ca2+ mobilization. Moreover, curcumin blocked neurotensin-stimulated IL-8 gene induction and protein secretion and, at a low concentration (i.e., 10 micromol/L), blocked neurotensin-stimulated colon cancer cell migration. CONCLUSIONS: Neurotensin-mediated induction of tumor cell IL-8 expression and secretion may contribute to the procarcinogenic effects of neurotensin on gastrointestinal cancers. Furthermore, a potential mechanism for the chemopreventive and chemotherapeutic effects of curcumin on colon cancers may be through the inhibition of gastrointestinal hormone (e.g., neurotensin)-induced chemokine expression and cell migration.

Calcium↗
PubMed1995

Effects of somatostatin on human satiety.

Somatostatin (ST) inhibits gastrointestinal motility and exocrine and endocrine secretions. In animals, ST has been demonstrated to decrease food intake. We investigated, in a randomized double-blind investigation in 10 healthy humans, the effects of an intravenous ST infusion compared to saline on subjective hunger feelings. After 1 h, a low dose of fat was given intraduodenally to induce the release of endogenous upper-intestinal satiety factors. Ninety minutes later sandwiches were served and eaten until satiation. In the first hour, when no intraduodenal fat was given, there was a significant decrease in feelings of hunger with ST (p < 0.05). During the intraduodenal fat infusion this pattern reversed with a trend towards less satiety with ST. Food intake during intraduodenal fat infusion tended to be higher during ST (305 +/- 42 g) than during saline (205 +/- 36 g) although not significantly. In the 5 h after the experiment hunger feelings were significantly less after ST. In conclusion, we found evidence for a satiety effect of ST in humans which reversed towards less satiety when intraduodenal intralipid, which presumably produced endogenous satiety factors, was given. Postmeal satiety is higher after ST.

Adult↗
PubMedDate not supplied

Gastrin and colon cancer: a unifying hypothesis.

Recently, a variety of studies in vivo as well as in vitro have demonstrated that gastrointestinal hormones can influence the rate of proliferation of neoplastic cells. The widespread use of omeprazole, which increases serum gastrin, coupled with the findings that omeprazole causes gastric carcinoid tumors in rats and that a significant number of patients with adenocarcinoma of the colon have increased serum gastrin have focussed attention on the relationship between gastrin and colon cancer. In the present paper, we have reviewed the experimental findings in humans, experimental animals, and colon cancer cells in tissue culture that bear on the possible relationships between gastrin and colon cancer. Based on these findings, we have proposed two hypotheses that can account for the increased serum gastrin that occurs in some patients with colon cancer.

Animals↗
PubMed1975

The motor-stimulating effect of natural motilin on the lower esophageal sphincter fundus, antrum and duodenum in dogs.

Natural motilin was investigated for its effect on gastrointestinal motor activity in anesthetized dogs. In doses starting from 10 ng/kg as single injection and 100 ng/kg-h as intravenous infusion, motilin induced phasic pressure changes in the lower esophageal sphincter (LES) and in the lumen of the fundus, antrum, and duodenum. Tachyphylaxis was seen in 6 out of 10 dogs. Motilin had no effect on isolated muscle strip preparations of the LES, fundus, antrum, and duodenum in this species.

Animals↗
PubMedDate not supplied

Effects of motilin and octapeptide of cholecystokinin on antral and duodenal myoelectric activity in the interdigestive state and during inhibition by secretin and gastric inhibitory polypeptide.

In conscious dogs prepared with gastric cannulae and antral and duodenal electrodes, intravenous administration of synthetic porcine motilin and CCK-OP in varying doses resulted in significant increases in the mean percent frequency of spike potentials on slow waves. Motilin was a more potent stimulant than CCK-OP. Motilin-stimulated spike potentials in both antrum and duodenum were significantly suppressed by either natural porcine secretin or synthetic porcine GIP. Secretin suppressed the spike potentials of the antrum stimulated by CCK-OP but not those of the duodenum. The spike potentials stimulated by CCK-OP could not be suppressed by GIP in the dosages employed.

