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 379 records · Page 21Linked to original sources
PubMed1985

An inhibitory protein of intestinal fluid secretion reverses neuronal GABA transport.

Intestinal challenge with cholera toxin induces the synthesis of a hormone-like protein which counteracts intestinal hypersecretion. This study shows that the protein also inhibits GABA transport across the plasma membrane of Deiters' cells in rabbits. The inhibitory action of the protein was dose dependent, and 10(3) times more potent than met 5-enkephalin, hitherto the most effective known inhibitor of GABA transport in vitro. The influence of the protein on the plasma membrane was reversible, and did not affect either postsynaptic binding or uptake of GABA.

Animals↗
PubMed1997

The enterotoxic effect of zonula occludens toxin on rabbit small intestine involves the paracellular pathway.

BACKGROUND & AIMS: Zonula occludens toxin is a novel toxin elaborated by Vibrio cholerae that modulates intestinal tight junctions. The aim of this study was to establish whether the permeabilizing effect of the toxin leads to intestinal secretion. METHODS: Rabbit intestine was mounted in Ussing chambers and exposed to increasing concentrations of purified toxin. The tissues were also fixed, exposed to zonula occludens toxin, and processed for fluorescence microscopy to determine the distribution of the toxin receptor within the intestine. Then purified toxin was simultaneously perfused in three distinct rabbit intestinal segments in vivo, and water and electrolyte absorption were measured. RESULTS: Zonula occludens toxin induced a time- and dose-dependent decrease of tissue resistance starting at a toxin concentration of 1.1 x 10(-13) mol/L. When tested in vivo, the toxin induced a secretion of water and chloride and the passage of polyethylene glycol 4000 in the bloodstream. Both the in vitro and in vivo effects of the toxin were observed only in the small intestine but not in the colon and paralleled the distribution of the toxin receptor within the intestine. CONCLUSIONS: The intestinal secretion induced by zonula occludens toxin follows the opening of tight junctions caused by the toxin, possibly representing a novel mechanism of intestinal secretion.

Animals↗
PubMed1995

Modulation of intestinal chloride secretion at basolateral transport sites: opposing effects of cyclic adenosine monophosphate and phorbol ester.

BACKGROUND: Although intestinal Cl secretion is largely regulated by apical Cl channels, we have shown that net secretory capacity can be controlled at a basolateral site, the Na-K-2Cl cotransporter (NKCC). Phorbol myristate acetate (PMA) was found to inhibit both cyclic adenosine monophosphate (cAMP)-regulated Cl secretion and basolateral NKCC function in parallel but not apical Cl channels. Because inhibition of NKCC function could occur by reducing the number of membrane NKCC units, we examined the effect of PMA on cAMP-regulated NKCC function and number. METHODS: NKCC function and number were assessed in the human intestinal line HT29cl.19A by bumetanide-sensitive uptake of rubidium 86 and by specific binding of 3H-bumetanide. RESULTS: The cAMP agonist forskolin enhanced bumetanide-sensitive 86Rb uptake and doubled the number of NKCCs. PMA decreased both basal and cAMP-stimulated uptake in time- and dose-dependent fashion. In addition, PMA down-regulated basal NKCC number and abolished cAMP-induced NKCC recruitment. CONCLUSIONS: PMA opposes the action of cAMP on NKCC function by reducing both basal numbers of NKCCs and cAMP-induced recruitment of NKCCs and not by reducing ion translocation per NKCC. These data further emphasize the potential for modulation of intestinal Cl secretion at basolateral sites.

Biological Transport↗
PubMed1984

The effect of variation in phosphorus intake on net intestinal phosphorus absorption, salivary phosphorus secretion and pathway of excretion in sheep fed roughage diets.

Mature sheep fitted with rumen and duodenal cannulae and fed either pelleted hay or grass diets were given supplements of Na2HPO4 by continuous infusion into the rumen and the effects on salivary phosphorus secretion, intestinal phosphorus absorption and pathway of excretion were studied. Little phosphorus was excreted in the urine in control periods and little increase was seen in response to phosphorus supplementation, most of the extra phosphorus given being recovered in the faeces. Infusion of phosphorus into the rumen led to an increase in the flow of phosphorus to the intestine, an increase in absorption, a rise in plasma phosphate level and an increase in salivary phosphorus secretion while withdrawal of supplementary phosphorus was seen to have the opposite effects. In separate studies short sections of the upper small intestine temporarily isolated from the normal flow of digesta were perfused with solutions containing NaH2PO4 (5-50 mmol.l-1). Phosphorus absorption increased with increasing concentration though the relationship was curvilinear such that absorptive efficiency fell from around 0.7 at 5 mmol.l-1 to around 0.35 at a concentration of 50 mmol.l-1. The significance of these results in relation to the control of phosphorus balance in ruminants is discussed.

