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At least 1,567 records · Page 87Linked to original sources
PubMed1987

Effects of preoptic injections of gastrin, cholecystokinin, secretin, vasoactive intestinal peptide and PHI on the secretion of luteinizing hormone and prolactin in ovariectomized estrogen-primed rats.

The effects of intracerebral injections of brain-gut peptides in the preoptic region on the secretion of luteinizing hormone (LH) and prolactin (PRL) were examined in ovariectomized, estrogen-primed rats. Gastrin or cholecystokinin-octapeptide injection in the preoptic region induced a moderate increase of circadian rise of LH secretion in some animals but no appreciable change in PRL secretion. Secretin injection was strikingly effective in increasing circadian rise of LH and PRL secretion. Vasoactive intestinal peptide injection completely abolished the occurrence of circadian rise of LH secretion whereas PHI injection facilitated LH secretion undergoing the circadian rhythm. The results suggest that those peptides act as neurotransmitters or neuromodulators in the preoptic region and are implicated in the regulation of LH and PRL secretion.

Animals↗
PubMed1984

Magnesium sulfate-induced water secretion in hamster small intestine.

We studied possible mechanisms of magnesium sulfate (MgSO4)-induced diarrhea. In vivo perfusion of hamster small intestine with an isotonic electrolyte solution containing 50 mM MgSO4 produced nearly three times as much fluid secretion as did a solution containing an equiosmotic amount of mannitol. We found that magnesium was absorbed at a faster rate than mannitol under these conditions, suggesting that differences in solute permeability do not explain the differences in secretory rates. Magnesium ion rather than sulfate appeared largely responsible for the effect as replacement of sulfate with chloride did not diminish the response. MgSO4 perfusion of a proximal intestinal segment did not affect water transport in an isolated distal segment suggesting that release of cholecystokinin or alterations in serum levels of other hormones were not responsible. Intestinal permeability, morphology, and cyclic nucleotide levels were normal after MgSO4 perfusion. Thus, MgSO4-induced diarrhea cannot be explained by the usual mechanisms, and additional processes responsible for intestinal secretion must exist.

Animals↗
PubMed1983

Vasoactive intestinal peptide evoked secretion of fluid and protein from rat salivary glands and the development of supersensitivity.

Vasoactive intestinal peptide (VIP) injected intravenously was found to induce a flow of saliva from both the parotid and the submaxillary gland in the rat. The secretion was slow in onset. The amount of saliva secreted from the parotid gland was less than that from the submaxillary gland. Parotid saliva was very viscous. VIP-evoked parotid saliva was more protein rich than both submaxillary saliva and saliva secreted in response to other sialagogue drugs including the beta-adrenergic receptor agonist isoprenaline. The effect of VIP was direct; it occurred after removal of the adrenals, after degeneration of intraglandular nerves and in the presence of autonomic blockers. A supersensitivity to VIP was demonstrable. In the parotid and the submaxillary glands the secretory response to VIP was enlarged following parasympathetic denervation and decentralization, respectively, while after sympathetic denervation supersensitivity was only found to develop in the submaxillary gland.

Adrenalectomy↗
PubMed1995

Caco-2 cells as a model for intestinal lipoprotein synthesis and secretion.

Caco-2 cells, an intestinal cell line derived from a human colorectal carcinoma that spontaneously differentiates under standard culture conditions, lends itself to the in vitro study of human gut in view of its efficient intestinal transport processes. Among its multiple biological functions are those related to the absorption, transport, and metabolism of lipids and lipoproteins. Despite their intestinal origin, confluent Caco-2 cell monolayers primarily express L-FABP for the uptake of apical dietary long chain fatty acids, incorporating them into triglycerides by the glycerol 3-phosphate pathway, and assembling very-low-density lipoprotein, high-density lipoprotein, and low-density lipoprotein. The monoacyl-glycerol pathway is inactive in Caco-2 cells. Furthermore, the secretion of newly synthesized triglyceride-rich lipoproteins is very restricted, despite abundant production of apolipoprotein (apo) B. The regulation of apoB synthesis and its mRNA editing at the enterocyte level has been intensively examined in Caco-2 cells. Luminal fatty acids, calcium ion, as well as vitamins and hormones are known to modulate the apoB-48/apoB-100 at the transcriptional and/or translational level. The regulation of 3-hydroxy-3-methylglutaryl-CoA reductase and acyl-CoA: (cholesterol acyltransferase), the key enzymes governing intracellular cholesterol handling, have also been extensively examined in Caco-2 cells. In many respects this cell line provides an excellent in vitro model for the investigation of intestinal lipoprotein metabolism; however, their limited secretion capacity remains a potential drawback to comparisons with the in vivo physiological state.

