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At least 523 records · Page 29Linked to original sources
PubMed1983

Tissue-specific synthesis of yolk proteins in Caenorhabditis elegans.

The primary site of yolk protein synthesis in the nematode, Caenorhabditis elegans, has been determined. In animals containing no gonadal cells (obtained by laser ablation of the gonadal precursor cells early in development), yolk proteins are present in abundance. This demonstrates that yolk proteins are made outside the gonad. An examination of proteins present in tissues isolated by dissection, and a comparison of proteins synthesized by isolated tissues incubated in vitro have identified the intestine as the major site of yolk protein synthesis. We propose that yolk proteins are synthesized in the intestine, secreted from the intestine into the body cavity, and taken up from the body cavity by the gonad to reach oocytes. The site of yolk protein synthesis has also been examined in four mutants that have largely male somatic tissues, but a hermaphrodite germ line. Here again, yolk proteins are produced by intestines in a hermaphrodite-specific manner. This suggests that sex determination is coordinately regulated in intestinal and germ line tissues.

Animals↗
PubMedDate not supplied

'In vivo' studies on the pathophysiological mechanism of Vibrio parahaemolyticus TDH(+)-induced secretion.

The thermostable direct haemolysin (TDH) is considered to be the major virulence factors of Vibrio parahaemolyticus; however, poor information is available about its mechanism of action. In our study we examined the capacity of two V. parahaemolyticus TDH-producers (strains 2067 and 3305) to induce fluid secretion in rat ileal loop and to reveal the role of calcium ions (Ca(2+)), calmodulin (CaM), and protein kinase C (PKC) in V. parahaemolyticus TDH(+)-induced fluid secretion. The results show that V. parahaemolyticus TDH(+) strains were able to induce secretion in small intestine; on the contrary, this ability was not evidenced in the V. parahaemolyticus TDH(-) strain used as negative control. The data suggest an enterotoxic activity of haemolysin. Calcium ionophore A23187 and 1-verapamil (calcium channel blocker), when injected alone, induced fluid accumulation in the control loops. A further increase in fluid accumulation (P<0.001) was noted when calcium ionophore was injected along with bacterial suspension of both TDH(+) strains and a significant decrease (P<0.001) in experimental loops when 1-verapamil was inoculated along with bacterial suspension. The other modulating agents increased fluid accumulation in both control and experimental loops, without significant differences with respect to the positive control. Our findings suggest that Ca(2+) appears to be an important messenger involved in the stimulation of intestinal secretion, contrary to PKC and calmodulin which do not appear to have any role.

Animals↗
PubMed1985

Chlorpromazine: adjuvant therapy for the metabolic derangements created by urinary diversion through intestinal segments.

The hyperchloremic metabolic acidosis which can occur following urinary diversion through intestinal segments has been managed with bicarbonate or citrate salts. However, satisfactory management is not always possible with this form of treatment. The development of this acidosis has been attributed to intestinal reabsorption of urinary solutes or intestinal secretion of bicarbonate. Intestinal absorptive and secretory processes are modulated by an adenylate cyclase-cyclic AMP system. Chlorpromazine inhibits the effect of cyclic AMP on the intestinal mucosal cell. The use of chlorpromazine in the management of the hyperchloremic metabolic acidosis following urinary diversion was investigated. A canine model employing an ileal segment between ureter and bladder and a rat model in which urine is diverted through the entire colon have been developed. Chlorpromazine (5 mg./kg./day) was found to be efficacious in the management of the metabolic derangements that occur in both of these models. A case study is presented in which conventional management of this syndrome with bicarbonate salts was unsuccessful. The use of chlorpromazine as an adjuvant treatment allowed correction of the acidosis.

Acidosis↗
PubMed1978

The effects of cholera toxin on intramural blood flow distribution and capillary hydraulic conductivity in the cat small intestine.

Blood flow distribution to the mucosa-submucosa and to the muscularis in the cat small intestine was investigated with a 85Kr elimination technique before and after exposing the intestinal mucosa for 30 min to cholera enterotoxin. In all experiments the toxin induced an intestinal secretion. Concomitantly, total intestinal blood flow was increased to a level 50 per cent above control 3 h after exposure. This vasodilatation reflected a doubling of mean blood flow in the mucosa--submucosa while muscularis blood flow remained unchanged. In another series of experiments the effect of cholera toxin on intestinal capillary hydraulic conductivity was investigated by determining the capillary filtration coefficient (CFC). A slight increase in CFC was noted during the 3 h observation period but this was not more pronounced than would have been expected from the concomitant vasodilatation. It is concluded that hemodynamic changes in the intestinal mucosa may be one of the several factors that probably are involved in the pathogenesis of cholera.

