Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “INTESTINAL SECRETIONS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 469 records · Page 26Linked to original sources
PubMed1990

5-HT2 and 5-HT3 receptor subtypes mediate cholera toxin-induced intestinal fluid secretion in the rat.

The mechanisms of diarrhea in Asiatic cholera have been studied extensively. Cyclic adenosine monophosphate, 5-hydroxytryptamine (5-HT), prostaglandins, and the function of neuronal structures have been implicated in the pathogenesis of cholera. To elucidate the action of 5-HT in mediating cholera secretion, in vivo experiments were performed in the rat jejunum. The inhibitory effects of the 5-HT2 receptor antagonist ketanserin and the 5-HT3 receptor antagonist ICS 205-930 were studied in cholera toxin- and 5-HT-induced fluid secretion. Both ketanserin and ICS 205-930 dose-dependently but only partially reduced the secretory effect of cholera toxin. The combination of the two blockers totally abolished cholera toxin-induced secretion without any influence on cholera toxin-induced increase in cyclic adenosine monophosphate. Prostaglandin E2- and bisacodyl-induced secretion was not affected by the combined administration of 5-HT2 and 5-HT3 antagonists. The present results provide evidence for an important role of 5-HT in cholera toxin-induced secretion. The data suggest a model in which cholera toxin may initiate the release of 5-HT from enterochromaffin cells. 5-Hydroxytryptamine may then cause prostaglandin E2 formation via 5-HT2 receptors and activation of neuronal structures via 5-HT3 receptors. These two effects may finally lead to the profuse fluid secretion which can be totally blocked by the combination of a 5-HT2 blocker and a 5-HT3 blocker.

Animals↗
PubMed1975

Diarrheagenic effect of volume expansion: intestinal fluid secretion without mucosal adenyl cyclase stimulation.

Rapid intravenous saline infusion causes secretion of isotonic fluid by the canine duodenum. The duodenal fluid secretion is not accompanied either by increased adenyl cyclase activity in the mucosal epithelial cells or by widening of the "tight junctions" between epithelial cells. These data clearly indicate that the diarrheagenic effect of volume expansion is not mediated by the adenyl cyclase system. Furthermore, these data provide support for the concept that, when increased mucosal adenyl cyclase activity is associated with gut fluid secretion, the adenyl cyclase stimulation is a primary event, and is not secondary to the transmucosal isotonic fluid movement.

Adenylyl Cyclases↗
PubMed2005

Histidine inhibits oxidative stress- and TNF-alpha-induced interleukin-8 secretion in intestinal epithelial cells.

We investigated the effect of several amino acids on the secretion of such inflammatory cytokines as interleukin-8 (IL-8) induced by hydrogen peroxide or tumor necrosis factor-alpha (TNF-alpha) in intestinal epithelial-like Caco-2 and HT-29 cells. We found that histidine, one of the conditionally essential amino acids, significantly inhibited both hydrogen peroxide- and TNF-alpha-induced IL-8 secretion and mRNA expression in Caco-2 cells and HT-29 cells. These inhibitions were dose dependent and the inhibition rate of hydrogen peroxide-induced IL-8 secretion reached more than 50% at a concentration of 25mM, with over 95% inhibition at a concentration of 50mM. TNF-alpha increased the transcriptional activity of the IL-8 promoter which was significantly inhibited by treating Caco-2 cells with histidine. Histidine also abolished the NF-kappaB-dependent activation of the IL-8 promoter induced by TNF-alpha. These results indicate that histidine inhibited the hydrogen peroxide- and TNF-alpha-induced IL-8 secretion at the transcriptional level in intestinal epithelial cells, suggesting that histidine has the potential to attenuate intestinal inflammation.

Cell Line↗
PubMed1998

Intestinal secretory factor released by macrophages stimulated with Clostridium difficile toxin A: role of interleukin 1beta.