Absorption↗
PubMed2000

Residual chloride secretion in intestinal tissue of deltaF508 homozygous twins and siblings with cystic fibrosis. The European CF Twin and Sibling Study Consortium.

BACKGROUND & AIMS: Cholinergic stimulation of chloride secretion is impaired in the intestines of patients with cystic fibrosis (CF). However, intestinal chloride secretion has been observed in patients with mild CF mutations. The aim of this study was to investigate residual Cl(-) secretion in the intestine of DeltaF508 homozygous CF patients, and examine the contribution of cystic fibrosis transmembrane conductance regulator (CFTR) and alternative Cl(-) conductances. Twins and siblings with identical CFTR genotypes were investigated to determine the impact of factors other than CFTR on chloride secretion. METHODS: Chloride secretion in rectal tissue was investigated by applying Ca(2+) and adenosine 3',5'-cyclic monophosphate (cAMP)-linked agonists before and after the inhibition of alternative Cl(-) conductances with 4,4'-diisothiocyanostilbene-2, 2'-disulfonic acid (DIDS). RESULTS: cAMP-mediated Cl(-) secretion was observed in 73% of patients, and 20% showed DIDS-sensitive Ca(2+)-activated Cl(-) secretion. This DIDS-sensitive alternative chloride conductance was seen only in CF patients who also responded to cAMP agonists. Chloride secretion was more concordant within monozygous twins than within dizygous pairs. CONCLUSIONS: These results suggest the presence of CFTR-mediated Cl(-) secretion in a subgroup of patients, implying that a portion of deltaF508 CFTR can be processed in vivo and function as a chloride channel in the apical membrane of intestinal cells. Moreover, a considerable number of deltaF508 homozygous patients express chloride conductances other than CFTR in their intestinal epithelia.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1975

Peculiar secretory IgA system identified in chickens. II. Identification and distribution of free secretory component and immunoglobulins of IgA, IgM, and IgG in chicken external secretions.

A homologue of a free secretory component (SC) was identified in chicken intestinal secretion by criteria based on its antigenic relationship with intestinal secretory IgA (SIgA), molecular size, sugar content, and electrophoretic mobility, as well as its elution characteristic from ion-exchange chromatography. SC was obtained in a form free from IgA from the intestinal secretion by salting out and DEAE chromatography, followed by density ultracentrifuguation or Sephadex G-200 gel-filtration. However, the free SC revealed some antigenic deficiency when compared to bound SC of intestinal SIgA and showed a failure of binding to serum-type-polymeric IgA of biliary IgA in vitro. Several kinds of chicken external secretions were examined for detection of SC and immunoglobulin classes of IgG, IgA, and IgM. In spite of the wide distribution of immunoglobulins in the external secretions, SC antigen could be detected only in intestinal secretion. Most IgA in the secretions had a molecular structure of a tetramer of serum-type IgA, lacking in SC and having 17S to 18.5S and 600,000 to 700,000 daltons. On the other hand, IgA in the intestinal secretion showed close similarity to the mammalian SIgA, associated with SC and having 11.2S and 350,000 daltons. Presence of antibody activity in the intestinal IgA to avian reovirus was confirmed by plaque reduction tests.

Animals↗
PubMed2000

Effect of zaldaride maleate, an antidiarrheal compound, on 16,16-dimethyl prostaglandin E2-induced intestinal ion secretion in rats.

The effect of zaldaride, a calmodulin inhibitor, on 16,16-dimethyl prostaglandin E2 (dmPGE2)-induced intestinal ion secretion was investigated in rats. Zaldaride inhibited the dmPGE2-induced increase in water content in the colon, but not that in the small intestine. In the colonic mucosa, zaldaride attenuated the dmPGE2-induced short-circuit current; however, it did not affect the forskolin or dibutyryl cAMP-induced effect. These results suggest that zaldaride inhibits dmPGE2-induced intestinal ion secretion by reducing the activity of Ca2+/calmodulin-dependent adenylate cyclase linked to a receptor, and the colon may be an important site in the action of zaldaride.

