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PubMed1985

Fe3+ transport by brush-border membrane vesicles isolated from normal and hypoxic mouse duodenum and ileum.

Studies of 59Fe3+ uptake by brush-border membrane vesicles prepared from mouse duodenum have indicated that uptake represents transport across the brush-border membrane which is rate-limited by the membrane-transfer step (Simpson, R.J. and Peters, T.J. (1984) Biochim. Biophys. Acta 772, 220-226). Further studies presented here reveal that the uptake rate represents the net influx rate for Fe3+ and is independent of Na+ in the medium and of the method of vesicle preparation. Uptake by brush-border membrane vesicles prepared from mouse distal ileum also represents predominantly transport and is higher than that observed with duodenal brush-border membrane vesicles. Studies of the initial uptake rate by vesicles prepared from normal and hypoxic mouse intestine demonstrated an increase in Fe3+ transport in duodenal vesicles only.

Animals↗
PubMed1991

Na+,K(+)-ATPase inhibition by an endogenous peptide, SPAI-1, isolated from porcine duodenum.

SPAI-1, a peptide isolated from porcine duodenum, has been shown to inhibit Na+,K(+)-ATPase in vitro (Araki et al. (1989) Biochem. Biophys. Res. Commun. 164, 496-502). The characteristics of ATPase inhibition by this novel peptide were examined. SPAI-1 inhibited Na+,K(+)-ATPase preparations isolated from various organs of dog or rat or from sheep kidney with similar potency. Three isoforms of rat Na+,K(+)-ATPase had similar sensitivity to inhibition by SPAI-1 although these isoforms had remarkable differences in their sensitivity to the inhibitory effect of ouabain. Ca(2+)-ATPase isolated from the sarcoplasmic reticulum of rabbit skeletal muscle was insensitive to inhibition by SPAI-1. Ouabain-insensitive Mg(2+)-ATPase activity was unaffected by low concentrations of SPAI-1, but was stimulated at high concentrations. SPAI-1 inhibited H+,K(+)-ATPase from hog stomach in concentrations similar to that required for Na+,K(+)-ATPase inhibition. These results indicate that SPAI-1 is a specific inhibitor for monovalent cation transporting ATPases.

Adenosine Triphosphatases↗
PubMed1984

Corticotropin-releasing factor is contained within perikarya and nerve fibres of rat duodenum.

Immunofluorescence microscopic studies revealed a corticotropin-releasing factor (CRF) staining within both myenteric plexus perikarya and nerve fibres of the rat duodenum. A CRF-immunofluorescence could be visualized also within nerve fibres close associated with myenteric and submucous blood vessels. Even the lamina propria contained CRF-immunoreactive nerve fibres, which were obviously often localized near the basal lamina.

Animals↗
PubMed1984

gamma-Melanotropin is contained within neurons, nerve fibres and nerve endings of rat duodenum.

Using an immunofluorescence microscopic technique a gamma 3-melanotropin staining is to recognize within neuronal cell bodies and nerve fibres as well as within nerve endings of the rat duodenum. These perikarya have a broad, gamma 3-melanotropin immunofluorescent cytoplasm rim which surrounds a round unstained cell nucleus. They possess often a pear-shaped cell body and are located mainly in the myenteric plexus, but also in the submucous plexus. gamma 3-Melanotropin immunoreactive nerve fibres and nerve fibre-strands are to see in the myenteric plexus neuropil and lamina propria as well as in interconnecting nerve strands lying between the longitudinal and circular smooth muscle layers. Nerve endings immunoreactive to gamma 3-melanotropin are in close association with submucosal blood vessels, probably arterioles, and smooth muscle cells of the circular smooth muscle layer.

Animals↗
PubMed1984

alpha-melanotropin and beta-endorphin-like immunoreactivities are contained within neurons and nerve fibers of the rat duodenum.

Both alpha-melanotropin and beta-endorphin were revealed by immunofluorescence microscopy studies within neurons and nerve fibers of the rat duodenum. An immunohistochemical staining for alpha-melanotropin was seen within neuronal cell bodies and nerve fibers bundles of the myenteric and submucous plexus. A beta-endorphin immunofluorescence was visualized within perikarya and nerve fibers of both the myenteric and submucous plexus. alpha-Melanotropin as well as beta-endorphin immunoreactivities were strictly localized to structures of the enteric nervous system. In crypts and epithelial cells only a non-specific staining was observed.