Animals↗
PubMed1982

Regulation of intestinal goblet cell secretion. II. A survey of potential secretagogues.

The factors that regulate the rate of mucus secretion in intestinal goblet cells are only partially defined. Autoradiographic and ultrastructural studies demonstrated that muscarinic cholinergic agents accelerate the exocytosis of mucus from goblet cells in the crypts throughout the small and large intestine, both in vivo and in mucosal organ culture. The present study seeks to identify other factors that may alter mucous secretory rates. Mucosal explants were exposed to potential secretagogues and inhibitors in the organ-culture system and analyzed by light and electron microscopy, alpha- and beta-Adrenergic agents, gastrointestinal regulatory peptides, serotonin, histamine, and dibutyryl cyclic nucleotides were tested over wide concentration ranges. With the exception of histamine, none of these agents accelerated or inhibited the exocytosis of mucous granules. Histamine was effective at the concentration of 10(-4) M and induced rapid, compound exocytosis by crypt goblet cells in mucosal explants from the colon but not from small intestine. The response to histamine was unaffected by atropine. Goblet cells on the mucosal surface released mucus by compound exocytosis when exposed to mustard oil, a nonspecific chemical irritant, but not when exposed to histamine or cholinergic agents.

Acetylcholine↗
PubMed1999

Part of quercetin absorbed in the small intestine is conjugated and further secreted in the intestinal lumen.

Rutin and quercetin absorption and metabolism were investigated in rats after in situ perfusion of jejunum plus ileum (15 nmol/min). In contrast to rutin, a high proportion of quercetin (two-thirds) disappeared during perfusion, reflecting extensive transfer into the intestinal wall. Net quercetin absorption was not complete (2.1 nmol/min), inasmuch as 52% were reexcreted in the lumen as conjugated derivatives (7.7 nmol/min). Enterohepatic recycling contribution of flavonoids was excluded by catheterization of the biliary duct before perfusion. After a 30-min perfusion period, 0.71 microM of quercetin equivalents were detected in plasma, reflecting a significant absorption from the small intestine. The differential hydrolysis of effluent samples by glucuronidase and/or sulfatase indicates that the conjugated forms released in the lumen were 1) glucuronidated derivatives of quercetin and of its methoxylated forms (64%) and 2) sulfated form of quercetin (36%). In vitro quercetin glucuronides synthetized using jejunal and ileal microsomal fractions were similar to those recovered in the effluent of perfusion. These data suggest that glucuronidation and sulfatation take place in intestinal cells, whereas no glucurono-sulfoconjugates could be detected in the effluent. The present work shows that a rapid quercetin absorption in the small intestine is very effective together with its active conjugation in intestinal cells.

Animals↗
PubMed2002

Transporter-mediated Drug Interactions.

Since 1994, researchers have isolated various genes encoding transporter proteins involved in drug uptake into and efflux from tissues that play key roles in the absorption, distribution and secretion of drugs in animals and humans. The pharmacokinetic characteristics of drugs that are substrates for these transporters are expected to be influenced by coadministered drugs that work as inhibitors or enhancers of the transporter function. This review deals with recent progress in molecular and functional research on drug transporters, and then with transporter-mediated drug interactions in absorption and secretion from the intestine, secretion from the kidney and liver, and transport across the blood-brain barrier in humans. Although the participation of the particular transporters in observed drug-drug interactions can be difficult to confirm in humans, this review focuses mainly on pharmacokinetic interactions of clinically important drugs.

Journal Article↗
PubMed1995

Diarrhoea in patients with diabetes mellitus.

Diarrhoea in patients with diabetes mellitus may be due to anorectal or rectal dysfunction that results in incontinence, intestinal secretion or rapid intestinal transit, or may be associated with disorders that typically cause malabsorption. The latter include small bowel bacterial overgrowth, coeliac sprue and pancreatic insufficiency. A practical algorithm for diagnosis and advances in therapy is discussed.

Chronic Disease↗
PubMed1996

Effect of pluronic L-81 on intestinal lipoprotein secretion in the rat.

