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PubMed1988

Control of glucagon-like immunoreactive peptide secretion from fetal rat intestinal cultures.

Some of the mechanisms underlying intestinal glucagon-like immunoreactive (GLI) peptide secretion from cultured fetal rat intestinal cells were investigated using modulators of the adenylate cyclase pathway [(Bu)2cAMP, theophylline, isobutylmethylxanthine], calcium fluxes (ionomycin, A23187), and protein kinase-C (phorbol ester). All of these agents were found to stimulate GLI peptide release, to 120-230% of paired control values (P less than 0.05-0.001). (Bu)2cAMP, but not the phorbol ester, also increased the total cell content of GLI peptides over the 2-h incubation period (P less than 0.05). No synergism between any of the three pathways was detected. When the mol wt distribution of the stored and secreted GLI peptides was determined in control and (Bu)2 cAMP-stimulated samples, 68 +/- 2% of the peptide corresponded to glicentin, while the remainder eluted with the same distribution coefficient as oxyntomodulin. No 3.5K glucagon was detected in any of the extracts. GLI peptide secretion by the cells was not altered by several pancreatic glucagon secretagogues (cortisol, bombesin, and prostaglandins E1 and D2), but was stimulated by the opioid peptide beta-endorphin (1 microM; P less than 0.02). These studies have indicated that the control of secretion of fetal rat intestinal GLI peptides is complex, involving activation of any one or a combination of the three major second messenger systems. A role for the adenylate cyclase pathway in regulating GLI peptide biosynthesis is also suggested.

1-Methyl-3-isobutylxanthine↗
PubMed1989

Pancreatic vasoactive intestinal polypeptide-secreting tumor: report of a case.

A 58-year-old Taiwanese woman was admitted to Mackay Memorial Hospital for evaluation profuse watery diarrhea. She presented with watery diarrhea, hypokalemia, and hypochlorhydria, and had experienced these problems for 2 years prior to admission. A pancreatic tumor with liver metastasis was noted by the ultrasound, abdominal CT scanning, and angiography studies. Surgical exploration disclosed an ill-defined ovoid tumor in the body and tail of the pancreas measuring 8 x 3 x 3 cm. The immunohistochemistry study of the tumor for VIP-immunoreactivity (VIP: vasoactive intestinal polypeptide) was markedly positive, and also stained slightly positive for other peptides, including pancreatic polypeptide (PP), calcitonin, glucagon, and neuron-specific enolase (NSE). Postoperatively, the patient recovered immediately from her symptoms and there has been no evidence of recurrence during the past 8 months of follow-up.

Adenoma, Islet Cell↗
PubMed1989

Intestinal apolipoprotein synthesis and secretion in the suckling pig.

The present studies report characterization of intestinal apolipoprotein (apoLp) synthesis and secretion in the suckling pig. Lipoproteins (d less than 1.006 g/ml) from mesenteric lymph were found to contain both apoB-100 and B-48, in addition to apoA-IV, E, A-I, and Cs. Lymph low density lipoproteins (LDL) and high density lipoproteins (HDL) contained mainly apoB-100 and apoA-I, respectively. Analysis of core cholesteryl ester fatty acid composition suggested filtration from plasma as the major source of lymph LDL and HDL. Dual radioisotope labeling of intestinal and hepatic apoLps in lymph, as well as immunoprecipitation of radiolabeled intestinal mucosa, demonstrated intestinal synthesis of apoB-48, A-IV, and A-I. There was no evidence for apoB-100 synthesis by intestinal mucosa. By contrast, piglet liver synthesized apoB-100, E, A-I, and Cs, but not apoB-48. Newly synthesized intracellular intestinal apoA-I was mainly (basic) isoform 1 (pI 5.58), while lymph and plasma HDL apoA-I were predominantly isoform 3 (pI 5.33), mature apoA-I. Lymph apoB (P less than 0.001) and apoA-I (P less than 0.04) mass output increased significantly during lipid absorption. Studies were subsequently conducted in fasting, fat-fed, bile-diverted, and sham-operated animals to determine the role of both dietary and biliary lipid in regulating intestinal apoLp biosynthesis. Proximal and distal small intestinal loops were pulse-radiolabeled with [3H]leucine, and apoB-48 and A-I were immunoprecipitated from cytosolic supernatants. Although a proximal to distal gradient in intestinal synthesis rates for both apoB and A-I was noted in all groups, the acute absorption of dietary lipid did not significantly increase apoB or A-I synthesis in either location. Complete removal of biliary lipid for 48 hr did not alter synthesis rates in jejunum or ileum. These studies suggest that mesenteric lymph apoLps in the suckling pig are derived both by filtration from plasma and by direct secretion from the intestine. Physiologic regulation of intestinal apoA-I and B-48 synthesis rates appears to be independent of luminal lipid availability.

