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At least 649 records · Page 36Linked to original sources
PubMed1995

Inhibition of intestinal chloride secretion by proanthocyanidins from Guazuma ulmifolia.

The antisecretory activity of Guazuma ulmifolia bark was examined in rabbit distal colon mounted in an Ussing chamber. Chloride secretion was stimulated by cholera toxin and prostaglandin E2 (PGE2). Guazuma ulmifolia extract (GUE) completely inhibited cholera toxin-induced secretion if the extract was added to the mucosal bath prior to the toxin. Adding the extract after administration of the toxin had no effect on secretion. GUE did not inhibit PGE2-induced chloride secretion. These results indicate an indirect antisecretory mechanism. SDS-PAGE analysis of cholera toxin treated with GUE confirmed this presumption. GUE specifically interacted with the A subunit of the toxin. Preliminary phytochemical examinations showed that the most active fraction contains procyanidins with a degree of polymerisation higher than 8.

Animals↗
PubMed1990

Oral immunization of mice with a live recombinant Yersinia enterocolitica O:9 strain that produces the cholera toxin B subunit.

The 70-kilobase pYV plasmid of Yersinia enterocolitica encodes a set of proteins called Yops that are produced during infection. To use Y. enterocolitica as a live carrier to present the cholera toxin B (CT-B) subunit to the immune system, we constructed an operon fusion between ctxB and the yop51 gene. This operon fusion was either cloned on an RSF1010-derived plasmid or integrated into the pYV plasmid itself. In Y. enterocolitica, both constructions directed the synthesis of free CT-B only under conditions of Yops production, i.e., at 37 degrees C in a medium deprived of Ca2+. Bacteria containing both types of recombinant plasmids were given orally to mice. A serum antibody response against CT-B was detected in both cases. A secretory immunoglobulin A activity specific to CT-B was also observed in the intestinal secretions. According to immunoblot analysis, the serum antibody response was only directed against the polymeric form of the B subunit. The ctxB gene was also inserted in frame within yop51, giving a chimeric Yop51-CT-B protein that was secreted into the surrounding medium. In this case, however, no antibody response was observed after oral inoculation of mice. This lack of response probably results from the inability of the hybrid protein to assemble into the polymeric form of the B subunit.

Animals↗
PubMed1995

Effect of gastric acid secretion on intestinal phosphate and calcium absorption in normal subjects.

BACKGROUND: Phosphate-induced hyperparathyroidism still represents an intriguing problem in dialysis patients. Postprandial hyperphosphataemia is considered to be the main stimulus to parathyroid hyperfunction, and therefore many efforts have focused on the use of phosphate binders to prevent phosphate absorption. METHODS: We investigated whether the pH-mediated gastric ionization of calcium phosphate dietary salts is necessary for its intestinal absorption. In eight normal subjects we measured 24-h urinary calcium phosphate excretion and the postprandial blood calcium phosphate profile after a meal containing 1 g of calcium and 2 g of phosphate salts in a crossover placebo-omeprazole study. On two occasions the subjects received either placebo or omeprazole 60 mg/day 2 days before and during the day test. RESULTS: Serum gastrin levels were measured as an indicator of achlorhydria and were 13.7 +/- 1 pg/ml after placebo and 30.4 +/- 4.7 after omeprazole (P < 0.003). Postprandial plasma phosphate profiles were not significantly different between the two studies (+36 +/- 8% after placebo and +24 +/- 8% after omeprazole, NS), while plasma calcium increased by +6.1 +/- 1% after placebo and decreased by -4.2 +/- 0.7% after omeprazole (P < 0.01). The 24-h urinary phosphate excretion was 1068 +/- 85 mg after placebo and 773 +/- 55 after omeprazole (P < 0.002), while the 24-h urinary calcium excretion was 360 +/- 21 after placebo and 238 +/- 15 after omeprazole (P < 0.0001). A negative relationship was observed between absolute changes in plasma gastrin and those in urinary calcium (P < 0.009) and phosphate (P < 0.05). CONCLUSIONS: The inhibition of gastric acid secretion by omeprazole significantly reduces both urinary phosphate and calcium excretion after an oral load. The behaviour of the postprandial calcium-phosphate plasma profile suggests that gastric acid inhibition is more effective in reducing calcium rather than phosphate dietary salts absorption in normal subjects.

