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PubMed1989

Effect of age on calcium uptake in isolated duodenum cells: role of 1,25-dihydroxyvitamin D3.

Uptake of Ca2+ in cells isolated from rat duodenum declined in the senescent rats. This age-related change was not due to an alteration in the rate of Ca2+ efflux or in the size of the cell. The decrease appeared specific, as alpha-methyl glucoside uptake was not altered. Cell population, as monitored by sucrase activity for villus cells, was not different between duodenal cells isolated from 6- and 24-month-old rats. Kinetic analysis shows the Vmax, the apparent maximum uptake capacity, decreased in the cells from senescent rats whereas the Km, the apparent affinity to Ca2+, was unchanged. Serum levels of 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] were determined as a function of age; the levels of 25OHD were not significantly different in 3-, 6-, 12-, and 24-month-old rats. On the other hand, serum 1,25-(OH)2D decreased throughout the age range studied. Since duodenal Ca2+ uptake is closely regulated by 1,25-(OH)2D3, we tested the hypothesis that low serum 1,25-(OH)2D in the senescent rats may have contributed to the decline in duodenal Ca2+ uptake. In vivo administration of 1,25-(OH)2D3 to senescent rats significantly enhanced Ca2+ uptake activity in the isolated duodenal cells. After 1,25-(OH)2D3 treatment, Ca2+ uptake activity in cells isolated from senescent rats was only slightly less than that in cells from adult rats. We conclude that duodenal Ca2+ uptake declined in the senescent rats, and this age-related change was most likely due to the low serum level of 1,25-(OH)2D and not the result of a decrease in any duodenal response to 1,25-(OH)2D3.

Aging↗
PubMed1996

PDX-1 is required for pancreatic outgrowth and differentiation of the rostral duodenum.

It has been proposed that the Xenopus homeobox gene, XlHbox8, is involved in endodermal differentiation during pancreatic and duodenal development (Wright, C.V.E., Schnegelsberg, P. and De Robertis, E.M. (1988). Development 105, 787-794). To test this hypothesis directly, gene targeting was used to make two different null mutations in the mouse XlHbox8 homolog, pdx-1. In the first, the second pdx-1 exon, including the homeobox, was replaced by a neomycin resistance cassette. In the second, a lacZ reporter was fused in-frame with the N terminus of PDX-1, replacing most of the homeodomain. Neonatal pdx-1 -/- mice are apancreatic, in confirmation of previous reports (Jonsson, J., Carlsson, L., Edlund, T. and Edlund, H. (1994). Nature 371, 606-609). However, the pancreatic buds do form in homozygous mutants, and the dorsal bud undergoes limited proliferation and outgrowth to form a small, irregularly branched, ductular tree. This outgrowth does not contain insulin or amylase-positive cells, but glucagon-expressing cells are found. The rostral duodenum shows a local absence of the normal columnar epithelial lining, villi, and Brunner's glands, which are replaced by a GLUT2-positive cuboidal epithelium resembling the bile duct lining. Just distal of the abnormal epithelium, the numbers of enteroendocrine cells in the villi are greatly reduced. The PDX-1/beta-galactosidase fusion allele is expressed in pancreatic and duodenal cells in the absence of functional PDX-1, with expression continuing into perinatal stages with similar boundaries and expression levels. These results offer additional insight into the role of pdx-1 in the determination and differentiation of the posterior foregut, particularly regarding the proliferation and differentiation of the pancreatic progenitors.

Animals↗
PubMed1986

Development of the enteric nervous system in chick embryonic duodenum in terms of the distribution of tubulin.

An immunohistochemical method that uses anti-tubulin was utilized to observe the development of the enteric nervous system in chick embryonic duodenum. Neural crest cells, and enteric neuroblasts, or enteric ganglia, which derive from neural crest cells were clearly shown as sharp immunoreactive regions of tubulin. The distributions of enteric neuroblasts and enteric ganglia in chick duodena were in agreement with results of previous reports in which different techniques were used. The initial stage at which cells of neural crest origin were present in the duodenal walls (4-day-old embryos) was earlier than the initial stage (about 6-day-old embryos) reported earlier. This was verified by transmission electron microscopy. Also, the tubulin that is a component of the enteric nervous system was shown to be stable at a low temperature. This tubulin-immunostaining method provides a useful histochemical technique with which to study the development of the enteric ganglion and the function of tubulin as a component of the enteric nervous system.