Animals↗
PubMed1986

Watery diarrhea syndrome caused by multihormonal malignant pancreatic islet cell tumor secreting somatostatin, vasoactive intestinal peptide, serotonin, and prostaglandin E--a clinicopathological, biochemical, immunohistochemical, and ultrastructural study.

The pathophysiological, biochemical, histological, ultrastructural, and immunohistochemical characters of a case of malignant pancreatic islet cell tumor with watery diarrhea syndrome were carefully investigated. Four hormones or mediators--somatostatin (SST), vasoactive intestinal peptide (VIP), serotonin, and prostaglandin E--were markedly elevated in the circulation. The diagnosis was further confirmed by exploratory laparotomy and autopsy. The contents of SST and VIP in tumor tissues were very high. Gel chromatography of tumor extract revealed single peaks for both SST and VIP. Immunohistochemical studies of tumor tissues showed numerous immunoreactive cells to anti-SST, moderate amount of VIP-positive cells, and a few hCG-, insulin-, and glucagon-positive cells. In conclusion, this is an unusual case of Verner-Morrison syndrome in which three kinds of bioactive hormones or mediators were simultaneously secreted; peptides, amine, and prostaglandin.

Adenoma, Islet Cell↗
PubMed1991

Regulation of peptide-YY synthesis and secretion in fetal rat intestinal cultures.

The regulation of intestinal peptide-YY (PYY) synthesis and secretion has not been well studied. We have used fetal rat intestinal cells in culture to examine the intra- and extracellular factors controlling the production of PYY. Immunohistochemical analysis demonstrated a distinct population of cells containing immunoreactive PYY (IR-PYY). When examined by HPLC, the IR-PYY stored and secreted by fetal rat intestinal cell cultures eluted as a single moiety with the same elution time as synthetic rat PYY. Pro-PYY mRNA transcript levels and secretion of IR-PYY into the cell medium were increased by activation of protein kinase-A with either a long-acting cAMP analog or forskolin. In contrast, IR-PYY secretion only was stimulated in a synergistic fashion through calcium- and protein kinase-C-dependent pathways (stimulated with A23187 and phorbol myristate acetate, respectively). The intestinal endocrine peptide, gastric inhibitory peptide, and the neurocrine peptide, gastrin-releasing peptide, were found to stimulate IR-PYY secretion in a dose-dependent fashion, with significant effects observed at concentrations as low as 10(-8) and 10(-12) M, respectively (P less than 0.05-0.001). Cholecystokinin and vasoactive intestinal peptide were without effect on IR-PYY secretion at doses of 10(-12)-10(-6) M. The fatty acid sodium oleate and the cholinergic agonist bethanechol were also found to stimulate IR-PYY secretion, each at a concentration of 10(-4) M (P less than 0.001). The results of the present study indicate that the synthesis and secretion of PYY by the rat intestine is under the regulatory control of a wide variety of extracellular agents, mediated by several intracellular signalling pathways.

1-Methyl-3-isobutylxanthine↗
PubMed1995

Effects of postoperative periods on glucose absorption and electrolyte secretion in the intestinal loop of sheep.

