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 1,621 records · Page 90Linked to original sources
PubMed1989

Intestinal alkaline phosphatase is secreted bidirectionally from villous enterocytes.

A fraction of intestinal alkaline phosphatase (IAP) is secreted into blood. To study this process, enzyme secretion was examined in a fetal (IRD-98) and a differentiated (Caco-2) intestinal cell line. Tissue-unspecific alkaline phosphatase (AP) activity in the IRD-98 cells increased 20-fold after addition of 1.5 mM sodium butyrate and 40 mM NaCl, but no AP activity was secreted into the medium. In contrast, newly synthesized IAP in Caco-2 cells was secreted into the medium. AP secretion increased with time and was inhibited by monensin. Medium AP was still partially bound to membranes as assessed by Triton X-114 phase separation and could be released by the addition of serum. Analysis by sodium dodecyl sulfate polyacrylamide gels and by isoelectric focussing showed that secreted AP gave a pattern similar to that of the AP released from membranes by phospholipase D treatment. When Caco-2 cells were grown on filters, AP activity was found in both basolateral (75%) and luminal (25%) media. These data demonstrate that the secretion of a particulate AP with extracellular release from the membrane can account for the appearance of the intestinal isozyme in both the serum and the lumen.

Adenocarcinoma↗
PubMed2000

Secretion of microbicidal alpha-defensins by intestinal Paneth cells in response to bacteria.

Paneth cells in mouse small intestinal crypts secrete granules rich in microbicidal peptides when exposed to bacteria or bacterial antigens. The dose-dependent secretion occurs within minutes and alpha-defensins, or cryptdins, account for 70% of the released bactericidal peptide activity. Gram-negative bacteria, Gram-positive bacteria, lipopolysaccharide, lipoteichoic acid, lipid A and muramyl dipeptide elicit cryptdin secretion. Live fungi and protozoa, however, do not stimulate degranulation. Thus intestinal Paneth cells contribute to innate immunity by sensing bacteria and bacterial antigens, and discharge microbicidal peptides at effective concentrations accordingly.

Animals↗
PubMed1997

Effect of ganglionic blocking compounds on in-vivo fluid secretion in the rat small intestine.

It is well-known that enteric, secreto-motor nerves mediate cholera toxin-induced fluid secretion in the rat small intestine. This notion is, in part, derived from experiments on anaesthetized animals in which the response to cholera toxin was antagonized by the ganglionic nicotinic receptor antagonist, hexamethonium. In the current study, such anti-secretory action of ganglionic blocking compounds was analysed in an experiment designed to minimize any possible negative effect of general anaesthesia on intestinal secretion. Rats were anaesthetized with ether for 5-10 min, during which time a jejunal loop (10-12 cm) was constructed. The loop was challenged with one of the secretagogues, cholera toxin, prostaglandin E1 (PGE1) or okadaic acid. Saline (control) or either of the ganglionic blockers, hexamethonium and chlorisondamine, was administered intravenously. The rats were killed 5 h (cholera toxin) or 1.5 h (PGE1 and okadaic acid) after challenge, and the amount of fluid accumulated in the loops was determined. Cholera toxin-induced secretion was unchanged by hexamethonium but reduced by approximately 80% by chlorisondamine. The difference in effect between the two blockers might relate to the duration of ganglionic blockade. Chlorisondamine blocked secretion induced by either PGE1 or okadaic acid by approximately 60%. It is suggested that the anti-secretory effect of ganglionic blocking compounds might be a result of blockade of secreto-motor nerves but other mechanisms, for example interference with haemodynamic factors, cannot be ruled out.

Alprostadil↗
PubMed1978

Inhibition by morphine of prostaglandin-stimulated fluid secretion in rat jejunum.