Animals↗
PubMed1990

[Bicarbonate secretion in the mucosal defensive mechanism of the duodenum. Acid neutralization with HCO3- in the lumen and mucus gel].

Bicarbonate secretion from the surface epithelial cells in the duodenum is an active process depending on tissue metabolism and blood flow, and regulated by humoral and neuronal factors as well as endogenous prostaglandins (PGs). The duodenal mucosa has been also able to respond luminal acid by a significant rise in alkaline secretion, mediated mainly by PGs, and the impairment of this process is involved in the pathogenic mechanism of various duodenal ulcer models. The mechanism of mucosal protection by HCO3- secretion is two ways: one is neutralization of luminal acid, and the other the establishment of pH gradient in the mucus gel with the aid of the physicochemical property of mucus. Although the majority of H+ is neutralized by secreted HCO3- in the lumen and mucus gel, the ultimate mucosal protection is ensured by removal of back-diffused H+ through intramucosal neutralization with HCO3- and translocation by blood flow. Thus, HCO3- secretion in collaboration with mucus plays an important role as the first line of defense (pre-epithelial barrier) in the duodenal mucosal protection.

Animals↗
PubMed1977

Depressive effect of epinephrine mediated via adrenergic beta-receptor in isolated rat colon and duodenum.

Differences in sensitivity to catecholamines between colon and duodenum were examined in tissues from the rat, monitoring the depressive effect of catecholamines on contractile response to acetylcholine (ACh). The sensitivity of colonic tissue to ACh was higher than that of duodenal. Epinephrine (Ep, 10(-7) g/ml) depressed the contractile response to ACh in the colonic tissue, but not in the duodenal. The depressive effect of Ep on the contractile response to ACh is attributed to the stimulation of adrenergic beta-receptors in the colonic tissue as the depression disappeared by pretreatment with propranolol (10(-6) g/ml). There was no difference on the depressive effect of papaverine on the contractile response to ACh, except when low concentrations were used. Dibutyryl cyclic AMP (10(-4) g/ml) depressed the contractile responses of both tissues to ACh. After treatment with Ep (10(-7) g/ml), cyclic AMP content was increased in the colonic tissue but not in the duodenal. However, papaverine (3 X 10(-6 g/ml) and a higher dose of Ep(10(-6) g/ml) increased cyclic AMP content in both tissues. The increase of cyclic AMP and the decrease of tension caused by Ep were not correlated in these tissues. However, a positive correlation was observed between the depressive effect of Ep on the contractile response to ACh and the increase of cyclic AMP content in these tissues.

Acetylcholine↗
PubMed1983

Studies on the site of action of neurotropin in experiments on denervation-supersensitivity of the duodenum and vas deferens of rats and mice.

In order to clarify to a greater extent its action on peripheral nerves, various experiments were conducted using denervated animals to determine the effects of the nervous sedative, Neurotropin (NSP, containing many types of polysaccharides), on the site considered to be the periphery of autonomic nerves and the central nervous system. The increase in response to ACh due to bilateral cardiac vagotomy was significantly inhibited by a daily administration of NSP, but the increase in the response to noradrenaline (NA) due to celiac sympathectomy was hardly affected by this administration. The supersensitivity to the muscarinic action of ACh or methacholine of a denervated rat vas deferens, owing to ablation of the serous membrane, was significantly inhibited by the daily administrations of NSP. However, supersensitivity to NA was hardly affected. NSP never had any effect on the increase in the NA response of the duodenum and vas deferens isolated from mice given 6-hydroxydopamine, an adrenergic degenerator. Thus, an inhibitory action of NSP on denervation-supersensitivity is conceivably exerted on the parasympathetic nerves, rather than on the sympathetic nerves, and on a muscarinic receptor site, instead of a nicotinic site.

Acetylcholine↗
PubMed1986

Changes of total acetylcholine content and the activity of related enzymes in SART (repeated cold)-stressed rat brain and duodenum.