This study was designed to determine the effect of postoperative periods on intestinal absorptive and secretory functions in the jejunal Thiry-Vella loop of sheep. The lumen was perfused with isotonic saline solution for 120 min at 1 ml/min. The secretory function was assessed by measuring the secretory response of water and electrolytes to PGE2 which was applied intraluminally at 100 microM during the second 30 min period. To measure glucose absorption, 10 mM isotonic glucose solution with its osmolality adjusted by adding NaCl was perfused. Measurements were taken at 1 week intervals for 3 months after surgery. Under basal conditions, water, sodium and chloride were absorbed, while potassium and bicarbonate were secreted. These net basal movements did not change throughout the 3 month period. PGE2 reversed the net absorptions of water, sodium and chloride to the net secretions, and significantly augmented bicarbonate secretion. Potassium secretion was not changed significantly by PGE2. These responses to PGE2 were not affected by the postoperative periods. Glucose absorption decreased gradually for 8 weeks after construction of the jejunal loop with a significant negative correlation to the postoperative period, and subsequently remained at a steady state of nearly 65% of the first week. This decrease in glucose absorption was prevented by regular perfusion of glucose. The results show that the Thiry-Vella loop of the ovine jejunum can be used to measure secretory function for 3 months or more after its construction, but it is essential to regularly perfuse the loop with glucose solution when this loop is used for absorptive experiments of glucose for a long time.

Animals↗
PubMed1976

Evidence for secretion of vasoactive intestinal peptide by tumours of pancreas, adrenal medulla, thyroid and lung: support for the unifying APUD concept.

Levels of vasoactive intestinal polypeptide (VIP) were measured by radioimmunoassay in plasma or tissue from thirty-five patients with watery diarrhoea, and in plasma of twenty-five normal controls. Plasma levels were between 0.6 and 11.0 ng/ml in thirty-one of the thirty-three patients in whom it was measured and too low to measure (less than 200 pg/ml) in the other two. Peptide levels were less than 200 pg/ml in twenty-three of the controls, but higher in the remaining two. All tissues from patients were "rich" in VIP (10 ng to 35 microgram per g). The aetiologic diagnoses included pancreatic islet-cell adenoma or adenocarcinoma, islet-cell hyperplasia, bronchogenic carcinoma, pheochromocytoma, ganglioneuroblastoma, medullary thyroid carcinoma, and retroperitoneal histiocytoma. The findings support the conclusions that: (1) VIP is a likely mediator of the water-diarrhoea syndrome; (2) the syndrome may result from a variety of tumours; (3) this or a related peptide hormone may be secreted by these tumours; and (4) these tumours may have a common embryonic origin.

APUD Cells↗
PubMed2000

Atorvastatin coadministration may increase digoxin concentrations by inhibition of intestinal P-glycoprotein-mediated secretion.

The effect of atovarstatin on digoxin pharmacokinetics was assessed in 24 healthy volunteers in two studies. Subjects received 0.25 mg digoxin daily for 20 days, administered alone for the first 10 days and concomitantly with 10 mg or 80 mg atorvastatin for the last 10 days. Mean steady-state plasma digoxin concentrations were unchanged by administration of 10 mg atorvastatin. Mean steady-state plasma digoxin concentrations following administration of digoxin with 80 mg atorvastatin were slightly higher than concentrations following administration of digoxin alone, resulting in 20% and 15% higher Cmax and AUC(0-24) values, respectively. Since tmax and renal clearance were not significantly affected, the results are consistent with an increase in the extent of digoxin absorption in the presence of atorvastatin. Digoxin is known to undergo intestinal secretion mediated by P-glycoprotein. Since atorvastatin is a CYP3A4 substrate and many CYP3A4 substrates are also substrates for P-glycoprotein transport, the influence of atorvastatin and its metabolites on P-glycoprotein-mediated digoxin transport in monolayers of the human colon carcinoma (Caco-2) cell line was investigated. In this model system, atorvastatin exhibited efflux or secretion kinetics with a K(m) of 110 microM. Atorvastatin (100 microM) inhibited digoxin secretion (transport from the basolateral to apical aspect of the monolayer) by 58%, equivalent to the extent of inhibition observed with verapamil, a known inhibitor of P-glycoprotein transport. Thus, the increase in steady-state digoxin concentrations produced by 80 mg atorvastatin coadministration may result from inhibition of digoxin secretion into the intestinal lumen.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1992

The effects of a high sodium diet on the metabolism and secretion of vasoactive intestinal peptide in the rabbit.