1 Anesthetized rats (225 to 300 g) were used to study the inhibitory effect of morphine on fluid secreted by the small intestine. 2 Small intestinal fluid secretion was stimulated by infusion of prostaglandin E1 (PGE1) into the aortic arch, the jejunum being more sensitive than the ileum. Infusion of PGE1 2 microgram/min caused maximal net fluid secretion in the jejunum but inhibited net fluid absorption in the ileum. 3 Morphine caused a dose-related inhibition of maximal PGE1-stimulated fluid secretion in the jejunum. At the higher doses of morphine used (5 to 20 mg/kg) the fluid transporting function of the jejunum was restored almost to normal net absorption. 4 The inhibitory effect of morphine on PGE1-stimulated fluid secretion was antagonized by naloxone. Naloxone caused a parallel shift to the right of the dose-response curve for morphine. 5 Two other narcotic analgesics were assayed relative to morphine and their descending order of potency was oxymorphone greater than morphine greater than pethidine. 6 It is suggested that the antisecretory effect of morphine in the small intestine may contribute to its efficacy as an anti-diarrhoeal drug. Further studies on the rat jejunum may show it to be a useful model for predicting narcotic drug activity and as such, may give some insight into the mechanisms of action of these drugs.

Animals↗
PubMed1986

Increased secretion of potassium in the rectum of humans with chronic renal failure.

Previous studies have shown that the intestinal excretion of potassium increases in patients with renal failure and serves to guard against severe potassium retention. It is not known, however, whether the rise in intestinal potassium excretion occurs because of an increase in intestinal potassium secretion or a reduction in potassium absorption. Therefore, studies were performed to evaluate the rate of potassium secretion in the human rectum of controls and subjects with renal insufficiency, using a dialysis bag technique. The results demonstrate that net potassium secretion was increased in subjects with renal failure (-5.2 +/- 0.9 microEq X min-1) compared with the control value of -2.0 +/- 0.4 microEq (P less than .05). This change in intestinal secretion of potassium was shown to be independent of the passive effects of plasma potassium. The rise in potassium secretion, however, correlated directly with an increase in transepithelial potential difference (lumen-negative). Although plasma aldosterone levels were higher in patients than in controls, the scatter of data precludes an assessment of the role of aldosterone in the mechanism of the rise in potassium secretion. These data suggest that augmented intestinal potassium excretion in patients with chronic renal insufficiency is caused by increased net potassium secretion in the large intestine, and highlight the role of the intestine in maintaining potassium balance.

Aldosterone↗
PubMed2002

Multiple pathways for fluoroquinolone secretion by human intestinal epithelial (Caco-2) cells.

1. Human intestinal epithelial Caco-2 cells, T84 cells, and MDCKII cells transfected with human MDR1, were used to investigate the mechanistic basis of transintestinal fluoroquinolone secretion. 2. The fluoroquinolone grepafloxacin was secreted across Caco-2 monolayers by a saturable process (V(max)=16.9 +/- 3.4 nmol.cm(-2).h(-1)). Net secretion was reduced by 2-deoxyglucose/azide treatment to reduce intracellular ATP. 3. Grepafloxacin inhibited [(14)C]-ciprofloxacin (100 microM) secretion across Caco-2 monolayers (K(0.5)=0.8 mM), and concurrently increased the cellular accumulation of ciprofloxacin from the basal medium, indicating inhibition of export across the apical membrane. 4. The unconjugated bile acid, cholic acid, was secreted across Caco-2 monolayers, and this secretion was sensitive to inhibition by the MRP-selective inhibitor MK-571, suggesting MRP2 involvement. Secretion of cholic acid (10 microM) across the apical membrane was also inhibited by grepafloxacin (K(0.5)=0.3 mM), but not by ciprofloxacin. 5. In MDCKII-MDR1 monolayers, net secretion of grepafloxacin was increased by 3.5 fold compared with untransfected controls. Neither ciprofloxacin nor cholic acid showed net secretion in either MDCKII or MDCKII-MDR1 monolayers, showing that in contrast to grepafloxacin, neither are substrates for MDR1. 6. In T84 monolayers, which express MDR1 but not MRP2, neither ciprofloxacin nor cholic acid was secreted, whilst the V(max) for grepafloxacin secretion was lower than in Caco-2 cells, which express both MDR1 and MRP2. 7. In conclusion, the transepithelial secretion of grepafloxacin is mediated by both MRP2 and MDR1, whereas ciprofloxacin is a substrate for neither. Grepafloxacin also competes for the ciprofloxacin-sensitive pathway, which remains to be elucidated.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1980

Entero-oxyntin: a stimulant of gastric acid secretion extracted from porcine intestine.