The hydrophobic nonionic detergent Pluronic L-81 has been shown to lower plasma very-low- and low-density lipoprotein cholesterol, thus preventing diet-induced atherogenesis. The major effect of this agent is a pronounced interference with intestinal lipid metabolism. For studying mesenteric lymph lipoproteins during detergent exposure, a combined micromorphological and biochemical assessment of mucosa and lymph during steady-state lipid absorption was performed. Pluronic L-81 was infused intraduodenally at a constant rate in combination with mixed micellar solutions or saline in mesenteric lymph fistula rats. Pluronic L-81 impairs transepithelial lipid flux during fat absorption, trapping export lipids within the enterocytes and leading to a cytosolic and endoplasmic reticulum lipid accumulation sparing the Golgi region. Pluronic L-81 markedly (P < 0.001) reduces mesenteric triglyceride, phospholipid, and total cholesterol secretion almost exclusively by a reduction of chylomicron formation. Chylomicron and very-low-density lipoprotein lipid composition was only insignificantly altered, except for somewhat higher phospholipid/triglyceride ratios. The chylomicron apoprotein pattern was almost unaffected. Thus, chylomicron formation decreased dramatically without major compositional alterations. The reduction of lipid and apoprotein secretion without particle augmentation is not in favour of a selective interference of Pluronic L-81 with intestinal apoprotein B-48 secretion.

Animals↗
PubMed1994

Role of platelet activating factor in the intestinal epithelial secretory and Chinese hamster ovary cell cytoskeletal responses to cholera toxin.

With the recent heightened concern about cholera around the world come new questions about the mechanism by which cholera toxin causes diarrhea. Peterson and Ochoa have suggested that prostaglandin synthesis is key to both the intestinal epithelial secretory and the CHO cell responses to cholera toxin [Peterson, J. W. and Ochoa, G. (1989) Science 245, 857-859]. Because platelet activating factor (PAF) can be a potent stimulus for prostaglandin synthesis, we examined its role in the intestinal and tissue culture effects of cholera toxin. We report that the specific PAF receptor antagonists BN 52021 and SR 27417 inhibit the effects of cholera toxin on intestinal secretion in rabbit ileal loops in vivo and on the cytoskeleton of Chinese hamster ovary cells in vitro. We also show that PAF itself can cause net fluid secretion in the rabbit model and that PAF potentiates the effects of cholera toxin on intestinal secretion. Finally, we demonstrate that cholera toxin stimulates significant PAF production (2.6-fold) in isolated T-84 intestinal epithelial cells. We conclude that cholera toxin stimulates PAF production and that PAF is involved in both the secretory and cytoskeletal responses to cholera toxin. These findings further support the involvement of additional mediators of cholera toxin effects other than mucosal cell cyclic AMP and help explain the effects of cholera toxin on prostaglandin synthesis.

Animals↗
PubMed1981

The lack of effect of propranolol on the intestinal phase secretion in the dog.

Four mongrel dogs were prepared with a Heidenhain pouch, a gastric fistula, and a 90-cm-long Thiry-Vella loop. After recovery, the jejunal loop was perfused for 3 h with either 5% liver extract or with 0.15 M NaCl, and measurements of gastric acid and pepsin secretion and serum gastrin levels were performed. The experiments were repeated during beta-adrenergic blockade induced by intravenous infusion of propranolol in a dose of 20 micrograms/kg/min. As control, propranolol was also given alone without intestinal perfusion. Perfusion of the jejunal loop with liver extract caused a significant acid secretion from the Heidenhain pouch and gastric fistula. In addition, significant pepsin secretion was obtained, but only from the gastric fistula. The serum gastrin levels remained unchanged during intestinal perfusion. Beta-adrenergic blockade did not influence any of these measurements. The results suggest that the intestinal-phase hormone also stimulates pepsin secretion in dogs. Furthermore, it seems that neither the release nor the action of this hormone is controlled by the beta-adrenergic nerves in the gut.

Animals↗
PubMed1984

[Motility inhibitors and secretion inhibitors].

Antidiarrheal substances interfering with either intestinal motility or intestinal secretion have been used for the management of acute diarrhea. Opiates are the motility inhibitors that appear particularly useful and among these drugs loperamide is the drug of choice due to its low risk of side effects. The question whether antisecretory effects of opiates observed in certain animal experiments is contributory to their antidiarrheal activity in man has not yet been definitely settled. With the exception of chlorpromazine that was felt to be especially useful in cholera, no other antisecretory drug has been used successfully against acute diarrhea. However, future development of new compounds may lead to drugs with potent anti-secretory activity but without unwanted extraintestinal side-effects.

Chlorpromazine↗
PubMed1998

Regulation of human lymphocyte IL-4 secretion by intestinal epithelial cell-derived interleukin-7 and transforming growth factor-beta.