Absorption↗
PubMed1980

Control of guinea pig intestinal electrolyte secretion by a delta-opiate receptor.

The effects of opioids on transepithelial potential difference and short-circuit current across guinea pig ileum stripped of one muscle layer were measured in vitro in Ussing chambers. Opioid peptides such as [DAla2, DLeu5]enkephalin and [DAla2, DMet5]enkephalin, which are primarily agonists at delta-opiate receptors, were able to reduce transepithelial potential difference and short-circuit current at concentrations as low as 1 nM. The narcotic drug etorphine was also very potent in reducing short-circuit current, but fentanyl and morphine, which are primarily agonists at mu-opiate receptors, were almost completely ineffective. Ketocyclazocine was relatively ineffective, and beta-endorphin had intermediate potency. All opioid effects could be reversed by the opiate antagonist naloxone. Somatostatin also reduced short-circuit current, but its effect was not reduced by naloxone. Chloride flux measurements indicated that the effect of etorphine on short-circuit current is associated with an enhancement of active Cl- absorption. The relative effects of opioids in this system suggest that their actions are being mediated by a specific delta-opiate receptor. In contrast, opioid effects on guinea pig intestinal smooth muscle seem to be primarily mediated by a mu-opiate receptor.

Animals↗
PubMed1994

Complementation of apolipoprotein B mRNA editing by human liver accompanied by secretion of apolipoprotein B48.

Mammalian small intestine secretes a truncated apolipoprotein B (apoB48) species as a result of tissue-specific post-transcriptional RNA editing. The human liver, by contrast, contains only unedited apoB mRNA and secretes only apoB100. We have recently isolated a cDNA clone from rat small intestine which encodes an apoB mRNA editing protein, REPR (Teng, B., Burant, C.F., and Davidson, N.O. (1993) Science 260, 1816-1819). The current study demonstrates that homogenates of Xenopus oocytes expressing REPR confer editing ability upon S100 extracts prepared from human liver when tested on a synthetic apoB RNA template in vitro. Transfection of REPR into HepG2 cells resulted in editing of endogenous apoB mRNA and the appearance of an apoB48-like protein in the media. Extracts prepared from these transfected cells edit mammalian apoB RNA templates when incubated alone and with enhanced efficiency in the presence of chicken intestinal S100 extracts. The results suggest that human liver expresses factor(s) which are critical to apoB mRNA editing and which allow functional complementation of REPR in vivo.

APOBEC-1 Deaminase↗
PubMed2005

Antisecretory factor modulates GABAergic transmission in the rat hippocampus.

Antisecretory Factor (AF) is a protein that has been implicated in the suppression of intestinal hypersecretion and inflammation. Intestinal secretion and inflammation are partly under local and central neural control raising the possibility that AF might exert its action by modulating neural signaling. In the present study we have investigated whether AF can modulate central synaptic transmission. Evoked glutamatergic and GABAergic synaptic transmissions were investigated using extracellular recordings in the CA1 region of hippocampal slices from adult rats. AF (0.5 microg/ml) suppressed GABA(A)-mediated synaptic transmission by about 40% while having no effect on glutamatergic transmission. Per oral administration of cholera toxin as well as feeding of rats with a diet containing hydrothermally processed cereals, known to upregulate endogenous AF plasma activity, mimicked the effect of exogenously administered AF on hippocampal GABAergic transmission. Our results identify AF as a neuromodulator and further raise the possibility that the hippocampus and AF are involved in a gut-brain loop controlling intestinal secretion and inflammation.

Animals↗
PubMed2003

Mechanisms of metabolic dyslipidemia in insulin resistant states: deregulation of hepatic and intestinal lipoprotein secretion.