1. In view of previous observations that the metabolism of vasoactive intestinal peptide (VIP) is significantly increased in sodium-depleted rabbits, we wished to determine whether a high sodium intake also leads to alterations in VIP metabolism. We performed metabolic clearance studies in rabbits maintained on a high sodium diet and normal control diets. These studies were performed both before and after the administration of 1.5 mmol kg-1 of sodium intravenously to observe the effects of an acute increase in body sodium. 2. The rabbits maintained on the high sodium diet had a significantly lower basal plasma VIP level (P less than 0.025), a lower metabolic clearance rate (MCR) of the peptide (P less than 0.025) and a lower secretion rate (P less than 0.005), compared with the normal control animals. These differences were maintained following the intravenous sodium infusion. 3. The administration of the intravenous sodium infusion resulted in a further decrease in MCR in the rabbits on the high sodium diet (P less than 0.05). 4. These results confirm that VIP metabolism is affected by high dietary intake of sodium, as well as a low sodium intake, adding further support to the hypothesis that VIP may be involved in sodium homeostasis.

Animals↗
PubMed1990

Effect of intestinal osmolality on insulin secretion to subsequent intravenous glucose or arginine in the rat.

To elucidate the effect of intestinal osmolality on insulin secretion, we investigated insulin response to a subsequent intravenous infusion of glucose or arginine after intragastric or intraduodenal mannitol or NaCl instillation in the rat. After anesthesia with intraperitoneal pentobarbital sodium, mannitol solution (10% or 20%) or 2.7% NaCl was instillated into the stomach or duodenum for 5 min at a flow rate of 0.5 ml/min, and 20% glucose (0.5 g/kg) or 10% L-arginine (0.5 g/kg) was infused bolus into the femoral vein 45 min after intestinal instillation. Insulin response to intravenous glucose was significantly higher in the rat with intragastric or intraduodenal mannitol or NaCl infusion than in control rats with intragastric or intraduodenal instillation of distilled water. Insulin response to intravenous arginine was almost the same in all groups. Subcutaneous preadministration of propranolol (0.4 mg/kg), atropine (1.2 mg/kg), or phentolamine (0.8 mg/kg) did not alter the present phenomenon. These results suggest that intestinal osmolality may enhance insulin release to intravenous glucose, but not to arginine in the rat.

Animals↗
PubMedDate not supplied

Surgical treatment of pancreatic vasoactive intestinal polypeptide-secreting tumor: a case report.

A 68-year-old woman presented with secretory watery diarrhea causing hypokalimia, hypoalbuminemia and dehydration for 5 years. Subsequent investigations including abdominal ultrasonography and computed tomography scanning revealed a mass measuring 7 x 6 cm in the pancreatic tail. The diagnosis of pancreatic VIPomas was suspected on the basis of clinical symptoms. The patient underwent distal pancreatectomy and splenectomy after resuscitation of electrolyte imbalance, dehydration and malnutrition. The pathological examination with histoimmunochemical stain confirmed the diagnosis. Postoperative course is uneventful and the patient does not have symptoms any longer during the follow-up period.

Aged↗
PubMed1975

The effects of phytate on intestinal absorption and secretion of zinc, and whole-body retention of Zn, copper, iron and manganese in rats.