A mucosal immune response to food antigens could result in detrimental hypersensitivity responses. Therefore, the response to many orally administered antigens is downregulated by mechanisms which are not completely understood. Intestinal epithelial cells (IEC) in these tissues may play a role in these regulatory mechanisms via their secreted cytokines. Experiments with human lymphocytes or isolated CD4(+) T cells cultured with 4-day culture supernatants from human colonic carcinoma cell lines revealed that the IEC cell lines normally secreted levels of IL-7 which could enhance IL-4, but not IL-2 or IFN-gamma, secretion by stimulated mixtures of lymphocyes, but not purified CD4(+) T cells. However, acid treatment of the IEC culture supernatants to activate latent TGF-beta resulted in a suppression IL-4, but not IL-2 or IFN-gamma, secretion. These results indicate that under normal conditions, IEC secrete latent TGF-beta and IL-7, the latter of which may enhance local IL-4 secretion. However, activation of the IEC-derived TGF-beta may suppress local IL-4 secretion to suppress the induction of local Th2-type responses to intestinal lumenal antigens.

CD4-Positive T-Lymphocytes↗
PubMed1991

Immune-related intestinal chloride secretion. III. Acute and chronic effects of mast cell mediators on chloride secretion by a human colonic epithelial cell line.

Excessive fluid and electrolyte secretion, resulting symptomatically in diarrhea, has been associated with mast cell activation in a variety of experimental and clinical settings. The present study has used a human colonic epithelial cell line to examine mechanisms underlying this phenomenon. Acute addition of mixed mast cell mediators (as a lysate of rat basophilic leukemia cells) to epithelial cells led to prompt and sustained chloride secretion. The response was partially inhibitable by an antihistaminic drug and an adenosine antagonist, suggesting that histamine, adenosine, and possibly other mediators are responsible for producing the acute effect. Supernatants from immunologically activated rat basophilic leukemia cells had similar effects. Chronic exposure of epithelial cells to the lysate mediator preparation, followed by washing, had no effect on their basal electrical or electrolyte-transporting properties. However, the chloride secretory response of the cells to subsequent addition of vasoactive intestinal peptide, carbachol, and heat-stable enterotoxin of Escherichia coli was significantly enhanced, whereas responses to an adenosine agonist or PGE1 were unaffected. This study has, therefore, demonstrated two ways in which mast cell mediators can directly influence intestinal epithelial cells to secrete more chloride and, hence, to enhance fluid secretion in the gut. The findings may be of relevance to our understanding of inflammatory diarrhea and may aid the development of novel therapies for this disorder.

Adenosine↗
PubMed1978

In vitro degradation of mouse, rabbit and dog antibodies to Vibrio cholerae by succus entericus.

Purified antibodies to Vibrio cholerae from mouse, rabbit and dog were digested in vitro by homologous intestinal secretions. When assessed with regard to their complement-dependent vibriocidal activity, IgG antibodies were generally more susceptible to degradation than IgM antibodies, High levels of tryptic inhibitors were required to inhibit this digestion. Rabbit IgG was unusual in being quite resistant to digestion. Gel filtration studies demonstrated that secretory IgA, isolated from mouse intestinal secretions, was resistant to proteolysis. Similar studies on dog IgG and mouse IgM demonstrated production of F(ab') 2-like fragments. Digestss of these antibodies, while devoid of Fc-mediated vibriocidal activity, retained significant protective activity for baby mice.

Animals↗
PubMed1980

Effect of nicotinic acid on cholera-induced fluid movement and unidirectional sodium fluxes in rabbit jejunum.

Cholera toxin produces intestinal secretion and elevation of intestinal cyclic AMP. Nicotinic acid has been shown to prevent these responses. The effect of nicotinic acid on cholera toxin-induced secretion could be caused by decreased plasma-to-lumen flux, increased lumen-to-plasma flux, or a combination of both. The purpose of this study was to define the effects of nicotinic acid on net fluid movement and unidirectional sodium fluxes in rabbit jejunal loops exposed to cholera toxin. In the untreated animals receiving no nicotinic acid, the cholera toxin-exposed loops secreted 0.91 ml/cm/4h above the control loops receiving no cholera toxin (p < 0.01). On the other hand, pretreatment with 100 mg/kg nicotinic acid caused a striking decrease in secretion in the cholera toxin loop, so that the cholera toxin loop was not significantly different from the control loop. Unidirectional sodium fluxes in untreated animals showed that cholera toxin caused an increase in the plasma-to-lumen flux and a decrease in the lumen-to-plasma flux. Both effects were abolished by pretreating the animals with nicotinic acid. These studies indicate that nicotinic acid prevents cholera toxin-induced secretion by restoring the unidirectional fluxes to control levels.

Animals↗