The growing epidemic of the metabolic syndrome is now well recognized and there is widespread effort to understand the pathogenesis of this complex syndrome and its major metabolic consequences. One of the severe complications accompanying insulin resistant states is the hypertriglyceridemia that appears to occur largely due to overproduction of triglyceride-rich, apolipoprotein B (apoB) containing-lipoproteins. As a result, mechanisms regulating the overproduction of these atherogenic apoB-containing lipoproteins have been the focus of much investigation in recent years. Both in vitro as well as in vivo models of insulin resistance are currently being used to further our understanding of the mechanisms involved in the deregulation of lipid metabolism in insulin resistant states. Evidence from these animal models as well as human studies has identified hepatic very low density lipoprotein (VLDL) overproduction as a critical underlying factor in the development of hypertriglyceridemia and metabolic dyslipidemia. In recent years, a dietary animal model of insulin resistance, the fructose-fed hamster model developed in our laboratory, has proven invaluable in studies of the link between development of an insulin resistant state, derangement of hepatic lipoprotein metabolism, and overproduction of apoB-containing lipoproteins. Evidence from the fructose-fed hamster model now indicates oversecretion of both hepatically-derived apoB100-containing VLDL as well as intestinal apoB48-containing triglyceride-rich lipoproteins in insulin resistant states. A number of novel intracellular factors that may be involved in modulation of VLDL have also been identified. This review focuses on these recent developments and examines the hypothesis that a complex interaction among enhanced flux of free fatty acids from peripheral tissues to liver and intestine, chronic up-regulation of de novo lipogenesis by hyperinsulinemia, and attenuated insulin signaling in the liver and the intestine may be critical to lipoprotein overproduction accompanying insulin resistance.

Animals↗
PubMed1991

Endothelin: a potent stimulator of intestinal ion secretion in vitro.

Effects of endothelin (ET) on electrical properties and Na+ and Cl- fluxes in stripped rabbit ileal mucosa were investigated in vitro in Ussing chambers. Results demonstrate that serosal addition of ET-1, ET-2, ET-3 or the precursor 38 amino acid 'big endothelin' produce dose-dependent increases in short-circuit current (Isc) with maximal effects at approx. 100 nM, 100 nM, 10 nM and 100 nM, respectively and half-maximal effects at 1.4 nM, 5 nM, 1.4 nM and 20 nM, respectively. Mucosal addition of ET-3 failed to elicit a response. Changes in Isc elicited by ET-3 are accompanied by decreases in net fluxes of both Na+ and Cl-. The cyclooxygenase inhibitors, indomethacin and piroxicam, inhibited the increase in Isc produced by ET-3 and indomethacin also abolished the changes in Na+ and Cl- fluxes produced by ET-3. However, no changes in the release of PGE2, thromboxane B2 or 6-keto-prostaglandin F1 alpha could be detected up to 20 min after the addition of ET-3. Preincubation of tissues with neuronal agonists or antagonists, antihistamines or an LTD4/LTE4 receptor antagonist, SKF 104353, failed to alter the response to ET-3. Furthermore, removal of serosal Ca2+ also failed to inhibit the change in Isc produced by ET-3. These results indicate that endothelin is a potent intestinal secretagogue which does not appear to elicit its response through stimulation of PGE2, thromboxane A2 or prostacyclin.

Animals↗
PubMed2000

Effect of zaldaride maleate, an antidiarrheal compound, on intracellular cyclic nucleotide-mediated intestinal ion secretion in rats.

The purpose of this study is to clarify the mechanisms of action of zaldaride, a calmodulin inhibitor. 16,16-Dimethyl prostaglandin E(2), forskolin, 8-bromo cAMP, nitroprusside, 8-bromo cGMP and Escherichia coli heat-stable enterotoxin STa increased the short-circuit current in rat colonic mucosa. Zaldaride at >/=10 microM significantly attenuated the 16,16-dimethyl prostaglandin E(2) and Escherichia coli heat-stable enterotoxin STa-induced increase in short-circuit current; whereas it did not affect other secretagogues-induced effects. These results suggest that zaldaride inhibits the activation of Ca(2+)/calmodulin-sensitive adenylate cyclase or guanylate cyclase linked to a receptor.

16,16-Dimethylprostaglandin E2↗
PubMed1998

[Chloride secretion in the intestinal epithelium: channels, ions, and intracellular signaling].