1. The inclusion of phytate (10 g/kg) in a purified diet containing zinc (15 mg/kg) fed to young male rats significantly reduced growth rate and food intake, and promoted a cyclic pattern of food intake characteristic of an uncomplicated Zn deficiency. The decreased growth rate could be accounted for by the reduced food consumption. 2. Rats maintained on a Zn-deficient diet (0.5 mg Zn/kg) were found to have a cyclic pattern of food intake and a very slight weight gain. The addition of phytate (10 g/kg) to the Zn-deficient diet promoted a net loss of mean body-weight. 3. Rats maintained on the Zn-supplemented diet containing phytate excreted significantly more Zn in their faeces than either pair-fed or ad lib.-fed control rats. Rats given the Zn-deficient diet supplemented with phytate excreted more Zn in their faeces than Zn-deficient control rats. 4. Dietary phytate significantly reduced the average daily accumulation (mug/d) and whole-body retention (relative to dietary intake) of iron, copper, manganese and Zn, whether or not the diet was supplemented with Zn. 5. The addition of phytate to the lumen fluid of ligated loops of rat duodenum maintained in situ significantly inhibited 65Zn absorption, compared with the control systems without added phytate. 6. Other studies using ligated duodenal and ileal loops indicated that Zn is secreted into the gut lumen and approximately one-third of this is normally reabsorbed. Recycling of endogenous Zn may be a significant process in the over-all body economy of this trace element. 7. The absorption of 65Zn added to the diet was significantly reduced by dietary phytate. Dietary phytate also reduced the biological half-life of body 65Zn from 61 to 211 h post-administration, possibly by inhibiting reabsorption of endogenous 65Zn and thus promoting a more rapid loss from the body.

Animals↗
PubMed1995

Effects of orally administered Clostridium butyricum MIYAIRI 588 on mucosal immunity in mice.

The activation of local mucosal immunity by Clostridium butyricum MIYAIRI 588 (CBM588) was investigated in germ-free mice. An increase of polyclonal IgA production in the small intestine or secretion into the intestinal lumen was observed in mice mono-associated with CBM588 and fed a diet containing killed vegetative cells of CBM588 (VCBM). However, fecal IgA of anti-CBM588 was rarely formed in mice administered CBM588 during 6 weeks from administration. Cholera toxin was administered orally to SPF mice fed a diet containing CBM588, and IgA secretion of anti-cholera toxin was enhanced in mice fed a VCBM diet. In addition, the production of IgA, IgM and IgG in Peyer's patch cell culture was increased in the presence of VCBM. These results suggest that oral administration of CBM588 stimulates polyclonal mucosal immune activity and shows adjuvant activity for anti-cholera toxin.

Adjuvants, Immunologic↗
PubMed2002

Activation of mucin exocytosis and upregulation of MUC genes in polarized human intestinal mucin-secreting cells by the thiol-activated exotoxin listeriolysin O.

The secreted thiol-activated cytolysin listeriolysin O (LLO) was responsible for L. monocytogenes-induced high-molecular glycoproteins (HMGs) exocytosis in cultured human mucosecreting HT29-MTX cells. By biochemical analysis we demonstrate that the majority of secreted HMGs in LLO-stimulated cells are of mucin origin. In parallel, analysis of the expression of MUCs genes showed that the transcription of the MUC3, MUC4 and MUC12 genes encoding for membrane-bound mucins was increased in LLO-stimulated cells. Upregulation of the MUC3 gene correlates with an increased expression of the membrane-bound MUC3 mucin. In contrast, increase in secretion of the gel-forming MUC5AC mucin develops without upregulation of the MUC5AC gene. Finally, results showed that NF-kappaB and AP-1 transcription factors were not involved in LLO-induced upregulation of MUCs genes in HT29-MTX cells, whereas L. monocytogenes infection was able to promote the degradation of IkappaB proteins in the cells.

Bacterial Proteins↗
PubMed1983

Effect of high vitamin A or tocopherol intake on hepatic lipid metabolism and intestinal absorption and secretion of lipids and bile acids in the chick.