Animals↗
PubMed1985

Ultrastructural evidence for beta-endorphin-like immunoreactivity in the nervous system of the rat duodenum.

Using a modified immunoelectron microscopic staining technique the opioid peptide beta-endorphin could be demonstrated within large dense-core vesicles (LDVs) which are localized in presumptive axons and dendrites of the duodenal myenteric plexus of the rat duodenum. Pre-absorption tests with synthetic beta-endorphin (10(-6)M, final concentration) abolished the beta-endorphin immunoreactivity, resulting in only beta-endorphin unstained vesicles. To demonstrate more clearly electron-dense beta-endorphin material within vesicles the ultrathin sections were not counterstained with heavy metal salts. These sections revealed that the beta-endorphin material is localized as 'cores' with a mean diameter of 35-50 nm within LDVs corresponding to cores of LDVs, which are 70-90 nm in mean diameter.

Animals↗
PubMed1977

Estimation of cholecystokinin-pancreozymin (CCK) in human plasma and tissue by a specific radioimmunoassay and the immunohistochemical identification of pancreozymin-producing cells in the duodenum of humans.

A reliable, sensitive, reproducible and specific radioimmunoassay for cholecystokinin-pancreozymin (CCK) has been developed, using rabbit antisera to highly purified porcine hormone. The natural occurring variant of CCK (39-CCK), in which the ordinary CCK is lengthened from its N-terminus by a hexapeptide, labelled with 125J, and repurified by column chromatography on Sephadex G-10 and on SP-Sephadex C-25, was used as tracer. Separation from antibody-bound labelled 39-CCK was carried out using a double antibody procedure. Non-specific interference with the assay system was abolished by ethanol extractions. Highly purified porcine CCK was used as standard. No significant crossreaction was found with gastrin, motilin, vasoactive polypeptide (VIP), gastric inhibitory polypeptide (GIP), natural and synthetic secretin, pancreatic glucagon or insulin. The sensitivity of the assay is approximately 40 pg/ml of test solution. The mean immunoreactive CCK concentration in 45 fasting normal subjects was 222 pg/ml increasing after food ingestion to 480 pg/ml. Somatostatin was able to abolish the stimulated CCK release. Elevated CCK concentrations were found in chronic pancreatitis. Immunohistochemical identification of pancreozymin cells was carried out either in surgical samples or in biopsy material. Approximately 1650 CCK cells per cross-section in the duodenum of humans have been found. The CCK cells usually appeared elongated, oval or pyramidal in shape and were observed to reach the lumen with their apical cell pole.

Animals↗
PubMed1980

Effects of delta-aminolaevulinic acid on contractile activity of rabbit duodenum.

delta-Aminolaevulinic acid (ALA) inhibited spontaneous contractions and contractions induced by acetylcholine, barium chloride or ouabain in rabbit duodenum preparations suspended in Ringe-Locke solution. Concentrations of ALA between 25--100 micrograms/ml reduced amplitude of spontaneous contractions and at levels above 200 micrograms ALA/ml spontaneous contractions caused. Muscle tone was decreased in proportion to logarithm of AL concentration between 25 and 1000 micrograms/ml. Gut ALA levels were increased by the treatment and returned to control values after washing, and pharmacological effects were full reversed. Neither tetrodotoxin nor atropine affected the gut's response to ALA. The response still occurred in calcium-free, high-calcium, potassium-free and high-potassium bathing fluid. Effects of ouabain resembled those of ALA only when gut had been pretreated with atropine; pretreatment with tetrodotoxin induced slight contracture. The observed pharmacological effects of ALA must be by actions additional to sodium pump inhibition.

Acetylcholine↗
PubMed1985

Tritiated thymidine radioautographic study on the origin and renewal of secretin cells in the rat duodenum.

The origin and renewal of secretin cells in the duodenum were investigated using the unlabeled antibody peroxidase-antiperoxidase technique and radioautography in rats killed at various times after single or multiple injections of [3H]thymidine. Secretin cells were spatially distributed from the upper crypt to the villus tip, being particularly numerous in the upper two-thirds of the duodenal villi. After a single injection of [3H]thymidine, there were no labeled secretin cells, indicating a lack of self-replicating activity. After repeated injections of the isotope, labeled secretin cells appeared and increased in number. They first occurred at the upper part of the crypt and the lower part of the villus, and later at the villus tip. All these cells were found to be labeled after continuous labeling for 120 h, which is considered to be the renewal time for this cell population.