Animals↗
PubMed1992

[Origin of secretions after denervation of the small intestine in the dog].

The origin of the severe diarrhea appearing after intestinal denervation or transplantation was studied on the 3rd and 14th postoperative days in 5 groups of dogs undergoing total or partial denervation. The net movements of water and electrolytes were investigated by employing an experimental model of intestinal perfusion in isolated loops in vivo. The active uptake of phenylalanine and beta-methylglucoside and Na(+)-K(+)-ATPase activity were used for in-vitro evaluation. Bacteriologic and histological specimens were also taken. Following total denervation with anastomosis, a considerable loss of water and electrolytes as well as numerous E. coli were found in the entire small intestine. This net secretion is due to the stagnation of bacteria in the presence of complete denervation and the absence of food since the animals in this group could not eat properly following general anesthesia and surgery. Consequently, peristalsis was not stimulated and bacterial overgrowth occurred. In the group denervation with pseudo-anastomosis, perfusion studies showed a decrease of absorption in the jejunum and minimal but significant secretion in the ileum. A high number of E. coli was also present. Since the mucosa remained intact, nutrition per os was resumed in the immediate postoperative period and excessive water and electrolyte loss was avoided. The high number of bacteria was due to a decrease in intestinal motility since complete denervation was performed. In the denervation group, water and electrolyte movements were identical to those observed in the preceding group but the entire intestine remained sterile.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Lipopolysaccharide binding protein and serum amyloid A secretion by human intestinal epithelial cells during the acute phase response.

The acute phase proteins LPS binding protein (LBP) and serum amyloid A (SAA) are produced by the liver and are present in the circulation. Both proteins have been shown to participate in the immune response to endotoxins. The intestinal mucosa forms a large surface that is continuously exposed to these microbial products. By secretion of antimicrobial and immunomodulating agents, the intestinal epithelium contributes to the defense against bacteria and their products. The aim of this study was to explore the influence of the inflammatory mediators TNF-alpha, IL-6, and IL-1beta on the release of LBP and SAA by intestinal epithelial cells (IEC). In addition, the induction of LBP and SAA release by cell lines of intestinal epithelial cells and hepatic cells was compared. The data obtained show that in addition to liver cells, IEC also expressed LBP mRNA and released bioactive LBP and SAA upon stimulation. Regulation of LBP and SAA release by IEC and hepatocytes was typical for class 1 acute phase proteins, although differences in regulation between the cell types were observed. Endotoxin did not induce LBP and SAA release. Glucocorticoids were demonstrated to strongly enhance the cytokine-induced release of LBP and SAA by IEC, corresponding to hepatocytes. The data from this study, which imply that human IEC can produce LBP and SAA, suggest a role for these proteins in the local defense mechanism of the gut to endotoxin. Furthermore, the results demonstrate that tissues other than the liver are involved in the acute phase response.

Acute-Phase Proteins↗
PubMed2006

Calcium-sensing receptor abrogates secretagogue- induced increases in intestinal net fluid secretion by enhancing cyclic nucleotide destruction.

The calcium-sensing receptor (CaSR) provides a fundamental mechanism for diverse cells to detect and respond to modulations in the ionic and nutrient compositions of their extracellular milieu. The roles for this receptor are largely unknown in the intestinal tract, where epithelial cells are normally exposed to large variations in extracellular solutes. Here, we show that colonic CaSR signaling stimulates the degradation of cyclic nucleotides by phosphodiesterases and describe the ability of receptor activation to reverse the fluid and electrolyte secretory actions of cAMP- and cGMP-generating secretagogues, including cholera toxin and heat stable Escherichia coli enterotoxin STa. Our results suggest a paradigm for regulation of intestinal fluid transport where fine tuning is accomplished by the counterbalancing effects of solute activation of the CaSR on neuronal and hormonal secretagogue actions. The reversal of cholera toxin- and STa endotoxin-induced fluid secretion by a small-molecule CaSR agonist suggests that these compounds may provide a unique therapy for secretory diarrheas.

Aniline Compounds↗
PubMed1996

The expression of complement protein 4 and IgG3 in luminal secretions.

