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At least 775 records · Page 43Linked to original sources
PubMed1982

Serum and intestinal secretory IgA in alcoholic cirrhosis of the liver.

Serum and intestinal secretory IgA (sIgA) were investigated in control subjects and patients with alcoholic cirrhosis of the liver. Intestinal secretions were sampled by intraluminal perfusion with a balloon catheter. Monomeric IgA and sIgA were assayed by reversed radial immunodiffusion and nephelometry after separation by Ultrogel column filtration. High levels of serum sIgA were found only in patients with severe cirrhosis accompanied by jaundice. The intestinal rate of secretion of sIgA measured in these patients was significantly lower than that observed in either controls or the patients with compensated cirrhosis. Such an intestinal sIgA deficiency, which could be explained either by a fall in small intestinal immunocyte synthesis or by a defect in the transenterocyte transport system, could be partially responsible for the high incidence of intestinal infection observed in severe cirrhosis.

Albumins↗
PubMedDate not supplied

Secretion of nitrogenous compounds in the small intestine of pigs.

Secretion of nitrogenous compounds in the small intestine of pigs. Acta Physiol. Pol., 1979, 30 (2): 319--326. The study was performed on pigs weighting 50 to 75 kg with temporarily isolated loops of one of the three parts of the small intestine: proximal, middle and terminal. For measurement of intestinal secretion the isolated loops were perfused with N-free solutions and the effluent was collected and analyzed. On a protein diet, under conditions of an isotonic osmotic pressure of the solution, secretion of nitrogen compounds in the upper part was twice that in the lower part of the small intestine, 0.97 against 0.48 g N/m/24 h. A hypertonic pressure increased secretion of N into the intestinal lumen. On a protein-free diet secretion of nitrogen compounds was markedly decreased. Soluble N amounted to about 90% of total N and alpha-amino-N to 50 to 79% of soluble N. Free amino acids made up about 65% and protein 33% of the total alpha-amino-N. There was a large proportion of threonine, 6.0--6.3%, and lysine, 8.0--8.7% in the total amino acids secreted into the intestine.

Animals↗
PubMed2001

Studies on the antidiarrhoeal effect of dragon's blood from Croton urucurana.

The red sap obtained by slashing the bark of Croton urucurana Baill. (Euphorbiaceae), also known as dragon's blood, was screened for a possible antidiarrhoeal activity on castor oil-induced diarrhoea in rats, cholera toxin-induced intestinal secretion in mice and on small intestinal transit in mice. Dragon's blood at an oral dose of 600 mg/kg caused in marked inhibition of the diarrhoeal response following castor oil administration as well as the intestinal fluid accumulation promoted by cholera toxin. At a similar dose the red sap significantly inhibited the small intestinal transit which was, however, found to be independent of the opioid mechanism. These results suggest a potential usefulness of the red sap from Croton urucurana Baill. in the control of secretory diarrhoea associated pathologies.

Animals↗
PubMed1997

Interruption of Escherichia coli heat-stable enterotoxin-induced guanylyl cyclase signaling and associated chloride current in human intestinal cells by 2-chloroadenosine.

Diarrhea induced by Escherichia coli heat-stable enterotoxin (STa) is mediated by a receptor guanylyl cyclase cascade. The present study establishes that an intracellular nucleotide-dependent pathway disrupts toxin-induced cyclic GMP (cGMP) production and the associated chloride (Cl-) flux that underlie intestinal secretion. Incubation of Caco 2 human intestinal epithelial cells with the nucleoside analog 2-chloroadenosine (2ClAdo) resulted in a concentration- and time-dependent inhibition of toxin-induced cGMP production. Inhibition of cGMP production correlated with the metabolic conversion of 2ClAdo to 2-chloroadenosine triphosphate. The effect of 2ClAdo did not reflect activation of adenosine receptors, inhibition of adenosine deaminase, or modification of the binding or distribution of STa receptors. Guanylyl cyclase activity in membranes prepared from 2ClAdo-treated cells was inhibited, in contrast to membranes from cells not exposed to 2ClAdo, demonstrating that inhibition of guanylyl cyclase C (GCC) was mediated by a noncompetitive mechanism. Treatment of Caco 2 cells with 2ClAdo also prevented STa-induced Cl- current. Application of 8-bromo-cGMP, the cell-permeant analog of cGMP, to 2ClAdo-treated cells reconstituted the Cl- current, demonstrating that inhibition of Cl- flux reflected selective disruption of ligand stimulation of GCC rather than the chloride channel itself. Thus, the components required for adenine nucleotide inhibition of GCC signaling are present in intact mammalian cells, establishing the utility of this pathway to elucidate the mechanisms regulating ST-dependent guanylyl cyclase signaling and intestinal fluid homeostasis. In addition, these data suggest that the adenine nucleotide inhibitory pathway may be a novel target to develop antisecretory therapy for enterotoxigenic diarrhea.