In SART-stressed rats regarded as pathologically diseased model animals with vagotonic-type autonomic imbalance, a decrease of total acetylcholine (T-ACh) content and enhancements of choline acetyltransferase (CAT) and acetylcholinesterase (AChE) activities were recognized in the basal ganglia and hypothalamus. In contrast, in the duodenum, an increase in T-ACh content and a decrease in AChE activity were found, while CAT activity showed no change. These findings suggest that in both brain areas of basal ganglia and hypothalamus in SART-stressed rats, ACh neurons may be activated.

Acetylcholine↗
PubMed1987

Impairment of acid-neutralizing capacity and lesion formation in the rat duodenum during hemorrhagic shock: comparative study with indomethacin.

The effects of hemorrhagic shock (HE) on duodenal pH, acid-neutralizing capacity and mucosal tolerance to acid were investigated in anesthetized rats, and they were compared with those of indomethacin. HE was performed by bleeding from the carotid artery to reduce arterial blood pressure to about 55 mmHg (3 ml of bleeding per 200 g of body weight), and indomethacin was given s.c. in a dose of 5 mg/kg. Duodenal pH was determined in the outflow from the proximal duodenum (1.7 cm) which was perfused with 10(-4) M HCl, and acid-neutralizing capacity was measured by back-titration of the perfusate to pH 4.0 with 10 mM HCl. Under these conditions, duodenal pH was kept at around 6.0 as the result of neutralization in the loop (approximately 8 microEq/hr). Both HE and indomethacin significantly decreased the pH and acid-neutralizing capacity. Administration of 16,16-dimethyl prostaglandin E2 (16-dmPGE2: 30 micrograms/kg, s.c.) significantly increased both pH and acid-neutralizing capacity in normal and indomethacin-treated rats, but failed to affect these parameters in rats under HE conditions. When the duodenal loop was perfused with 50 mM HCl for 1.5 hr, both HE and indomethacin induced extensive damage in the mucosa. Pretreatment with 16-dmPGE2 significantly reduced the formation of duodenal lesions induced by indomethacin but not by HE. These results suggest that HE as well as indomethacin impaired duodenal acid-neutralizing capacity to reduce the tolerance to acid of the mucosa. The deleterious effects of HE on the mucosa may be mainly due to a decreased mucosal blood flow, but not due to a deficiency of endogenous prostaglandins.

Acid-Base Equilibrium↗
PubMed1989

Histamine-induced villous damage in the rat duodenum.

A single s.c. administration of histamine dose-dependently (5-20 mg/kg) induced villous damage of the proximal duodenum in 24-hr fasting rats. Time course studies indicate that histamine (20 mg/kg) induced severe exfoliation of the epithelial cells at the villous tips of the duodenal mucosa 0.5 hr after administration. The damage, however, tended to heal with time, and recovery was nearly complete 8 hr later. This villous damage was significantly inhibited by pretreatment with sodium bicarbonate given orally or cimetidine, omeprazole and NC-1300 given subcutaneously. Histamine (20 mg/kg) significantly stimulated gastric acid secretion and lowered the intraduodenal pH for 1 hr. Gastric content was significantly greater than that in the control group for 1 hr after histamine administration, probably due to stimulated gastric secretion and delayed emptying. We conclude that a single administration of histamine induces microscopical duodenal damage by stimulation of gastric acid secretion, but the damage heals with time, probably as a result of the short periods of acid stimulation and delayed emptying.

Animals↗
PubMed1990

Stimulation by prostaglandin E2 of alkaline secretion in the rat duodenum: comparative study with hypertonic NaCl.