Animals↗
PubMed1987

Subcellular localization of pepsinogen II in stomach and duodenum by the immunogold technique.

We have determined the ultrastructural localization of pepsinogen II (PG II) in aldehyde-osmium fixed, resin-embedded ultrathin sections of human gastric fundic and pyloric gland mucosa and duodenum using the protein A immunogold technique and antiserum specific for PG II. Chief cells contained homogeneous, finely granular secretory granules that were uniformly PG II-positive. In contrast, mucous neck, pyloric gland, and Brunner's gland cells contained secretory granules consisting of an eccentrically placed dense core surrounded by a clear matrix; PG II immunoreactivity was concentrated over the dense core of these biphasic granules. Pyloric gland cells also contained monophasic secretory granules having the same electron density, texture, and PG II immunoreactivity as the nucleoids of biphasic granules and clear vesicular granules that were PG II-negative. Vesicular granules also were found in Brunner's gland cells. The Golgi region of pyloric gland cells contained small PG II-positive monophasic granules adjacent to small PG II-negative vesicular granules. This observation suggests that biphasic granules may form in the Golgi region of pyloric gland cells by fusion of PG II-containing monophasic granules and PG II-unreactive vesicular granules.

Brunner Glands↗
PubMed1988

Relationship of the motor activity of the antrum, pylorus, and duodenum to gastric emptying of a solid-liquid mixed meal.

The postprandial motor activity of the antrum, pylorus, and duodenum in 15 healthy volunteers was compared with the profiles of emptying of the solid and liquid components of a meal. The liquid component of the meal emptied rapidly in an exponential manner, whereas the solid remained in the fundus of the stomach until approximately 80% of the liquid had emptied and then emptied in a linear manner. The onset of solid emptying was associated with an increase in the rate of occurrence of antral pressure waves (p less than 0.05), and the half-time for solid emptying (t1/2 - lag period) was inversely correlated (p less than 0.05) with the rate of coordinated contractions involving the antrum. The substitution of 25% dextrose in normal saline as the liquid component of the meal increased the half-time for liquid emptying from a median of 8 to 40 min (p less than 0.01), increased the lag period for solid emptying from 40 to 87 min (p less than 0.01), and increased the rate of occurrence of isolated pyloric pressure waves during the solid lag phase from 7 to 58/h (p less than 0.05), but did not affect the slope of solid emptying or the rate of coordinated contractions involving the antrum during the solid emptying period.

Adolescent↗
PubMed1989

Major pathway for putrescine synthesis induced by 1 alpha,25-dihydroxyvitamin D3 in chick duodenum.

We have reported that a single injection of 1 alpha,25-dihydroxyvitamin D3 into vitamin D-deficient chicks produces a marked accumulation of putrescine in the duodenum by an interconversion pathway. In the present study, we examined the effect of N1,N2-bis(2,3-butadienyl)-1,4-butanediamine, a specific irreversible inhibitor of polyamine oxidase, on the duodenal putrescine synthesis induced by 1 alpha,25-dihydroxyvitamin D3. Addition of N1,N2-bis(2,3-butadienyl)-1,4-butanediamine to an assay mixture completely inhibited the activity of duodenal polyamine oxidase in vitro. Prior administration of N1,N2-bis(2,3-butadienyl)-1,4-butanediamine to chicks completely blocked the 1 alpha,25-dihydroxyvitamin D3-induced increase in duodenal accumulation of putrescine in vivo. The increase of the duodenal accumulation of putrescine by 1 alpha,25-dihydroxyvitamin D3 in vitamin D-deficient chicks coincided quantitatively with the amount of N1-acetylspermidine synthesized from spermidine after the injection of the vitamin into the chicks pretreated with the inhibitor of polyamine oxidase. These results clearly indicate that spermidine N1-acetyltransferase plays a preferential role in the increase in duodenal putrescine synthesis by 1 alpha,25-dihydroxyvitamin D3. The rapidly proliferating and maturing epithelium of small intestines will provide a good model for investigating the role of the interconversion of polyamine metabolism in cell growth and differentiation.

Acetyltransferases↗
PubMed1990

Cysteamine induces cholecystokinin release from the duodenum. Evidence for somatostatin as an inhibitory paracrine regulator of cholecystokinin secretion in the rat.