Clostridium difficile toxin A is associated with enterocolitis in animals and humans. However, the mechanisms of its secretory and damaging effects are not totally understood. In this work, we examined the intestinal secretion of electrolytes and water caused by supernatants from macrophages stimulated with toxin A in rabbit ileal mucosa mounted in Ussing chambers. We also investigated the mechanism by which the intestinal secretory factor (ISF) is released from stimulated macrophages. Supernatants from macrophages stimulated with toxin A caused potent intestinal secretion (change in short-circuit current [DeltaIsc], 76 microA x cm-2; P < 0.01). The release of the ISF was pertussis toxin sensitive (reduction, 61%; P < 0.01) and was also reduced (P < 0.05) by a protein synthesis inhibitor (67%), protease inhibitors (57%), a phospholipase A2 inhibitor (54%), a cyclo-oxygenase inhibitor (62%), a dual cyclo- and lipoxygenase inhibitor (48%), a platelet-activating factor (PAF) receptor antagonist (55%), and tumor necrosis factor alpha (TNF-alpha) synthesis inhibitors (48%). However, this release was not inhibited by a lipo-oxygenase inhibitor. Monoclonal anti-interleukin 1beta (IL-1beta) but not anti-IL-1alpha antibody blocked (72%; P < 0.01) the secretory action of the ISF, as did recombinant human IL-1 receptor antagonist (80%; P < 0.01). High levels of IL-1beta (3,476 pg/ml) were detected by an enzyme-linked immunosorbent assay in the above supernatants. Furthermore, the addition of IL-1beta to the serosal side caused a potent secretory effect (DeltaIsc, 80 microA x cm-2; P < 0.01). These results show that macrophages stimulated with toxin A release an ISF capable of provoking intestinal secretion. The regulation of this factor is dependent upon the activation of the G protein. In addition, prostaglandins, PAF, and TNF-alpha are involved in the release of the ISF. We conclude that IL-1beta is probably the ISF released by macrophages in response to toxin A.

Animals↗
PubMed2000

Somatostatin receptor scintigraphy: the definitive technique for characterizing vasoactive intestinal peptide-secreting tumors.

Vasoactive intestinal peptide-secreting tumors (VIPomas) are extremely rare and difficult to diagnose. The authors describe a patient who was found to have a VIPoma after 3 years of symptoms. Somatostatin receptor scintigraphy using indium-labeled octreotide localized her tumor and prompted a surgical resection. This is the preferred imaging study for the earliest, most accurate, and cost-effective identification of VIPomas and their metastases.

Female↗
PubMed1980

Enhancement by cholera toxin of IgA secretion from intestinal crypt epithelium.

Studies of the effects of cholera toxin on the intestine have produced conflicting results regarding stimulation of IgA secretion. In the present study rabbit ileal loops were perfused with saline, and the IgA content of the perfusate was assessed by immunoradiometric assay. Crypt epithelial IgA content in biopsies was studied by immunofluorescence. Cumulative loop fluid IgA production 300 minutes after exposure to cholera toxin was 6216 +/- 993 microgram/cm compared with 4646 +/- 953 microgram/cm in controls (P < 0 . 20). However, rate of fluid IgA production above baseline at 300 minutes was 1742 +/- 181 microgram/h/cm in cholera loops and 1049 +/- 310 microgram/h/cm in controls, and the mean difference between the cholera and control loops was statistically significant (P < 0 . 05). In biopsies, mean rank of crypt epithelial IgA at 300 minutes was decreased compared with controls (P < 0 . 05). The findings of increased rate of fluid IgA production and decreased epithelial IgA suggest that a single dose of cholera toxin enhanced secretion of IgA from crypt epithelium into the intestinal lumen, although the magnitude of the enhancement was not great.

Animals↗
PubMed2003

Short fasting dramatically decreases rat duodenal secretory responsiveness to orexin A but not to VIP or melatonin.