Action Potentials↗
PubMed1983

Effect of antrectomy on small intestinal structure and function in the rat.

Antrectomy reduced the levels of circulating gastrin but did not change jejunal morphology. In vitro and in vivo absorption as well as the activity of some brush border enzymes were increased. The observed alterations are discussed on the basis of antrectomy-induced alterations in the release of gastrointestinal hormones, gastric and pancreatic secretion and gastric emptying.

Animals↗
PubMed1987

Effect of a long-acting somatostatin analogue (SMS 201-995) on postprandial gastric emptying of 99mTc-tin colloid and mouth-to-caecum transit time in man.

The effect on gut motility of a single subcutaneous injection of 50 micrograms of the long-acting somatostatin analogue, SMS 201-995, was investigated in 8 normal volunteers who took a drink containing 99mTc and lactulose with a mixed meal. The rate of gastric emptying was assessed by disappearance of the isotope from the stomach area as measured by a gamma camera, and mouth-to-caecum transit time (MCTT) was measured by the appearance of hydrogen in the breath. Gastric emptying was accelerated, with a significant reduction of the time taken to 50% isotope disappearance (37.2 +/- 3.3 min during control study vs 23.3 +/- 3.4 min after SMS injection; p less than 0.01). In contrast, MCTT was prolonged from 57.3 +/- 9.4 min (control) to 203.6 +/- 14.7 min after SMS (p less than 0.001).

Adult↗
PubMed1995

Specificity of phospholipase D activation by cholecystokinin and phorbol myristate acetate but not by carbamylcholine and A23187 in rat pancreatic acini.

The gastrointestinal hormone cholecystokinin and the muscarinic agonist carbamylcholine are involved in pancreatic enzyme secretion through phospholipase C activation and production of the second messengers inositol trisphosphate and diacylglycerol. However, cholecystokinin induces growth of the pancreas whereas carbamylcholine does not. This study investigated the possibility of a specific cellular signalling transduction system through which cholecystokinin may induce pancreatic growth. Rat pancreatic acini were preincubated with 3H choline or 3H myristic acid to label phosphatidylcholine. They were then stimulated by caerulein, phorbol myristate acetate, and carbamylcholine; choline and phosphocholine release as well as phosphatidic acid and phosphatidylethanol production were measured to establish phospholipase D (PLD) activation. Caerulein, phorbolester and carbamylcholine increased phosphocholine release. Choline release was induced early by caerulein and later by phorbolester but not by carbachol. PLD was activated by caerulein and phorbolester but not by carbamylcholine. Increased intracellular calcium by A23187 had no effect on PLD activation but its chelation by BAPTA prevented caerulein-induced PLD activation. In conclusion, PLD seems to be selectively activated by caerulein and phorbol ester by two different mechanisms which are insensitive to carbamylcholine. It is suggested that the PLD pathway might be the cellular signalling system leading to pancreatic growth.

Alkaloids↗
PubMed1994

Effect of mode of delivery, parity and umbilical blood gas on first meconium passage in full-term healthy neonates.

The various physiologic factors which might influence the time of first meconium passage were studied in 62 healthy full-term newborn infants. Thirty-two babies were born vaginally and 30 by elective cesarean section. Infants born vaginally were more acidotic and passed first stool earlier compared to those born by cesarean section. The same applies to vaginally delivered babies when comparing babies born to primipara and others. Acidosis is a presumed mechanism, and a role of gastrointestinal hormones is suggested to be the possible mediator of increased motility in these babies.

Acidosis↗
PubMed1969

The gastrointestinal stimulus to insulin release. I. Secretin.