Possible involvement of increased mucosal permeability in the stimulation by prostaglandin E2 (PGE2) of duodenal HCO3- secretion was investigated in rats. PGE2 (0.3, 1 mg/kg, s.c.) dose-dependently increased HCO3- secretion in the duodenum with a significant elevation of transmucosal potential difference (PD); the PD was increased from -4.5 +/- 0.3 mV to -10.0 +/- 1.5 mV (mucosa negative) at 1 mg/kg. These responses caused by PGE2 were abolished by sacrificing the animals with saturated KCl (i.v.). Although a significant increase of HCO3- output was observed after exposure of the mucosa to 1 M NaCl (0.5 ml), this response was accompanied by a significant reduction of PD and was not abolished after KCl injection. The mucosal permeability determined by Evans blue (1%, i.v.) was not affected by PGE2, while 1 M NaCl markedly elevated the amount of extravasated dye in both the luminal content and the mucosa. Stimulation of HCO3- output by PGE2 was significantly mitigated by ouabain (3 mg/kg, s.c.) or prior exposure of the mucosa to 1 M NaCl. These results suggest that stimulation by PGE2 of duodenal HCO3- secretion is not simply due to the increased mucosal permeability, but depends rather on both the Na/K ATPase activity and the intact perfusion of the organ. The HCO3- response as induced by 1 M NaCl may result from the increased permeability and is accompanied by a marked reduction of PD.

Animals↗
PubMed2006

Distribution of the cystine/glutamate antiporter system xc- in the brain, kidney, and duodenum.

System x(c)(-), one of the main transporters responsible for central nervous system cystine transport, is comprised of two subunits, xCT and 4F2hc. The transport of cystine into cells is rate limiting for glutathione synthesis, the major antioxidant and redox cofactor in the brain. Alterations in glutathione status are prevalent in numerous neurodegenerative diseases, emphasizing the importance of proper cystine homeostasis. However, the distribution of xCT and 4F2hc within the brain and other areas has not been described. Using specific antibodies, both xCT and 4F2hc were localized predominantly to neurons in the mouse and human brain, but some glial cells were labeled as well. Border areas between the brain proper and periphery including the vascular endothelial cells, ependymal cells, choroid plexus, and leptomeninges were also highly positive for the system x(c)(-) components. xCT and 4F2hc are also present at the brush border membranes in the kidney and duodenum. These results indicate that system x(c)(-) is likely to play a role in cellular health throughout many areas of the brain as well as other organs by maintaining intracellular cystine levels, thereby resulting in low levels of oxidative stress.

Amino Acid Transport System y+↗
PubMed2002

Invertase, maltase, lactase, and peroxidase activities in duodenum of BB rats.

The development of immune-mediated diabetes in BB rats may involve a defect of the gastrointestinal tract (GI), as suggested by increased gut permeability. This study aimed at measuring invertase, maltase, lactase, and peroxidase activities in the duodenum of diabetesprone BioBreeding (BBdp) rats and control BioBreeding rats (BBc) given free access to NIH-07 diet up to the time of killing at 60 66 d of age. After washing the entire small intestine, the duodenal mucosa was scraped off in the first 5-cm segment from the pylorus and frozen in distilled water. Invertase, maltase, and lactase activities were measured by monitoring the conversion of [U-(14)C]sucrose, [U-(14)C]maltose, and [D-[1-(14)C]glucose] lactose to radioactive hexoses, which were phosphorylated in the presence of adenosine triphosphatase and yeast hexokinase and then separated from their precursor by ion-exchange chromatography. Peroxidase activity was measured by a spectrophotometric procedure. In the BBdp rats, the activity of invertase, maltase, and lactase averaged, respectively, 70.2 +/- 4.4, 81.2 +/- 4.3, and 75.7 +/- 4.1% (n = 16 and p < 0.001 in all cases) of the control values found in BBc rats of the same sex. Inversely, after exclusion of two female BBc rats with abnormally high plasma D-glucose concentration, the activity of peroxidase in the BBdp rats averaged 157.4 +/- 20.0% (n = 16; p < 0.02) of the mean control value recorded in BBc rats of the same sex (100.0 +/- 9.3%; n = 14). These findings are compatible with the view that a proinflammatory state of the GI associated with compromise function may precede the occurrence of pancreatic insulitis in BBdp rats and, possibly, human subjects with type 1 diabetes.

Animals↗
PubMed2005

Ferroportin is expressed on the mucous granule membrane of a subpopulation of goblet cells in the duodenum of the rat.