Orexins are involved in the central nervous control of appetite and behavior, and in addition, they are present in endocrine cells and/or neurons in the intestine. The role of these peptides in peripheral regulation of intestinal secretion has not been investigated. We thus compared the effects of orexin A and some established secretagogues on duodenal HCO3- secretion in fed rats with effects in rats exposed to short (overnight) food deprivation. Rats were anesthetized with thiobarbiturate, a 12-mm segment of proximal duodenum with intact blood supply was cannulated in situ, and the alkaline secretion was titrated by pH stat. Secretagogues were supplied specifically to the duodenum by close intra-arterial infusion. Orexin A (60-600 pmol x kg(-1) x h(-1)) caused marked and dose-dependent stimulation of the duodenal secretion in fed animals but did not affect secretion in overnight food-deprived animals. Similarly, short fasting caused a 100-fold increase in the amount of the muscarinic agonist bethanechol (from 50 to 5,000 nmol x kg(-1) x h(-1)) required for stimulation of the secretion. In contrast, the secretory responses to VIP (50-1,000 pmol x kg(-1) x h(-1)) and melatonin (20-200 nmol x kg(-1) x h(-1)) were not affected. The appetite-regulating peptide orexin A is thus a stimulant of intestinal secretion, but the response to this peptide as well as the muscarinic agonist bethanechol is markedly dependent on previous intake of food. Overnight fasting is a standard experimental procedure in studies of gastrointestinal function and pathophysiology in humans and animals. Studies made on neuroendocrine control of intestinal secretion may require reevaluation with respect to feeding status.

Animals↗
PubMed1983

The role of pancreatico-biliary secretions in intestinal adaptation after resection, and its relationship to plasma enteroglucagon.

Two groups, each containing 16 male Wistar rats, had either 75 per cent small bowel resection or jejunal transection; 8 animals from each group; had previously been subjected to pancreatico-biliary diversion. All animals were killed 12 days after the operation, plasma enteroglucagon levels were measured and crypt cell production rate (CCPR) at different sites of the remaining small intestine was measured using a metaphase arrest technique with vincristine. In each of the resected groups there was a significant increase in the CCPR and enteroglucagon levels compared with the transected groups. Furthermore it was found that the CCPR and enteroglucagon levels were higher in the resected group without the pancreatico-biliary diversion compared with the resected group with the diversion. This study, although it confirms the importance of pancreatico-biliary secretions in intestinal adaptation, could also indicate that a humoral factor may be important in the control of intestinal cell proliferation. Our findings do not exclude the possibility that enteroglucagon could be a candidate for such a role.

Adaptation, Physiological↗
PubMed2000

Involvement of an organic anion transporter (canalicular multispecific organic anion transporter/multidrug resistance-associated protein 2) in gastrointestinal secretion of glutathione conjugates in rats.

We investigated the role of cMOAT/MRP2 (canalicular multispecific organic anion transporter/multidrug resistance-associated protein 2) in the intestinal secretion of organic anions by comparing the behavior in Sprague-Dawley (SD) rats and Eisai hyperbilirubinemic rat (EHBR) whose cMOAT/MRP2 is hereditarily defective. After i.v. administration of 1-chloro-2,4-dinitrobenzene (30 micromol/kg), the biliary and intestinal excretion of its glutathione conjugate 2, 4-dinitrophenyl-S-glutathione (DNP-SG), a substrate for cMOAT/MRP2, was significantly reduced in EHBR compared with SD rats. This result also was confirmed by Ussing chamber studies; DNP-SG showed 1.5-fold greater serosal-to-mucosal flux compared with the mucosal-to-serosal flux in SD rats, whereas a similar flux was observed in both directions in EHBR. In addition, metabolic inhibitors reduced the preferential serosal-to-mucosal flux of DNP-SG in SD rats. In everted sac studies, intestinal secretion clearance, defined as the efflux rate of DNP-SG into the mucosal side divided by the area under the curve on the serosal side, was significantly lower in the jejunum of EHBR than that in SD rats. Northern blot analyses demonstrated the highest mRNA level of cMOAT/MRP2 in the jejunum, which is in good agreement with the results of the everted sac studies. These results suggest that cMOAT/MRP2 is involved in the secretion of organic anions in the small intestine.