A peptide that further augments gastric acid secretion in cats, maximally stimulated by pentagastrin, was identified in porcine upper small intestine. Since the peptide stimulated basal and maximally pentagastrin-stimulated acid secretion to the same extent, it appears to act on a receptor different from the gastrin receptor and thus may be designated entero-oxyntin, a mediator of the intestinal phase of acid secretion.

Animals↗
PubMed1993

Transforming growth factor-beta and IL-1 beta act in synergy to enhance IL-6 secretion by the intestinal epithelial cell line, IEC-6.

Intestinal epithelial cells are a potentially important source for a number of cytokines that may modulate the immune response at the intestinal mucosa. We have recently begun to study the mechanisms that regulate IL-6 production by intestinal epithelial cells using the nontransformed crypt-like rat intestinal epithelial cell line IEC-6 as a model. Culture of the IEC-6 cells with human rIL-1 beta resulted in an enhanced secretion of IL-6 by the cells. RT-PCR analysis of IL-1 beta-treated cells showed an enhanced level of IL-6 mRNA at 4 h, suggesting that IL-1 beta enhanced IL-6 gene expression. In a previous study, transforming growth factor-beta (TGF-beta 1) was also found to enhance IL-6 secretion by the IEC-6 cells and because both IL-1 beta and TGF-beta may be present in inflamed mucosal tissue, the effect of adding both cytokines together was next investigated. Culture of the IEC-6 cells with both TGF-beta 1 and IL-1 beta resulted in a synergistic enhancement of IL-6 secretion that was seen even at high levels of both TGF-beta and IL-1 beta. IL-6 mRNA levels from cells treated with both TGF-beta 1 and IL-1 beta were also determined to be enhanced when compared to that of cells treated with IL-1 beta or TGF-beta 1 only, as determined by RT-PCR analysis. Pretreatment of the IEC-6 cells with TGF-beta 1 for 2 or 3 days before addition of the IL-1 beta induced the IEC-6 cells to differentiate and become more sensitive to stimulation by IL-1 beta. Subsequent experiments determined that TGF-beta enhanced the capacity of the IEC-6 cells to bind labeled IL-1 beta indicating that TGF-beta may have enhanced the expression of IL-1 receptors on the cells. These results suggest that the intestinal epithelial cell may represent an important source of IL-6 in inflammatory responses at the intestinal mucosa and that TGF-beta could potentiate this function.

Animals↗
PubMed1984

Vasoactive intestinal polypeptide (VIP) in the pig pancreas: role of VIPergic nerves in control of fluid and bicarbonate secretion.

Vasoactive intestinal polypeptide (VIP) in the pig pancreas is localized to nerves, many of which travel along the pancreatic ducts. VIP stimulates pancreatic fluid and bicarbonate secretion like secretin. Electrical vagal stimulation in the pig causes an atropine-resistant profuse secretion of bicarbonate-rich pancreatic juice. In an isolated perfused preparation of the pig pancreas with intact vagal nerve supply, electrical vagal stimulation caused an atropine-resistant release of VIP, which accurately parallelled the exocrine secretion of juice and bicarbonate. Perfusion of the pancreas with a potent VIP-antiserum inhibited the effect of vagal stimulation on the exocrine secretion. It is concluded, that VIP is responsible for (at least part of) the neurally controlled fluid and bicarbonate secretion from the pig pancreas.

Animals↗
PubMed2006

Vasoactive intestinal peptide stimulates mucus secretion, but nitric oxide has no effect on mucus secretion in the ferret trachea.