Salt and water secretion by epithelial cells is required to hydrate the mucosal surface of both gastrointestinal and respiratory tracts. Intestinal secretion is the result of active transcellular chloride transport by epithelial cells lining the crypts. Defective chloride secretion is responsible for many common disorders such as secretory diarrhea and cystic fibrosis. In this review we deal with the most relevant issues regarding epithelial transcellular chloride secretion. We first consider the principles of membrane transport and transport protein function. Then, we briefly discuss the use of state-of-the-art techniques for electrophysiological studies such as "patch-clamp" and microfluorometry. The epithelial chloride secretion model is described according to observations made in both native tissue and cultured intestinal epithelial cells. Next, we consider the intracellular signaling cascades involved in the regulation of membrane transport systems and transcellular chloride secretion. Finally, the clinical implications of the most recent findings are commented, with emphasis on potential molecular targets for the treatment of cystic fibrosis and secretory diarrhea.

Cell Membrane↗
PubMedDate not supplied

[Severe acute diarrhea associated to classic enteropathogenic Escherichia coli (EPEC): clinical features and fecal losses in hospitalized infants].

UNLABELLED: Enteropathogenic Escherichia coli (EPEC) strains are the most prevalent enteropathogenic agents isolated in the stools of hospitalized infants with severe acute diarrhea in São Paulo. These microorganisms induce a severe intestinal secretion of fluids and electrolytes that can cause dehydration leading to hospital admission in the majority of the cases. OBJECTIVES: This investigation aims at the following objectives: 1) to study the clinical features of acute diarrhea in male infants who were hospitalized owing to EPEC infection; 2) to determine the fecal fluid losses, formula intake and variation of the body weight during the evolution of the disease. PATIENTS AND METHODS: Thirty eight male infants with acute diarrhea due to EPEC strains were studied. The clinical and epidemiological features of the patients were recorded and the different EPEC serogroups were identified. The infants were kept in a metabolic bed in order to allow the collection of stools and urine separately during the whole period of the disease, and daily metabolic balances were also obtained. The mean duration of the metabolic study was 5.8 days, and during this period of time 220 daily metabolic balances were accumulated and analyzed. RESULTS: The main clinical features of the studied group were as follows: age below 12 months; low birth weight; precocious weaning; severe protein-calorie malnutrition. EPEC 0111 was the most frequent serogroup identified, present in 68.4% of the infants. The average daily fecal fluid losses were 66 ml/kg and the mean daily formula intake was 85.2 ml/kg. Cow's milk was the most precocious food utilized and the infants who received cow's milk feeding presented the largest stool losses in comparison with lactose free formulas and total parenteral nutrition. CONCLUSION: EPEC strains are able to induce moderate to severe fecal fluid losses in infants and the duration of diarrhea is usually below 15 days, although in several circumstances diarrhea can show a protracted evolution owing to food intolerance associated or not with intestinal secretion.

Acute Disease↗
PubMedDate not supplied

Giardiasis. Functional, immunological and histological study of the small bowel. Therapeutic trial with a single dose of tinidazole.

Fourteen patients between the ages of 9 months and 5 years with chronic diarrhea and giardiasis were studied. Ten were eutrophic and 4 undernourished. The parasitological diagnosis was based on stool examination, a trophozoite search in duodenal aspiration, mucus adhered to mucosa and parasite identification in the intestinal biopsy material. Functional intestinal absorption studies, IgA determination in intestinal secretions and immunofluorescence studies were made. After the tests, tinidazole in suspension was administered at 60-70 mg/kg in one single oral dose. Patients were clinically re-evaluated and tests were done again after 30 days. The purpose of this paper was to evaluate the changes in the functional morphologic and immunologic studies and the therapeutic efficacy of the drug in a single dose. Nine patients had good clinical results, 2 fair and 3 were not evaluated due to celiac disease. All had negative results on the parasitological tests after treatment. There was no relationship between the number of parasites and the severity of symptoms. There was no significant difference between stool fat and d-xylose at the time of diagnosis and 30 days after the administration of tinidazole. The lactose tolerance test presented a significant difference (p less than 0.05) in the disaccharide absorption after treatment. The secretory IgA revealed significantly lower value (p less than 0.01) with respect to the normal values. The immunofluorescence showed productive IgA cells in all cases. The histologic changes were: mild enteropathy (grade I) in 6 patients; moderate (grade II) in 5; and severe (grade III-IV) in 3. Improvement of the mucosa was seen in 6 patients.