2-Chloroadenosine↗
PubMed1992

Human colonic epithelial cells, HT29/C1, treated with crude Bacteroides fragilis enterotoxin dramatically alter their morphology.

Bacteroides fragilis has been associated with causation of diarrheal disease in livestock and humans. To date, conventional tissue culture and animal assays used to detect the biologic activity of bacterial enterotoxins have failed with enterotoxigenic B. fragilis. Although enterotoxigenic B. fragilis stimulates intestinal secretion in lamb and calf ligated intestinal loops, infant rabbits, and adult rabbits with ligated ceca, these animal systems are costly and complicated, which limits their usefulness for identification of enterotoxigenic B. fragilis strains. Using the cloned human colonic-epithelial-cell line HT29/C1, we have developed an in vitro assay that is 89% sensitive and 100% specific in detecting enterotoxigenic B. fragilis strains as defined by the lamb ligated-intestinal-loop assay. Subconfluent HT29/C1 cells treated with concentrated bacterium-free culture supernatants of enterotoxigenic B. fragilis strains develop specific and striking morphologic changes including loss of cell-to-cell attachments, rounding, swelling, and, in some cases, pyknosis. These morphologic changes are initially visible at 1 h after treatment and progress over at least the first 24 h. This tissue culture assay should prove useful in epidemiologic studies of enterotoxigenic B. fragilis and may facilitate basic studies to identify the B. fragilis toxin(s) and its mechanism of action.

Bacterial Toxins↗
PubMed2003

[Effects of octreotide on small bowel obstructions in rats].

BACKGROUNDS/AIMS: Gastrointestinal decompression by nasogastric or intestinal tubes developed in 1930s has been the only treatment modality for inoperable intestinal obstruction. We hypothesized that the octreotide, a potent inhibitor of intestinal secretion, has a therapeutic potential in intestinal obstruction. METHODS: Forty Sprague-Dawley rats were randomly assigned to four groups. The rats were subjected to complete or partial ileal obstruction. The treated rats received octreotide (100 microgram/kg) while the controls received the same quantity of saline every 12 hours for 24 or 48 hours. After 24 or 48 hours, the volumes of the small bowel contents were measured. The volumes of supernatant and the concentrations of electrolytes in the small bowel contents after centrifugation were also analyzed. The ileal segments proximal to obstruction were harvested, fixed, and stained, and the pathological changes were evaluated with mucosal damage scores. RESULTS: There were no statistical differences in the volume and the electrolyte composition of intestinal fluid among the 4 groups. In the 48 hour complete obstruction group, the octreotide-treated rats showed statistically lower mucosal damage scores than the control rats (p<0.05). CONCLUSIONS: Octreotide exerts mucosal protecting effect on the complete intestinal obstruction rat model.

Animals↗
PubMed1993

Guanylin stimulation of Cl- secretion in human intestinal T84 cells via cyclic guanosine monophosphate.

Intestinal salt and fluid secretion is stimulated by Escherichia coli heat-stable enterotoxins (ST) through activation of a membrane guanylate cyclase found in the intestine. Guanylin is an endogenous intestinal peptide that has structural similarity to the bacterial peptides. Synthetic preparations of guanylin or E. coli ST 5-17 stimulated Cl- secretion in T84 cells cultured on semipermeable membranes as measured by increases in short circuit current (Isc). The guanylin/ST receptors appeared to be on the apical surface of T84 cells, since addition of guanylin to the apical, but not basolateral, reservoir stimulated Isc. Bumetanide added to the basolateral side effectively inhibited the Isc responses of T84 cells to either guanylin or ST 5-17. Guanylin appeared to be about one-tenth as potent as ST in stimulating transepithelial Cl- secretion. Guanylin and E. coli ST 5-17 both caused massive (> 1,000-fold) increases in cGMP levels in T84 cells, but guanylin was less potent than ST. Both peptides fully inhibited the binding of 125I-ST to receptor sites on intact T84 cells. The radioligand binding data obtained with guanylin or ST 5-17 best fit a model predicting two receptors with different affinity for these ligands. The Ki values for guanylin were 19 +/- 5 nM and 1.3 +/- 0.5 microM, whereas the Ki values for ST 5-17 were 78 +/- 38 pM and 4.9 +/- 1.4 nM. We conclude that guanylin stimulated Cl- secretion via the second messenger, cGMP, in T84 human colon cells. At least two guanylin receptors with different affinities for these ligands may exist in the cultured T84 cells. It may be postulated that guanylin is an endogenous hormone that controls intestinal Cl- secretion by a paracrine mechanism via cGMP and that E. coli ST stimulates Cl- secretion by virtue of an opportunistic mechanism through activation of guanylin receptors.