Vasoactive intestinal peptide (VIP) and nitric oxide (NO) are neurotransmitters involved in the regulation of bronchial and pulmonary vascular tone. Published studies of the effects of VIP on airway mucus secretion have yielded conflicting results. The purpose of this study was to determine the effect of VIP on mucus secretion in the ferret trachea and if this effect was influenced by NO. We used a sandwich enzyme-linked lectin assay to measure mucin secretion and a turbidimetric assay to measure lysozyme (serous cell) secretion from ferret tracheal segments. VIP (10(-7) M) increased mucin secretion over 2 h. VIP (10(-9) to 10(-5) M) stimulated mucin secretion in a dose-dependent fashion. VIP-induced mucin secretion was partially blocked by a VIP receptor antagonist (a chimeric VIP-pituitary adenylate cyclase-activating peptide analog, VIP receptor antagonist) at a 10-fold excess concentration. At all concentrations tested, neither NG-nitro-L-arginine methyl ester, an inhibitor of NO synthase, nor S-nitroso-N-acetyl-penicillamine, an NO donor, had any significant effect on constitutive or VIP-induced mucus secretion. We conclude that VIP-stimulated mucin and lysozyme secretion was both time dependent and dose dependent and that NO neither stimulates nor inhibits mucus secretion in the ferret trachea.

Animals↗
PubMed1988

Aging-associated changes in murine intestinal immunoglobulin A and M secretions.

The aging effect on the quantity of intestinal IgA and IgM class-specific immunoglobulins secreted and the quality of intraluminal intestinal IgA was studied in 5- to 6-month-old and 24- to 28-month-old male BALB/c mice. The level of IgA increased in the intestinal juice from the aged mice, while the IgM level remained unchanged. These alterations were similar to those found in serum, but the effect of age on serum IgA was profound, almost a threefold increase, in contrast to an increase of just under 35% in intestinal secretions. The ratio of dimeric to total IgA in the small intestine decreased in the older mice, though that of serum was unchanged. In contrast, the total amounts of dimeric IgA in the small intestinal lavage fluid did not change between the two age groups, while the dimeric IgA in serum in older mice were 4.5 times as high as those of young mice. The binding of purified intestinal dimeric IgA to antigens from normal habitant enteric bacteria (gamma streptococci and Enterobacter agglomerans) declined in the old mice. In the immunochemical studies, using SDS-PAGE and isoelectric focusing, the purified intestinal IgA from the young and old mice showed no major differences. Thus, the findings in aged small intestinal perfusates that the increased content of intraluminal IgA is due to an increased monomeric IgA, but not to a reduced dimeric IgA, which remains unchanged, and that the binding capacity of the dimeric IgA to the bacterial antigens is diminished, suggest that the level of the natural secretory IgA antibody is decreased. These altered quantitative and functional features of intraluminal intestinal IgA observed in the aged mice appear to be due to the complex heterogeneous effects of senescence on gut-associated lymphoid tissues, and may contribute to age-related impairment in gut humoral immune function.

Aging↗
PubMed1976

A fraction isolated from porcine upper small intestine stimulating pepsin secretion in the cat.

The preliminary purification of a material, apparently distinct from any hitherto isolated gastrointestinal hormone, with pepsin release stimulating activity in the cat is described. This material has shown no inhibitory effect on pentagastrin-stimulated secretion of acid, no effect of its own on gastric acid secretion and antral motility, and only a weak stimulatory effect on pancreatic secretion of bicarbonate.

Animals↗
PubMed2000

Zinc transport and metallothionein secretion in the intestinal human cell line Caco-2.

Caco-2, a human cell line, displays several biochemical and morphological characteristics of differentiated enterocytes. Among these is the ability to transport zinc from the apical to the basal compartment. This process was enhanced following exposure by the apical compartment to increasing concentrations of the metal. High pressure liquid chromatography fractionation of the media obtained from cells labeled with radioactive zinc showed that metallothioneins (MTs), small metal-binding, cysteine-rich proteins), were present in the apical and basal media of controls as well as in cells grown in the presence of high concentrations of zinc. Following exposure to the metal, the levels of Zn-MTs in the apical medium increased, while in the basal compartment the greatest part of zinc appeared in a free form with minor changes in the levels of basal MTs. Metabolic labeling experiments with radioactive cysteine confirmed the apical secretion of MTs. A stable transfectant clone of Caco-2 cells (CL11) was selected for its ability to express constitutively high levels of the mouse metallothionein I protein. This cell line showed an enhanced transport of the metal following exposure to high concentrations of zinc and a constitutive secretion of the mouse metallothionein I protein in the apical compartment. Together, these findings strongly support the hypothesis of a functional role between the biosynthesis and secretion of MTs and the transport of zinc in intestinal cells.

Animals↗