To determine whether cholecystokinin secretion is regulated by endogenous somatostatin, somatostatin deficiency was induced in vivo with cysteamine (250 mg/kg body wt, IV) or anti-somatostatin antiserum in anaesthetized rats and in vitro with cysteamine (30 micrograms/mL) in a rat duodenum-incubation system. Cholecystokinin secretion was assessed in vivo by measuring amylase in duodenal perfusates collected at 10-minute intervals for 1 hour and in vitro by a carboxy-terminal radioimmunoassay. Cysteamine induced a marked decrease in duodenal immunoreactive somatostatin both in vivo (50%) and in vitro (60%). The rate of amylase secretion increased from 9.7 +/- 2.1 U (mean +/- SE) to 28.0 +/- 4.8 U at 20 minutes (P less than 0.001). The cholecystokinin-receptor antagonist CR-1392 abolished amylase response for 30 minutes, whereas the more potent antagonists Asperlicin (18.0 mg/kg body wt, IV) and L-364,718 (0.25 mg/kg body wt, IV) caused prolonged blockade. The rate of amylase secretion in gastrectomized animals increased from 7.2 +/- 2.0 U to 15.0 +/- 2.2 U 20 minutes after cysteamine administration (P less than 0.01), indicating that the effect was not due to the presence of gastrin. In vitro, cysteamine caused a nearly fourfold increase in cholecystokinin secretion compared with controls (63.1 +/- 4.9 vs. 15.2 +/- 3.7, respectively; P less than 0.001). In vivo immunoneutralization of circulating somatostatin with a high-affinity and high-capacity antiserum produced no significant change in the rate of amylase secretion. These results suggest that cholecystokinin secretion is tonically inhibited by somatostatin and that this effect is mediated by locally secreted (paracrine) but not by circulating somatostatin.

Amylases↗
PubMed1992

Regulation of transferrin, transferrin receptor, and ferritin genes in human duodenum.

To gain insights at the molecular level into the expression of iron-regulated genes [transferrin (Tf), transferrin receptor (TfR), and ferritin H and L subunits] in human intestinal areas relevant to iron absorption, the steady-state levels of specific messenger RNAs (mRNAs) were analyzed in gastric and duodenal samples obtained from 6 normal subjects, or 10 patients with anemia, 14 patients with untreated iron overload, and 8 patients with various gastrointestinal disorders. No Tf mRNA was detected in human gastroduodenal tissue, confirming earlier findings in the rat. In normal subjects, although higher levels of ferritin H- and L-subunit mRNAs were consistently found in duodenal than in gastric samples, no differences in the content of TfR transcripts were detected. However, a dramatic increase in TfR mRNA levels was specifically found in duodenal samples from subjects with mild iron deficiency but severe anemia. This response of the TfR gene is presumably secondary to decreased cellular iron content due to its accelerated transfer into the bloodstream, as also indicated by the low levels of ferritin subunit mRNAs found in the same tissue samples, and is not linked to faster growth rate of mucosal cells because no changes in duodenal expression of histone, a growth-related gene, were detected. In patients with secondary iron overload, a down-regulation of duodenal TfR gene expression and a concomitant increase in ferritin mRNA content were documented. On the contrary, a lack of TfR gene down-regulation and an abnormally low accumulation of ferritin H- and L-subunit mRNAs were detected in the duodenums of subjects with idiopathic hemochromatosis. Whether these molecular abnormalities in idiopathic hemochromatosis are relevant to the metabolic defect(s) of the disease is presently unknown.

Adult↗
PubMed1992

DNA patterns of Helicobacter pylori isolated from gastric antrum, body, and duodenum.

Biopsy specimens for culture of Helicobacter pylori were obtained from two different sites in the antrum, gastric body, and duodenal cap in 20 patients during endoscopic investigation of dyspepsia. H. pylori was identified in 64 isolates obtained from 15 of the 20 patients. Analysis of chromosomal DNA from these isolates of H. pylori showed that 13 of 15 patients harbored a single strain of H. pylori throughout their stomach and duodenum. Two differing H. pylori types were found in two patients. Unique DNA patterns were shown in each of the 15 patients. The genetic heterogeneity of H. pylori is unexplained but it could be of considerable value for epidemiological studies.

Biopsy↗
PubMed1992

Ontogeny of procholecystokinin maturation in rat duodenum, jejunum, and ileum.