Bacterial Toxins↗
PubMed1979

[Bile acids in duodenal juice of infants and children. Normal values, lognormal distribution, and age-dependence of the total quantity and the distribution of bile acids (author's transl)].

43 gastroenterologically healthy infants and children were investigated during the basic secretion period and after the injection of secretin/pankreozymin in order to establish the total quantity and also the distribution of the secreted bile acids. The total concentration and quantity were enzymatically determined while column and thin-layer chromatography were utilized to separate the bile into 34 different bile acids. Quantified results for bile salts were read directly from the thin-layer sheet with the help of a Chromatogram-Spectrophotometer Zeiss KM 3. While the total quantity of bile acids was found to be independent of age, the composition of bile changed during the first years of life. The percentage of cholic acids decreased from 50% in infants to 35% in older children. At the same time, deoxycholic acids went up from 3% to 13%, and chenodeoxycholic acids increased by 5%. The percentage of glycine and taurine conjugated bile salts, however, remained constant after to the second month of life, the former at 58% and the latter at 35%. In comparison, rather small amounts of unconjugated acids and sulfates were secreted, 0,5% and 6% respectively. The latter were distributed in the same sequence as the nonsulfated bile acids. Lithocholic acids (2,6%) and ursodeoxycholic acids (4,3%) were regularly present in the intestinal secretion.

Age Factors↗
PubMed1978

Some comparative properties and localization of porcine jejunal adenylate cyclase.

Cholera toxin is thought to cause intestinal secretion by activating adenylate cyclase and increasing intracellular 3',5'-cyclic AMP concentrations in intestinal mucosa. Cholera toxin causes profuse secretion of fluid into ligated intestinal loops of both pigs and rabbits, but cholera toxin-induced increases in 3',5'-cyclic AMP concentration are much lower in the pig than in the rabbit. Porcine jejunal adenylate cyclase was examined for unusual properties which might account for a lack of 3'-5'-cyclic AMP accumulation after treatment with cholera toxin. The divalent cation requirements, the pH optimum, and the stimulation by fluoride ion were unremarkable. The Km for ATP was 0.11 mM with negative cooperativity indicated by a Hill coefficient of 0.83. Triton X-100 was inhibitory and guanosine diphosphate methylenephosphate stimulated enzyme activity. Adenylate cyclase activity was highest in the basal and lateral membrane fractions of jejunal mucosa and relatively low in brush-border preparations. Pretreatment of pig jejunum with cholera toxin caused a 30-40% activation of the crude and of the partly purified enzyme. A relatively low activation of adenylase cyclase in pig jejunal mucosa, compared with rabbit, may account for the absence of 3',5'-cyclic AMP accumulation after cholera-toxin treatment in the pig.

Adenylyl Cyclases↗
PubMed2006

Luminal glucose sensing in the rat intestine has characteristics of a sodium-glucose cotransporter.

The presence of glucose in the intestinal lumen elicits a number of changes in gastrointestinal function, including inhibition of gastric emptying and food intake and stimulation of pancreatic and intestinal secretion. The present study tested the hypothesis that Na(+)-glucose cotransporter (SGLT)-3, a member of the SGLT family of transport proteins, is involved in detection of luminal glucose in the intestine. Gastric emptying, measured in awake rats, was significantly inhibited by perfusion of the intestine with glucose (60 and 90 mg); this effect was mimicked by alpha-methyl glucose (nonmetabolizable substrate of SGLT-1 and -3) but not 2-deoxy-d-glucose (substrate for GLUT-2) or isoosmotic mannitol. Gastric motility and intestinal fluid secretion, measured in anesthetised rats, were significantly inhibited and stimulated, respectively, by duodenal glucose but not galactose, which has a much lower affinity for SGLT-3 than glucose. Duodenal glucose but not galactose stimulated the release of 5-HT into mesenteric lymph and stimulated the discharge of duodenal vagal afferent fibers. mRNA for SGLT-3 was identified in the duodenal mucosa. Together these data suggest that detection of glucose in the intestine may involve SGLT-3, possibly expressed by enterochromaffin cells in the intestinal mucosa, and release of 5-HT.