The effect of high dietary vitamin A or tocopherol, or both, on lipid absorption and secretion in the gastrointestinal tract and on serum and hepatic lipids was determined in the chick. High dietary vitamin A increased secretion of cholesterol, bile acids, phospholipids and fatty acids to the duodenum, and tocopherol enhanced cholesterol and bile acid secretion to the duodenum. No differences in over-all absorption were observed. Serum cholesterol was depressed by vitamin A and hepatic lipids were enhanced, except phosphatidyl choline which was depressed. Tocopherol increased hepatic triglycerides and cholesterol. In vitro fatty acid synthesis from lactate by liver homogenates was enhanced by vitamin E and cholesterogenesis enhanced by both vitamin A and tocopherol. delta 9 Desaturation was also enhanced by vitamin E. It is concluded that both vitamin A and tocopherol affect the hepatic synthesis and catabolism of cholesterol and that vitamin E also influences fatty acid metabolism.

Animals↗
PubMed1996

Vasoactive intestinal polypeptide-secreting tumours: biology and therapy.

VIP-secreting tumours are rare, but they produce a dramatic clinical picture, the most prominent feature being profuse, watery diarrhoea and hypokalaemia. VIPomas are malignant and require sophisticated diagnostic and localization techniques in order to identify their presence. Delays in diagnosis are the rule rather than the exception. Improvements in the diagnosis of VIPomas appear to result in an increase in resectability rates. A definitive diagnosis is aided by the determination of plasma VIP concentrations through the use of sensitive radioimmunoassays. With heightened awareness of this syndrome, increasing numbers of patients can be identified and more effective treatments developed for the refractory and recurrent tumours.

Diagnosis, Differential↗
PubMed1975

Intestinal lipid absorption: evidence for an intrinsic defect of chylomicron secretion by normal rat distal intestine.

Intracellular triglyceride accumulation and delayed chylomicron secretion were demonstrated in distal but not in proximal rat intestine following prolonged steady state fat absorption. After 1 and 4 hr of intraduodenal triolein infusion, the mucosal triglyceride content in distal intestinal segments was greatly increased compared with proximal segments. Electron microscopy at each time interval disclosed greater quantities of lipid droplets within the distal cells and these were much larger than the intracellular droplets in the proximal cells, some attaining an enormous size (9000 mum). When proximal and distal cells were compared at intervals after cessation of a 4 hr triolein infusion, the differences in intracellular lipid accumulation were also evident because, even after 6 hr the distal cells were still filled with large droplets, whereas the proximal cells were almost devoid of fat. These results indicate a basic cellular difference between proximal and distal intestine in the processing of fat and, in contrast to current concepts, suggest that defective chylomicron secretion is not necessarily associated with limited B-apoprotein availability.

Animals↗
PubMed2000

Listeriolysin O-induced stimulation of mucin exocytosis in polarized intestinal mucin-secreting cells: evidence for toxin recognition of membrane-associated lipids and subsequent toxin internalization through caveolae.

Lysteriolysin O (LLO) induces a microtubule-dependent activation of mucin exocytosis in the human mucin-secreting HT29-MTX. Cholesterol inhibits the LLO-induced mucin exocytosis, whereas the oxidized form of cholesterol had no inhibitory effect. LLO-induced mucin exocytosis inhibited by cholesterol can be restored by enzymatic treatment with cholesterol oxidase. Inhibition of cholesterol synthesis in HT29-MTX cells results in a decrease in the LLO-induced mucin exocytosis. Other lipids such as gangliosides are able to inhibit the LLO-induced mucin exocytosis, suggesting that the binding of the toxin occurs at a multiplicity of membrane-associated lipids acting as receptors. Incubation of the toxin with lipids such as cholesterol or gangliosides does not decrease binding of LLO to target membranes. The present work also provides evidence that the LLO-induced mucin exocytosis develops independently of the pore-forming activity of the toxin. Finally, we demonstrated that the toxin associates with detergent-insoluble glycolipid microdomains (DIGs) containing VIP/21 caveolin, allowing internalization of the toxin and subsequent activation of the mucin exocytosis.

Bacterial Toxins↗