Administration, Oral↗
PubMed1996

Peptone stimulates CCK-releasing peptide secretion by activating intestinal submucosal cholinergic neurons.

In this study we tested the hypothesis that peptone in the intestine stimulates the secretion of the CCK-releasing peptide (CCK-RP) which mediates CCK secretion, and examined the enteric neural circuitry responsible for CCK-RP secretion. We used a "donor-recipient" rat intestinal perfusion model to quantify the CCK-RP secreted in response to nutrient stimulation. Infusion of concentrated intestinal perfusate collected from donor rat perfused with 5% peptone caused a 62 +/- 10% increase in protein secretion and an elevation of plasma CCK levels to 6.9 +/- 1.8 pM in the recipient rat. The stimulatory effect of the intestinal washings was abolished when the donor rats were pretreated with atropine or hexamethonium but not with guanethidine or vagotomy. Mucosal application of lidocaine but not serosal application of benzalkonium chloride which ablates the myenteric neurons in the donor rats also abolished the stimulatory action of the intestinal washings. Furthermore, treatment of the donor rats with a 5HT3 antagonist and a substance P antagonist also prevented the secretion of CCK-RP. These observations suggest that peptone in the duodenum stimulates serotonin release which activates the sensory substance P neurons in the submucous plexus. Signals are then transmitted to cholinergic interneurons and to epithelial CCK-RP containing cells via cholinergic secretomotor neurons. This enteric neural circuitry which is responsible for the secretion of CCK-RP may in turn play an important role in the postprandial release of CCK.

Animals↗
PubMed1982

In vivo identification of muscarinic receptors on rat colonic epithelial cells. Binding of [3H]-quinuclidinyl benzilate.

(1) We have demonstrated that intravenously administered [3H]-quinuclidinyl benzilate binds to rat colonic and ileal epithelial cells. The binding was prevented by pretreatment with atropine and QNB. (2) Binding was stereoselective in favor of dexetimide, the biologically more active optical isomer of benzetimide. (3) The results with intestinal epithelial cells were qualitatively the same as those obtained using heart and gut muscle as controls. (4) QNB inhibited pilocarpine-induced fluid accumulation in ligated gut segments. (5) The results support the concept that cholinergic receptors, which mediate intestinal secretion, exist on rat intestinal epithelial cell membranes.

Animals↗
PubMed1989

Effect of somatostatin analog (SMS 201-995) on in vivo intestinal fluid transport in rats. A limited systemic effect.

Somatostatin analog, SMS 201-995, effectively inhibits the release of hormones from gastrointestinal endocrine tumors and reduces hormonally mediated diarrheas. Its clinical efficacy in nonhormonally mediated diarrhea is limited, despite a potent antisecretory and proabsorptive effect in vitro. The effect of serosal addition of SMS 201-995 on in vitro short-circuit current responses in rat intestine is dependent upon chloride and more marked in colon and ileum than jejunum. In contrast, in vivo loop studies demonstrated that systemic administration of SMS 201-995 for five consecutive days produced a paradoxical decrease in basal colonic fluid absorption with no effect in jejunum or ileum. Furthermore, systemically administered SMS 201-995 did not alter cholera toxin-stimulated intestinal secretion. We conclude that despite a previously identified intestinal antisecretory and proabsorptive effect of SMS 201-995 in vitro, this effect is not seen in vivo and may explain the limited use of SMS 201-995 as an antidiarrhoeal agent in nonhormonally mediated diarrhoea.

Animals↗
PubMed1986

Physiological aspects of absorption and secretion in intestine.

Two differently oriented approaches in intestinal physiology can be distinguished. One, mainly based on in vitro experiments, seeks explanations at the level of the epithelium itself. The other, mainly based on in vivo experiments, looks for explanations at the level of regulatory nervous and endocrine mechanisms and their interaction. These two approaches complement each other.

Animals↗