ATP-Binding Cassette Transporters↗
PubMed2002

MAP kinases contribute to IL-8 secretion by intestinal epithelial cells via a posttranscriptional mechanism.

The intracellular pathways that regulate intestinal epithelial gene expression are poorly understood. In this study we examined the roles of extracellular signal-regulated kinase (ERK) and p38 in the expression of interleukin-8 (IL-8) and intercellular adhesion molecule-1 (ICAM-1) using the human intestinal cell line HT-29. HT-29 cells were treated with tumor necrosis factor-alpha (TNF-alpha) in the presence or absence of ERK and p38 pathway inhibitors. TNF-alpha treatment resulted in increased IL-8 and ICAM-1 protein and mRNA synthesis, increased ERK and p38 activity, and activation of the transcription factors activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB). Inhibition of the ERK and p38 pathways attenuated IL-8 secretion but did not alter ICAM-1 expression. Furthermore, AP-1 and NF-kappaB DNA binding was not affected by ERK and p38 inhibition. In contrast, ERK and p38 inhibition resulted in the accelerated degradation of the IL-8 mRNA, suggesting that in HT-29 cells, p38 and ERK contribute to TNF-alpha-stimulated IL-8 secretion by intestinal epithelial cells via a posttranscriptional mechanism that involves stabilization of the IL-8 transcript.

Cell Line↗
PubMed1982

Intestinal HCO3- secretion in Amphiuma: stimulation by mucosal Cl- and serosal Na+.

The requirement for Na+ and Cl- in the bathing media to obtain a maximal HCO3- secretory flux (JHCO3-) across isolated short-circuited Amphiuma duodenum was investigated using titration techniques and ion substitution. Upon substitution of media Na+ with choline, HCO3- secretion was markedly reduced. Replacement of media Cl- produced a smaller reduction of JHCO3-. The presence of Cl- enhanced HCO3- secretion only if Na+ was also in the media. Elevation of media Na+ or Cl- in the presence of the other ion produced a saturable increase of JHCO3-. In the presence of Na+, Cl- stimulated JHCO3- when added to the mucosal but not the serosal medium. In the presence of Cl-, Na+ elevated JHCO3- when added to the serosal but not the mucosal medium. The ability of mucosal Cl- to stimulate JHCO3- was not apparently dependent on mucosal Na+. Simultaneous addition of 10 mM Cl- to the Na+ -free mucosal medium and 10 mM Na+ to the Cl- -free serosal medium stimulated JHCO3- above levels produced by serosal Na+ alone. In conclusion, intestinal HCO3- secretion required mucosal Cl- and serosal Na+ and did not involve mucosal NaCl cotransport. The results are consistent with a mucosal Cl- absorptive mechanism in series with parallel basolateral Na+ -H+ and Cl- -HCO3- exchange mechanisms.

Animals↗
PubMed1997

Novel p53 mutation in a malignant tumor secreting vasoactive intestinal peptide.

OBJECTIVE: To assess involvement of p53 mutations in development of pancreatic endocrine tumors. DESIGN: Survey of sporadic pancreatic endocrine tumors. SETTING: Hospital referral centers, mainly in the Los Angeles, Calif, area. PATIENTS: We obtained fresh surgical specimens from 25 patients (convenience sample) with no family history of endocrine tumors and no evidence of multiple endocrine neoplasia 1 or von Hippel-Lindau disease. Preoperative tests included serum peptide analysis. MAIN OUTCOME MEASURES: DNA was prepared from tumor specimens. We screened exons 5 through 8 of the p53 gene using single-strand conformation polymorphism analysis, followed by DNA sequencing when a variant was detected. RESULTS: A three-base deletion mutation (codon 239) was found in one malignant tumor secreting vasoactive intestinal peptide. CONCLUSIONS: p53 appears to have a limited role in development of pancreatic endocrine tumors. However, evidence from one of our patients suggests it may be involved in tumor progression in uncommon cases.