Expression and processing of procholecystokinin (proCCK) in rat intestine during development were examined using sequence-specific immunoassays, cleavage with processing-like enzymes, and chromatography. Fetal proCCK concentrations were similar in duodenum, jejunum, and ileum, but the maturation to CCK followed different courses: duodenal CCK increased from 14 pmol/g in the fetus to 86 pmol/g 4 days after birth and then declined to 17 pmol/g in the adult. In jejunum, CCK varied from 34 pmol/g in the fetus to 127 pmol/g at day 7, decreased to 54 pmol/g at day 21, and increased again to 93 pmol/g in the adult. Ileal CCK decreased from 20 pmol/g in the fetus to 10 pmol/g postnatally. Whereas duodenal proCCK after birth matured completely to carboxyamidated CCK, jejunoileal proCCK matured only partially. Chromatography showed an increase of tyrosine-sulfation and proteolytic processing of N-terminal sequences. At day 7 jejunal cholecystokinin octapeptide (CCK-8) constituted only a minute fraction of the carboxyamidated CCK, of which less than half was sulfated. However, in the adult jejunum, CCK-8 constituted a significant fraction, which was completely sulfated. It is concluded that the CCK gene is well expressed at propeptide level in the fetal small intestine. Postpartum maturation of proCCK, however, is late and differs in the three parts of the small intestine. The belated maturation supports the hypothesis that factors other than CCK regulate pancreatic growth in fetal and neonatal life.

Amino Acid Sequence↗
PubMed1993

Stimulation of mucosal alkaline secretion in rat duodenum by dopamine and dopaminergic compounds.

BACKGROUND: The catechol-O-methyl-transferase (COMT) inhibitor nitecapone, which prevents mucosal degradation of dopamine, and some dopamine receptor agonists ameliorate gastroduodenal mucosal damage. Therefore, their effects on mucosal bicarbonate secretion were studied. METHODS: Duodenum just distal to the Brunner's glands area was cannulated in situ in anesthetized rats. Bicarbonate secretion into the luminal perfusate and transmucosal electrical potential difference (PD) were recorded. RESULTS: Intravenous dopamine (50 micrograms.kg-1 x h-1) increased bicarbonate secretion twofold, and a higher rate of infusion (250 micrograms.kg-1 x h-1) resulted in a further increase. Neither dose affected the PD. The dopamine D1 agonist SKF-38393 (10-50 micrograms/kg) and the COMT inhibitor nitecapone (50-500 micrograms/kg) caused dose-dependent increases in secretion, similar to that observed with dopamine. Domperidone, a peripherally acting dopamine antagonist, inhibited the stimulatory effects of SKF-38393 and nitecapone. Hexamethonium or the alpha-adrenoceptor antagonist phentolamine, in contrast, did not affect the response to nitecapone. Intracerebroventricular administration of nitecapone was without effect. CONCLUSIONS: A probable electroneutral component of duodenal mucosal bicarbonate secretion is stimulated via peripheral dopamine D1 receptors. This may contribute to the previously observed ulceroprotective actions of dopaminergic compounds.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1995

Acetazolamide inhibits basal and stimulated HCO3- secretion in the human proximal duodenum.

BACKGROUND/AIMS: Carbonic anhydrase activity plays a role in electrolyte transport in many tissues. This study examined the effect of the carbonic anhydrase inhibitor acetazolamide on human basal and prostaglandin E2- and acid-stimulated duodenal mucosal bicarbonate secretion and transmucosal electrical potential difference. METHODS: Seven healthy volunteers participated in four separate experiments. The variables included oral acetazolamide vs. control test and, as agonists of bicarbonate secretion, either luminal acidification or luminal prostaglandin E2. The proximal 4 cm of the duodenum (i.e., the duodenal bulb) was isolated between balloons as previously described and perfused with an HCO(3-)-containing (24 mmol/L) balanced electrolyte glucose-containing (10 mmol/L) solution. RESULTS: Acetazolamide treatment significantly decreased mean basal HCO3- secretion and basal transmucosal potential difference. After luminal acidification, duodenal mucosal bicarbonate increased significantly after both acetazolamide treatment (mean, 626; 95% CI, 91-1160 mumol.cm-1.h-1) and in the control tests (mean, 868; 95% CI, 652-1084 mumol.cm-1.h-1). However, acetazolamide treatment significantly decreased prostaglandin E2-stimulated HCO3- secretion from 461 (95% CI, 307-615) to 222 (95% CI, 121-324) mumol.cm-1.h-1. CONCLUSIONS: Duodenal mucosal carbonic anhydrase activity has an important function in the regulation of basal and prostaglandin E2-stimulated human duodenal mucosal bicarbonate transport.

Acetazolamide↗