The gastrointestinal stimulus to the release of insulin has been investigated in man by the use of a radioimmunoassay for secretin. Serum secretin levels rose rapidly after the oral ingestion of glucose or protein and preceded the elevation of serum insulin. An intravenous infusion of highly purified secretin caused a release of insulin when the serum secretin levels were within the physiological range. Infusion of hydrochloric acid into the duodenum caused an elevation of serum secretin and serum insulin levels in normal subjects. A similar response of secretin and insulin was seen after intravenous infusion of pentagastrin even when the acid stimulus to the duodenum was prevented. The latter observation suggests that pentagastrin (and probably gastrin) releases secretin by a direct humoral effect which is later fortified by the arrival of gastric acid in the duodenum. These studies suggest that secretin participates in the augmentation of insulin release after oral stimuli, and that a rapid sequence of humoral events takes place, gastrin releasing secretin and secretin releasing insulin. Subsequently secretin release would be augmented by a local stimulus in the duodenum and insulin release by the rising level of blood glucose or amino acids. This humoral system, which could also involve other gastrointestinal hormones, would provide a mechanism for facilitating the release of insulin to coincide with the onset of metabolite absorption.

Adult↗
PubMed1971

Secretion of glucagon from the isolated, perfused canine pancreas.

Using the isolated, perfused canine pancreas preparation, previously described, the interrelationship of the secretion of pancreatic glucagon and insulin was studied after stimulation with glucose, gastrointestinal hormones, and the amino acid arginine. The results confirm the concept that pancreatic glucagon is a hormone of "glucose need" and suggest that it may be important in a moment to moment control of glucoregulation. The secretion of pancreatic glucagon was stimulated after infusion of gastrin, pancreozymin, and arginine, while no increase was associated with secretin infusion. The magnitude of the increase was closely related to the glucose concentration present in the perfusion medium, being higher and more pronounced during perfusion with low concentrations of glucose (25 mg/100 ml or 50 mg/100 ml). Stimulation of insulin secretion was seen after glucose, gastrin, pancreozymin, secretin, and arginine. The magnitude of the increase was again closely related to the glucose concentration present, this time being higher and more pronounced during perfusion with high glucose concentrations (150 mg/100 ml). Secretion of both pancreatic hormones always followed a biphasic response pattern after the stimuli mentioned, similar to the characteristic release pattern previously described for insulin after an increment in glucose concentration. In order to elucidate whether endogenous pancreatic glucagon possesses an insulinogenic action, as it has been shown to be the case with the administration of exogenous pancreatic glucagon, the time interrelationship of the secretion of pancreatic glucagon and insulin was investigated by determining the initial rise of the hormones after stimulation with gastrin, pancreozymin, and arginine. The rise of glucagon and insulin occurred simultaneously, i.e. inside a 10 sec period. This does not, however, exclude with certainty an insulinogenic role of pancreatic glucagon.

Animals↗
PubMed1988

Dietary regulation of rat intestinal cholecystokinin gene expression.

Cholecystokinin (CCK) is a gastrointestinal hormone produced by discrete endocrine cells in the upper small intestine and released after ingestion of a meal. The present study was designed to determine if enhanced CCK secretion is associated with increases in intestinal CCK mRNA levels. Rats, prepared with indwelling intraduodenal cannulae, were first fed an elemental diet that did not stimulate CCK release. Next, as a means of stimulating CCK secretion, soybean trypsin inhibitor was perfused for up to 24 h. Trypsin inhibitor administration increased plasma CCK levels from 0.9 +/- 0.1 to approximately 5 pmol/liter. RNA was prepared from the proximal small intestine at various times after trypsin inhibitor perfusion and mRNA levels analyzed by hybridization with a CCK cDNA probe. After 12 and 24 h of trypsin inhibitor treatment there were three- and fourfold increases, respectively, in CCK mRNA levels. In comparison, there was no change in beta-actin mRNA levels. To determine if regulation of CCK mRNA was at the level of CCK gene transcription, labeled transcripts from nuclear run-on incubations were hybridized to immobilized CCK cDNA. In trypsin inhibitor-treated rats, a two- to threefold increase in transcriptional activity was observed, whereas beta-actin gene transcription levels were unaltered. These studies indicate that stimulation of CCK secretion is associated with an increase in intestinal CCK mRNA content resulting from an increase in CCK gene transcription.