Codon↗
PubMed2005

CD36 deficiency impairs intestinal lipid secretion and clearance of chylomicrons from the blood.

CD36 mediates the transfer of fatty acids (FAs) across the plasma membranes of muscle and adipose cells, thus playing an important role in regulating peripheral FA metabolism in vivo. In the proximal intestine, CD36 is localized in abundant quantities on the apical surface of epithelial cells, a pattern similar to that of other proteins implicated in the uptake of dietary FAs. To define the role of CD36 in the intestine, we examined FA utilization and lipoprotein secretion by WT and CD36-null mice in response to acute and chronic fat feeding. CD36-null mice given a fat bolus by gavage or fed a high-fat diet accumulated neutral lipid in the proximal intestine, which indicated abnormal lipid processing. Using a model in which mice were equipped with lymph fistulae, we obtained evidence of defective lipoprotein secretion by directly measuring lipid output. The secretion defect appeared to reflect an impaired ability of CD36-null enterocytes to efficiently synthesize triacylglycerols from dietary FAs in the endoplasmic reticulum. In the plasma of intact mice, the reduced intestinal lipid secretion was masked by slow clearance of intestine-derived lipoproteins. The impaired clearance occurred despite normal lipoprotein lipase activity and likely reflected feedback inhibition of the lipase by FAs due to their defective removal from the plasma. We conclude that CD36 is important for both secretion and clearance of intestinal lipoproteins. CD36 deficiency results in hypertriglyceridemia both in the postprandial and fasting states and in humans may constitute a risk factor for diet-induced type 2 diabetes and cardiovascular disease.

Animals↗
PubMed1977

Exclusion of pancreatic exocrine secretion from intestine in the pig: existence of a digestive compensation.

The apparent digestibility of a diet was studied over a period of 87 days after ligature of the pancreatic duct, in the growing pig. Sham operated pigs were used as controls. Feces and urine collections were made during three periods of 10 days each. Mean daily gain of sham operated pigs was higher (560 g/day) than that of pancreatic duct ligated pigs (421 g/day), throughout the experiment. Within the first period (15-24 days after ligature), the apparent digestibility of nitrogen was most affected (-35.6%) while that of energy decreased by 12.1% as compared to values obtained in sham operated pigs. Nitrogen retention was similar in all pigs. Between the 1st (15-25 days) and the 3rd period (78-87 days) after exclusion of the pancreatic secretion from intestine, the apparent digestibility of nitrogen increased by 20% and that of energy by 6%, which might suggest digestive compensation. At the end of the experiment, weights of empty small intestine and liver were significantly higher in the pancreatic duct ligated pigs. The origin of the digestive compensation is discussed.

Animals↗
PubMed1987

Mechanisms underlying the small intestinal fluid secretion caused by arachidonic acid, prostaglandin E1 and prostaglandin E2 in the rat in vivo.

Prostanoids were given intraluminally (PGE2) or infused close intra-arterially (PGE1 and PGE2) or arachidonic acid was administered intraluminally to denervated jejunal segments of the rat in vivo. These experimental manoeuvres caused a net fluid secretion, although a 1,000-fold higher concentration of the prostanoids was needed from the luminal than from the vascular side. I.v. hexamethonium or serosally applied lidocaine diminished the induced fluid secretion suggesting that the prostanoids act mainly by eliciting local secretory reflexes in the enteric nervous system. This nerve-mediated secretion is not accompanied by any increase in tissue cAMP. However, at higher i.a. concentrations of PGE2 there seems to be a non-neurogenic effect on the enterocytes associated with an increase in tissue cAMP.

Alprostadil↗