BACKGROUND: Factors regulating proximal small-intestinal luminal concentrations of IgG3, the predominant IgG subclass at this site, are unclear. This study determined whether luminal IgG3 concentrations are related to those of complement protein 4 (C4), an acute-phase reactant predominantly derived from local mucosa. METHODS: Proximal small-intestinal luminal and peripheral blood IgG subclass and C4 concentrations were measured by radial immunodiffusion in 30 adult subjects without predisposition to disturbed mucosal immunity. Mucosal C4 immunoreactivity and the presence or absence of small-intestinal bacterial overgrowth were determined in all subjects. Caecal luminal concentrations of IgG3 and C4 were measured in a separate cohort of eight asymptomatic subjects. RESULTS: Proximal small-intestinal luminal C4 and IgG subclass concentrations were not significantly influenced by the presence of absence of small-intestinal bacterial overgrowth (P > 0.2). Nor did plasma C4 levels significantly influence C4 concentrations in small-intestinal luminal secretions (P > 0.2). Mucosal immunoreactivity for C4 was present in every subject. A significant correlation was found between C4 and IgG3 concentrations in proximal small-intestinal luminal secretions (P < 0.0005) and also in caecal secretions (P < 0.05) but not in peripheral blood (P > 0.1). CONCLUSIONS: Common factors, not including the presence or absence of small-intestinal bacterial overgrowth, regulate luminal concentrations of C4 and IgG3. Local investigation is mandatory when assessing mucosal immune mechanisms.

Cecum↗
PubMed2000

Somatostatin receptor subtype-5 mediates inhibition of peptide YY secretion from rat intestinal cultures.

Somatostatin-14 (S-14) and somatostatin-28 (S-28) bind to five distinct membrane receptors (SSTRs), but S-28 has higher affinity for SSTR-5. Whether S-28 acting through SSTR-5 regulates inhibition of peptide YY (PYY) secretion was tested in fetal rat intestinal cell cultures. S-28 and S-14 caused dose-dependent inhibition of PYY secretion stimulated by gastrin-releasing peptide, but S-28 was more potent than S-14 (EC(50) 0.04 vs. 13.2 nM). PYY was inhibited by two analogs with affinity for SSTR-5, BIM-23268 and BIM-23052, more potently than S-14 and as effectively as S-28. The SSTR-5 analog L-362855 suppressed PYY equivalent only to S-14, but the structurally related peptide L-372588 (Phe to Tyr at position 2) was equipotent to S-28, whereas L-372587 (Phe to Tyr at position 7) caused no inhibition. An SSTR-2 analog decreased PYY secretion similar to S-14, and an SSTR-3 analog was ineffective. PYY secretion stimulated by phorbol 12-myristate 13-acetate and by forskolin was also more potently suppressed by S-28 and the octapeptide SSTR-5 analogs. The results indicate that S-28 mediates inhibition of gastrin-releasing peptide-stimulated PYY secretion through activation of SSTR-5 and includes suppression of cAMP- and protein kinase C-dependent pathways. Substitution of a single hydroxyl group confers differences in SSTR-5 agonist properties, suggesting region specificity for the intrinsic activity of this receptor subtype.

Animals↗
PubMed1988

Apolipoprotein B-100 is the major form of this apolipoprotein secreted by human intestinal Caco-2 cells.

Although the discovery of stop codon has explained the mechanism for the formation of the intestinal marker, apolipoprotein B-48, the dispute regarding the presence of apolipoprotein B-100 in the intestine is still unsettled. To further investigate the characteristics of intestinal apolipoprotein B, the newly developed human colonic adenocarcinoma Caco-2 cells which express functional properties of the differentiated enterocytes, were used. SDS-polyacrylamide gel electrophoresis analyses of the intact culture medium or its lipoproteins of d less than 1.23 g/ml showed the presence of only a single protein band of apolipoprotein B-100 with no detectable apolipoprotein B-48. After immunoblotting with oligoclonal antibodies to the amino-terminal peptide of apolipoprotein B, a trace amount of apolipoprotein B-48 was observed in the isolated lipoproteins, but not in the intact culture medium. These results suggest that apolipoprotein B-100 is the major form of apolipoprotein B secreted by human intestinal cells.

Adenocarcinoma↗
PubMed1985

[Effect of natriuretic factor on sodium secretion in the small intestine].