16,16-Dimethylprostaglandin E2↗
PubMed1991

Intestinal mucin secretion in streptozotocin-diabetic rats: lack of response to cholinergic stimulation and cholera toxin.

In diabetic rats, intestinal mucin secretion is unusually high compared with that in normal rats. These studies demonstrate that mucin synthesis is also increased in the diabetic intestine. alpha- and beta-adrenergic agonists or antagonists did not affect mucin output in either normal or diabetic animals, suggesting that altered release in diabetes was not due to goblet cells responding abnormally to adrenergic agents. The cholinergic agonist bethanechol caused a dose-dependent and atropine-sensitive increase in mucin secretion from the normal intestine but had no effect on mucin release from diabetic tissue. Atropine alone did not reduce mucin secretion from the diabetic intestine to levels found in normal tissue. Cholera toxin caused an approximately fivefold increase in mucin output from normal rats but had no effect on mucin secretion from diabetic animals. Thus, goblet cell responses to cholinergic stimulation and cholera toxin in the diabetic intestine are markedly impaired. However, loss of cholinergic control does not appear to be responsible for altered baseline mucin secretion in diabetes.

Animals↗
PubMed1995

Molecular cloning and expression of a pituitary gland protein modulating intestinal fluid secretion.

Antisecretory factor (AF) is a protein known to inhibit intestinal fluid secretion induced by cholera toxin. cDNA clones, expressing immunoreactivity to AF were isolated from a human pituitary gland library and sequenced. The sequence contained 1309 base pairs plus a poly(A) tail; Northern blot analysis of pituitary RNA confirmed this size. One large open reading frame was found to code for 382 amino acids. The protein was expressed in pGEX-lambda 1T/Escherichia coli and purified. The recombinant AF was extremely potent, 9 ng (2.10(-13) mol), giving a significant antisecretory activity against cholera toxin-induced fluid secretion in rat. Antiserum against recombinant AF was used in immunohistochemical and Western blot analysis. Sections from human pituitary glands manifested specific intracellular staining in cells exclusively located in the anterior part. Both recombinant AF and AF extracted from pituitary gland appeared in SDS-polyacrylamide to have a molecular mass of 60 kDa, although the renal value was 41 kDa. The protein sequence manifested homology (29% identity) with one protein, a putative Saccharomyces cerevisiae 30-kDa protein of unknown function.

Amino Acid Sequence↗
PubMed1998

Butyrate enhances interleukin (IL)-8 secretion by intestinal epithelial cells in response to IL-1beta and lipopolysaccharide.

Intestinal epithelial (Caco-2) cells secrete the chemokine, IL-8, after stimulation with IL-1beta, but not after lipopolysaccharide. Butyrate is a short chain fatty acid derived from the metabolism of intestinal contents by gut bacteria. Butyrate concentrations reflect, therefore, the bacterial microenvironment established within the intestine. We hypothesized that butyrate may alter the secretion of IL-8 by intestinal epithelial cells in response to stimulation by IL-1beta or lipopolysaccharide. Caco-2 cells were incubated in varying concentrations of sodium butyrate (0-20 mM) for 24 h before stimulation with lipopolysaccharide or IL-1beta. IL-8 secretion was measured over 24 h by ELISA. IL-8 mRNA accumulation was detected by Northern blots. Lipopolysaccharide induced the secretion of IL-8 only after Caco-2 cells cells had been cultured with sodium butyrate. Furthermore, butyrate significantly enhanced IL-8 secretion by cells stimulated with IL-1beta. Butyrate also increased IL-8 mRNA accumulation in stimulated Caco-2 cells. Intestinal epithelial cells can, therefore, be primed by butyrate to become activated by lipopolysaccharide and proinflammatory cytokines. This may represent a mechanism by which intestinal epithelial cells can regulate intestinal inflammation in response to changes in the intestinal milieu.

Blotting, Western↗
PubMed1985

Intestinal iodide secretion and its dependence upon mucosal I- permeability.