Animals↗
PubMed1998

Exendin(9-39)amide is an antagonist of glucagon-like peptide-1(7-36)amide in humans.

The gastrointestinal hormone, glucagon-like peptide-1(7-36)amide (GLP-1) is released after a meal. The potency of synthetic GLP-1 in stimulating insulin secretion and in inhibiting glucagon secretion indicates the putative physiological function of GLP-1. In vitro, the nonmammalian peptide, exendin(9-39)amide [ex(9-39)NH2], is a specific and competitive antagonist of GLP-1. This in vivo study examined the efficacy of ex(9-39)NH2 as an antagonist of exogenous GLP-1 and the physiological role of endogenous GLP-1. Six healthy volunteers underwent 10 experiments in random order. In each experiment, a 30-min period of euglycemia was followed by an intravenous infusion of glucose for 150 min that established a stable hyperglycemia of 8 mmol/liter. There was a concomitant intravenous infusion of one of the following: (1) saline, (2) GLP-1 (for 60 min at 0.3 pmol . kg-1 . min-1 that established physiological postprandial plasma levels, and for another 60 min at 0.9 pmol . kg-1 . min-1 to induce supraphysiological plasma levels), (3-5) ex(9-39)NH2 at 30, 60, or 300 pmol . kg-1 . min-1 + GLP-1, (6-8) ex(9-39)NH2 at 30, 60, or 300 pmol . kg-1 . min-1 + saline, (9 and 10) GIP (glucose-dependent insulinotropic peptide; for 60 min at 0.8 pmol . kg-1 . min-1, with saline or ex(9-39)NH2 at 300 pmol . kg-1 . min-1). Each volunteer received each of these concomitant infusions on separate days. ex(9-39)NH2 dose-dependently reduced the insulinotropic action of GLP-1 with the inhibitory effect declining with increasing doses of GLP-1. ex(9-39)NH2 at 300 pmol . kg-1 . min-1 blocked the insulinotropic effect of physiological doses of GLP-1 and completely antagonized the glucagonostatic effect at both doses of GLP-1. Given alone, this load of ex(9-39)NH2 increased plasma glucagon levels during euglycemia and hyperglycemia. It had no effect on plasma levels of insulin during euglycemia but decreased plasma insulin during hyperglycemia. ex(9-39)NH2 did not alter GIP-stimulated insulin secretion. These data indicate that in humans, ex(9-39)NH2 is a potent GLP-1 antagonist without any agonistic properties. The pancreatic A cell is under a tonic inhibitory control of GLP-1. At hyperglycemia, the B cell is under a tonic stimulatory control of GLP-1.

Adult↗
PubMed1998

Distribution and expression of adrenomedullin in human gastrointestinal tissue.

Adrenomedullin (AM) is a biologically active peptide recently isolated from phaeochromocytoma. We report here the distribution and characterization of immunoreactive AM and gene expression of AM in human gastrointestinal tissue. Using a sensitive radioimmunoassay system for the peptide, immunoreactive human AM was detected in the stomach, duodenum, jejunum, ileum and colon. The AM concentration of these tissues was about 0.4-0.8 pmol/g wet tissue. Reverse phase and gel filtration high-performance liquid chromatographies showed that most of the immunoreactive AM in stomach and jejunum was identical to authentic human AM. By northern blot analysis, human AM mRNA was found to be expressed ubiquitously in the human gastrointestinal tissues. Furthermore, an immunohistochemical study revealed that immunoreactive AM cells were present in the gastrointestinal glands. These results suggest that AM may play some role as a gastrointestinal hormone.

Adrenomedullin↗