Animals↗
PubMed1975

Jejunal fluid and electrolyte secretion in carcinoid syndrome.

To evaluate the pathogenesis of the diarrhea of carcinoid syndrome, triple-lumen jejunal-perfusion studies were performed in three patients with carcinoid syndrome and diarrhea and eleven control subjects. In contrast to the net absorption observed in the control subjects during perfusion with an isotonic mannitol-saline solution, net secretion occurred in two of the three carcinoid-syndrome patients. Glucose absorption and glucose-stimulated fluid absorption were normal in the carcinoid-syndrome patients. Methysergide controlled the diarrhea and in one patient net absorption was observed during methysergide therapy. These studies suggest that intestinal secretion may be one of the pathogenetic factors responsible for the diarrhea of carcinoid syndrome and provide additional evidence of the importance of intestinal electrolyte secretion in the genesis of many diarrheal states.

Aged↗
PubMed1974

Luminal distension as a possible consequence of experimental intestinal perfusion.

In an experimental jejunal perfusion study, distress in healthy subjects occurred during eight out of 16 perfusions in which intestinal secretion was provoked. Calculation demonstrates the volumetric consequences of inadequate recovery of secretory perfusates, and analysis of the perfusion studies shows that distress was significantly associated with poor recovery of the perfusate. These observations are pertinent to increasing interest in the phenomenon of intestinal fluid secretion.

Carbon Radioisotopes↗
PubMed1982

Effects of nitrogen, phosphorus, and caffeine on calcium balance in women.

The effects of different levels of nitrogen, phosphorus, and caffeine intake on calcium balance and on certain of its components were assessed in 170 studies in normal middle-aged, but still premenopausal women. Statistically significant negative associations with calcium balance were found for nitrogen and for caffeine, but no effect could be found for phosphorus. Higher nitrogen intakes were associated with proportionately higher levels of urinary calcium; higher phosphorus intake was associated with slightly lower levels of urinary calcium but also with slightly more intestinal secretion of calcium. Since these two effects were opposite in direction, there was no net association of different phosphorus intakes with calcium balance. Caffeine intake was associated with higher levels of both urinary calcium and intestinal calcium secretion. None of the three intake variables was associated with differences in calcium absorption efficiency. Both the nitrogen and the caffeine effects were proportional to intake. The magnitude of the effects observed was such that a 50% increase in intake of nitrogen above the group mean intake value would be predicted to result in calcium balance shift of -0.032 gm/day. For caffeine, the corresponding calcium balance shift would be predicted to be -0.006 gm/day.

Adult↗
PubMed1978

The effect of oral immunisation with heat stable Escherichia coli antigens on the sensitivity of pigs to enterotoxins.

It was found that oral immunisation of pigs with heat stable Escherichia coli antigens resulted in a decrease in the sensitivity of the porcine intestine to both the heat stable (ST) and the heat labile (LT) and the heat labile (LT) form of the enterotoxin produced by enterotoxigenic strains. Antitoxic factors capable of neutralising LT, but not ST, could be passively transferred in the intestinal secretions of the immunised animals.

Administration, Oral↗
PubMed2002

Microsomal triglyceride transfer protein (MTP) inhibitors: discovery of clinically active inhibitors using high-throughput screening and parallel synthesis paradigms.

The inhibition of microsomal triglyceride transfer protein (MTP) blocks the hepatic secretion of very low density lipoproteins (VLDL) and the intestinal secretion of chylomicrons. Consequently, this mechanism provides a highly efficacious pharmacological target for the lowering of low density lipoprotein (LDL) cholesterol and reduction of postprandial lipemia. The combination of these effects could afford unprecedented benefit in the treatment of atherosclerosis and consequent cardiovascular disease. The promise of this therapeutic target has attracted widespread interest in the pharmaceutical industry. Independent efforts have yielded strikingly similar series of lipophilic amide inhibitors. The way in which the evolutionary paths of distinct inhibitor series have tended to converge through the course of robotics-assisted synthesis efforts is illustrated with candidates from Bristol-Myers Squibb and Pfizer. Hanging in the balance with the exceptional potency of the compounds presented are the potential adverse effects due to blockage of intestinal fat absorption and hepatic lipid secretion. Finding a degree of efficacy that can be safely tolerated defines the dilemma surrounding the advancement of these compounds to clinical practice.

Animals↗