Iodide secretion across different regions of rat small intestine has been investigated in vitro using the standard Wilson-Wiseman technique. Net I- secretion was observed along the entire small intestine, being significantly higher in the central region. Anaerobic conditions, ouabain (2 mM) and Na+ free Ringer solution prevented net I- secretion, whilst both theophylline (1 mM) and carbachol (0,1 mM) enhanced the observed basal intestinal I- secretion. Furthermore, Ca2+-deprived bathing solutions significantly reduced intestinal I- secretion. Epithelial I- uptake from both mucosal and serosal sides was measured by using a Ussing-type chamber technique. The initial rate of I- uptake across the mucosal membrane was significantly higher in the central region than in the proximal part of rat small intestine. No significant differences were observed in the rate of I- uptake from the serosal side. These studies suggest that mucosal I- permeability might determine the direction of net I- intestinal transport and that cytosolic Ca2+ may be a physiological regulator of intestinal I- transport.

2,4-Dinitrophenol↗
PubMed2003

Influence of P-glycoprotein, transfer clearances, and drug binding on intestinal metabolism in Caco-2 cell monolayers or membrane preparations: a theoretical analysis.

Studies on the Caco-2 cell monolayer system that contained cytochrome P450 and P-glycoprotein activities had advanced the theory that increased intestinal metabolism resulted with increased drug efflux due to an increase in mean residence time (MRT) in the system. To confirm or refute the claim, we developed compartmental models to study the effects of intestinal secretion on the MRT and rates of metabolism under first-order and nonlinear conditions. The theoretical examinations showed that under first-order conditions, intestinal secretion increased the MRT of drug in all compartments but failed to increase the rate of metabolite formation or the total amount of metabolite formed. Instead, reduced metabolic rates arose with increased efflux from cell, either into the apical or the basolateral compartment. By contrast, under saturable metabolic conditions, there were some conditions found whereby rates of metabolism increased with intestinal secretion and rapid reabsorption, albeit the total amount of metabolite formed eventually equaled the administered dose. Intestinal secretion failed to induce higher rates of metabolism for other conditions (saturable cellular binding, cellular efflux, or cell entry). With saturation of metabolic enzymes, drug efflux brought about desaturation, and, upon rapid recovery of drug into the cellular compartment, higher rates of metabolite formation were attained. The simulation study showed that, under first-order conditions, intestinal secretion reduced the rate of metabolism even though the MRT was prolonged within the cell preparation. With nonlinear metabolism, however, instances may exist whereby higher rates of metabolism would result with secretion.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMedDate not supplied

Recent advances with thyrocalcitonin.

Thyrocalcitonin (TCT) is a 32 amino acid peptide hormone similar, but not identical, in structure from fish to man. Mammals produce the hormone in non-follicular thyroidal "C-cells" which can be identified visually using recently developed immunocytochemical methods. Although TCT exerts effects on the gut and kidney, bone seems to be the primary target tissue. The ability of TCT to restrict calcium fluxes from bone to blood and to inhibit bone resorption explains its utility for treating certain metabolic bone diseases, e.g. Paget's disease. The bone effects also account for the ability of TCT to combat a hypercalcemic challenge. Recent work suggests close relationships and a possible closed-loop feedback system between the gut and thyroid. In animals, gastrin is a potent TCT secretagogue; studies in man indicate that TCT, in turn, can effect gastric acid secretion and intestinal secretion of water and electrolytes. This gastrin-TCT relationship may help control levels of blood calcium during intestinal absorption of calcium following feeding. The ability of gastrin to stimulate TCT release has been applied clinically for the early diagnosis of medullary thyroid carcinoma (MTC), a C-cell tumor. Subclinical or questionable cases of MTC have been identified reliably using a simple, rapid provocative test involving pentagastrin injection and evaluation of blood samples by radioimmunoassay for elevated levels of TCT.

Amino Acid Sequence↗
PubMed1993

Pigeon breeders' lung; IgG subclasses to pigeon intestinal mucin and IgA antigens.