In dogs with Tiri-Vella fistula, the natriuretic factor increases the secretion of the intestinal fluid and its content of sodium. In rats with increased content of natriuretic factor, the water and sodium absorption diminishes in the intestine whereas the secretion of 22Na into the intestine lumen is increased.

Animals↗
PubMed1979

Role of gastric antrum in gastric and intestinal phases of gastric secretion in dogs.

1. The gastric and intestinal phases of gastric secretions were selectively evoked before and after the removal of the antral mucosa in four dogs provided with a special cannula that allowed complete separation of the stomach and duodenum without interrupting neural connexions between them. 2. The gastric phase induced by 5% liver extract meal administered into the stomach at various distension pressures (ranging from 0 to 15cm H2O) resulted in an increase in acid output to about 56% of the histamine maximum and in a marked rise in serum gastrin. 3. Following resection of the antral mucosa, the gastric acid response to meal of liver extract was reduced by about 50% and serum gastrin response was completely eliminated. Exogenous gastrin (G-17) given during the gastric phase induced by such a meal in dogs with antral mucosectomy failed to restore acid output to pre-resection level. 4. Intestinal perfusion of meal of liver extract in graded amounts stimulated gastric acid secretion to about 30% of histamine maximum acid output and raised significantly serum gastrin level. 5. Antral mucosectomy abolished almost completely both gastric acid and serum gastrin response to intestinal meal of liver extract. 6. Exogenous gastrin given during the intestinal meal of liver extract failed to restore acid output to the pre-resection level, suggesting that this procedure greatly reduced the secretory capacity of the oxyntic glands. 7. We conclude that the antral gland area plays an important role in the gastric phase and that it is a prerequisite for the intestinal phase of gastric secretion.

Animals↗
PubMed1996

Systematic and intestinal antibody-secreting cell responses and correlates of protective immunity to human rotavirus in a gnotobiotic pig model of disease.

Neonatal gnotobiotic pigs orally inoculated with virulent (intestinal-suspension) Wa strain human rotavirus (which mimics human natural infection) developed diarrhea, and most pigs which recovered (87% protection rate) were immune to disease upon homologous virulent virus challenge at postinoculation day (PID) 21. Pigs inoculated with cell culture-attenuated Wa rotavirus (which mimics live oral vaccines) developed subclinical infections and seroconverted but were only partially protected against challenge (33% protection rate). Isotype-specific antibody-secreting cells (ASC were enumerated at selected PID in intestinal (duodenal and ileal lamina propria and mesenteric lymph node [MLN]) and systemic (spleen and blood) lymphoid tissues by using enzyme-linked immunospot assays. At challenge (PID 21), the numbers of virus-specific immunoglobulin A (IgA) ASC, but not IgG ASC, in intestines and blood were significantly greater in virulent-Wa rotavirus-inoculated pigs than in attenuated-Wa rotavirus-inoculated pigs and were correlated (correlation coefficients: for duodenum and ileum, 0.9; for MLN, 0.8; for blood, 0.6) with the degree of protection induced. After challenge, the numbers of IgA and IgG virus-specific ASC and serum-neutralizing antibodies increased significantly in the attenuated-Wa rotavirus-inoculated pigs but not in the virulent-Wa rotavirus-inoculated pigs (except in the spleen and except for IgA ASC in the duodenum). The transient appearance of IgA ASC in the blood mirrored the IgA ASC responses in the gut, albeit at a lower level, suggesting that IgA ASC in the blood of humans could serve as an indicator for IgA ASC responses in the intestine after rotavirus infection. To our knowledge, this is the first report to study and identify intestinal IgA ASC as a correlate of protective active immunity in an animal model of human-rotavirus-induced disease.

Animals↗
PubMed2000

Increased zinc absorption but not secretion in the small intestine of metallothionein-null mice.

Metallothionein (MT) has been assigned a role in intestinal Zn absorption and secretion. The influence of MT was investigated in isolated segments of the small intestine from mice lacking the expression of MT I and II genes (MT-/-). To measure Zn absorption, washed 10- to 12-cm segments of the proximal and distal small intestine of MT-/- and control MT+/+ mice were filled with 65Zn as ZnSO4 (10 microg/mL), and the amount of 65Zn appearing in the external buffer was measured over 4 h. To measure Zn secretion, the same procedure was followed using everted gut segments. The 65Zn absorption from the small intestine was significantly greater in MT-/- mice, but only in the absence of albumin. In the proximal small intestine, the inclusion of 2% albumin in the external buffer significantly increased Zn absorption from 6.8% (no albumin) to 13.2% (with albumin) for MT-/-, and from 4.9% (no albumin) to 14.2% (with albumin) for MT+/+. In the distal segment, the respective values, with and without albumin respectively were 9.5% and 15.1% for MT-/- mice and 4.3% and 16.1% for MT+/+ mice. Regarding 65Zn secretion, there was no difference between MT+/+ and MT-/- in either segment. However, the rate of secretion was higher in the proximal small intestine for both genotypes. Although it can be demonstrated that MT limits Zn absorption under controlled conditions in vitro, the ability of albumin to overcome this effect emphasizes the importance of circulating ligands in Zn transport.

Albumins↗
PubMed2002

Active sulfate secretion by the intestine of winter flounder is through exchange for luminal chloride.

SO4(2-) transport by winter flounder intestine in Ussing chambers was characterized. With 50 mM SO4(2-) (physiological level) bathing the lumen, net absorption (lumen to blood) dominated. Under short-circuited conditions, 1 mM SO4(2-) on both sides, net active SO4(2-) secretion occurred (8.55 +/- 0.96 nmol. cm(-2). h(-1)). NaCN (10 mM), ouabain (10(-4) M), and luminal DIDS (0.2 mM) inhibited net secretion. Removal of luminal Cl- and HCO3- together (Cl--HCO3-) or Cl- alone blocked net secretion, whereas removal of luminal HCO3- alone increased net secretion. SO4(2-) uptake into foregut brush-border membrane vesicles was stimulated by a trans-Cl- gradient (in > out) and unaffected by a trans-HCO3- gradient (in > out). Short-circuiting with K+ (in = out) and valinomycin had no effect on Cl--stimulated SO4(2-) uptake, suggesting electroneutral exchange. Satiety (i.e., full stomach) stimulated the unidirectional absorptive flux, eliminating net secretion. It was concluded that the intestine is a site of SO4(2-) absorption in marine teleosts and that active SO4(2-) secretion is in exchange for luminal Cl-.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2000

Human intestinal epithelial cells secrete interleukin-1 receptor antagonist and interleukin-8 but not interleukin-1 or interleukin-6.

BACKGROUND: There is growing evidence that intestinal epithelial cells (IECs) are involved in the mucosal immune system. AIM: To assess the pattern of cytokines secreted by IECs and lamina propria mononuclear cells (LPMNCs). To achieve this, the expression and secretion of interleukin (IL)-1, IL-1 receptor antagonist (IL-1ra), IL-6, and IL-8 in human primary colonic and ileal IECs and LPMNCs from the same patient were studied. METHODS: IECs and LPMNCs were isolated from surgical specimens or endoscopic biopsy samples. mRNA expression was investigated by northern blot analysis. Secretion of IL-1beta, IL-6, IL-8, and IL-1ra was measured by enzyme linked immunosorbent assay. RESULTS: IL-1ra mRNA levels were higher in IECs than in LPMNCs in all probands. IL-8 mRNA was only present in low amounts in the IECs from two controls. In none of the specimens were IL-1beta and IL-6 mRNA present in IECs. Transcripts encoding IL-1beta, IL-1ra, IL-6, and IL-8 were identified in LPMNC preparations of all specimens. IECs from normal mucosa produced no detectable amounts of IL-1beta or IL-6, whereas LPMNCs did. IECs secreted some IL-8 (65 (9) pg/10(5) cells) but significantly more was generated by LPMNCs (408 (43) pg/10(5) cells, p<0.0001). However, IECs secreted more IL-1ra than did LPMNCs (120 (12) v 94 (11) pg/10(5) cells). In acute inflammation, IEC IL-1ra secretion was significantly increased. A correlation between secreted IL-1ra and the macroscopical degree of inflammation was found in Crohn's disease (r = 0.64, p<0.0001, n = 36) and ulcerative colitis (r = 0. 76, p<0.0001, n = 24). CONCLUSIONS: IECs from normal mucosa express and secrete IL-1ra and low amounts of IL-8, but no IL-1 or IL-6. In inflamed mucosa the secretion of IL-1ra by IECs is slightly increased but may be not sufficient to antagonise the greatly increased production of proinflammatory cytokines by LPMNCs and the IECs themselves.

Epithelial Cells↗