Sera from all symptomatics with pigeon breeders' lung and many non-symptomatic pigeon breeders react specifically with the pigeon antigens and in particular pigeon intestinal secretions and isolated pigeon intestinal mucin and IgA. In sera from all 82 precipitin-positive pigeon breeders investigated, IgG1 reacted with both IgA and mucin, while IgG2 reacted predominantly with mucin only. Sera from all 32 symptomatic patients with pigeon breeders' lung demonstrated an IgG3 reaction with mucin, but only three sera showed reactivity against IgA and this was very weak. In contrast, only three out of 27 pigeon breeders with pulmonary pathology other than pigeon breeders' lung and only three out of 23 sera from healthy pigeon breeders showed detectable IgG3 reactivity with mucin. IgG4 from eight sera only reacted with mucin (n = 7) or IgA (n = 1) and showed no consistent pattern between subject groups. Precipitin-negative sera from 30 volunteers with no previous pigeon exposure showed no IgG subclass reactivity with either the pigeon intestinal secretions or the isolated mucin and IgA antigens. These results show specific IgG2 and IgG3 subclass reactivity to pigeon intestinal mucin antigen in precipitin-positive sera from pigeon breeders. Further IgG3 subclass reactivity specific to pigeon mucin is strongly associated with sera from patients with the active pigeon breeders' lung disease.

Adolescent↗
PubMed1994

[Effect of somatostatin-14 in simple mechanical obstruction of the small intestine].

In order to investigate the properties of somatostatin-14 we studied an experimental model of simple mechanical and closed loop occlusion. Forty-eight New Zealand rabbits were assigned randomly to three groups of 16: group C (controls) was operated and treated with saline solution (4 cc/Kg/h); group A was operated and initially treated with saline solution and an equal dose of somatostatin-14 (3.5 micrograms/Kg/h; and group B was operated and treated in the same manner as group A, but later, 8 hours after the laparotomy. The animals were sacrificed 24 hours later; intestinal secretion was quantified, blood and intestinal fluid chemistries were performed and specimens of the intestine were prepared for histological examination. Descriptive statistical analysis of the results was performed with the ANOVA, a semi-quantitative test and the covariance test. Somatostatin-14 produced an improvement in the volume of intestinal secretion in the treated groups compared with the control group. The results were statistically significant in group B treated after an 8-hour delay: closed loop (ml): 6.40 +/- 1.12, 2.50 +/- 0.94, 1.85 +/- 0.83 and simple mechanical occlusion (ml): 175 +/- 33.05, 89.50 +/- 9.27, 57.18 +/- 21.23, p < 0.01 for groups C, A and B C, A and B respectively. Net secretion of Cl and Na ions was also improved, p < 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Effects of 5-hydroxytryptamine on the transintestinal electrical activity and cardiovascular function of fawn-hooded rats in-vivo.

Fawn-hooded rats, which have abnormal serotonergic function, were used to investigate the receptors involved in 5-hydroxytryptamine (5-HT)-induced intestinal secretion. The effects of 5-HT on secretion by the small intestine and proximal colon, monitored as increased transintestinal electrical activity, and on cardiovascular function, measured as changes in heart rate and blood pressure, were compared in fawn-hooded and Wistar rats. The maximum fall in heart rate induced by 5-HT (mediated by 5-HT3 receptors) was greater in fawn-hooded than in Wistar rats. ED50 values (the doses resulting in 50% of the maximum effect) for the 5-HT2-mediated increases in systolic pressure were lower for both 5-HT and 5-methoxytryptamine in the fawn-hooded group. The prolonged fall in diastolic pressure mediated by 5-HT1-like receptors was significantly attenuated in fawn-hooded rats, with the maximum responses to 5-HT, 5-methoxytryptamine and 6-hydroxyindalpine reduced to 21%, 42% and 28%, respectively, of the values obtained for Wistar rats. In fawn-hooded rats the small intestine was less sensitive to the effects of 5-HT (ED50 = 47 nmol kg(-1); ED50 for Wistar rats = 23 nmol kg(-1)) and the maximum colonic response to 5-methoxytryptamine was greater (7.0 mV compared with 4.3 mV in Wistar rats), but other indices did not differ for the two strains. The responses to 6-hydroxyindalpine were similar in fawn-hooded and Wistar rats. It is concluded that although the cardiovascular response of fawn-hooded rats to 5-HT challenge is very different from that of Wistar rats, this difference is not reflected in marked alterations in 5-HT-induced intestinal secretion. This is consistent with 5-HT stimulating secretion via the activation of several different receptor subtypes so that any changes in the receptor profile in fawn-hooded rats results in little alteration in the overall intestinal response.

Animals↗