Ferroportin is a basolateral transporter involved in the release of iron from cells. In addition to expression on the basolateral membrane of enterocytes, ferroportin is also seen on the microvillus membrane. This led us to consider that ferroportin might be expressed by other cells of the intestine where it contributes to iron metabolism. Ferroportin gene and protein expression in rat duodenum was studied by in situ hybridisation and immunohistochemistry, respectively in rats with different efficiencies of iron absorption. Ferroportin mRNA localised to enterocytes of the villus only. Ferroportin was demonstrated in enterocytes and in 30% of goblet cells. In goblet cells it localised to the mucous granule membrane. In iron-loaded intestine some goblet cells contained iron suggesting that ferroportin may transport iron into the mucous granule where it would be lost during discharge of mucous. The finding of ferroportin in iron deficient goblet cells also suggests an additional role to iron excretion.

Animals↗
PubMed1986

Low-sodium resistant non-adrenergic inhibitory neurotransmission in the guinea-pig duodenum.

The evoked inhibitory potentials (i.p.s) in the longitudinal smooth muscle cells of the guinea-pig duodenum were recorded intracellularly. The i.p.s were not blocked by adrenergic blocking agents, guanethidine (10(-6) g/ml), propranolol (10(-6) g/ml) and phentolamine (10(-6) g/ml), and atropine (10(-6) g/ml). Tetrodotoxin (10(-7)-10(-6) g/ml) abolished the non-adrenergic non-cholinergic i.p.s evoked by single or repeated stimulation without changes in the resting membrane potential of the longitudinal smooth muscle. In the presence of atropine (10(-6) g/ml), acetylcholine (5 X 10(-9)-7 X 10(-7) g/ml) had no effect on the amplitude of the i.p.s d-tubocurarine (2 X 10(-5) g/ml) reduced the amplitude of the i.p.s and produced a small depolarization in the muscle membrane. The longitudinal muscle membrane was slightly depolarized by Li-solution and the i.p.s could be evoked in the Li-solution for a long period, accompanying with the slight decrease in the amplitude of the i.p.s. In the choline-solution, the depolarization of the muscle membrane and the slight increase in the amplitude of the i.p.s were obtained. The i.p.s were abolished in the Ca2+-free choline-solution. In the sucrose-solution, the decrease of the resting membrane potential of the longitudinal smooth muscle was observed and the amplitude of the i.p.s was gradually reduced during the perfusion of the sucrose-solution. Chloride deficiency had no considerable effect on the amplitude of i.p.s. The results obtained suggest that the non-adrenergic non-cholinergic inhibitory neurotransmission is low-sodium resistant and the excitation-secretion coupling in the non-adrenergic non-cholinergic inhibitory nerves is mainly dependent on the external calcium ions but not sodium ions.

Acetylcholine↗
PubMed1989

Spread of the single spike activity in the myenteric plexus of the guinea-pig duodenum.

The spontaneous single spikes in the myenteric plexus of the guinea-pig duodenum were recorded extracellularly. The myenteric plexus neurones in the cardiac region of the stomach also exhibited the spontaneous single spike activity. The frequency of these spikes was at low level. By the treatment with a high Mg and Ca-free Krebs solution, the single spikes were abolished. The generation of the single spikes was also inhibited by d-tubocurarine. These results suggest the presence of nicotinic neurotransmission in the myenteric plexus. The field stimulation could not evoke the single spike activity. The single spike activities of the myenteric plexus neurones were recorded by two electrodes situated in a ganglion or at two different ganglia. The simultaneous recordings by two different spots showed that there were corresponded and non-corresponded spikes. The former may be due to the conduction of excitation. The values of the correspondence ratio were calculated and the values ranged from 39.1% to 69.6% in a ganglion and ranged from 55.2% to 94.2% in different ganglia. The single spikes may spread over 10 mm in a longitudinal direction. These results suggest that the intra- and interganglionic interactions appear within the myenteric plexus and ganglia are interconnected into a functional integrative circuitry.

Action Potentials↗
PubMed1999

Number and size of myenteric neurons of the duodenum of adult rats with acute diabetes.

This study had as its purpose to assess the effects of acute diabetes induced by streptozotocin (35 mg/kg body weight) on the number and size of the myenteric neurons of the duodenum of adult rats considering equally the antimesenteric and intermediate regions of the intestinal circumference. Experimental period extended for a week. Neuronal counts were carried out on the same number of fields of both regions of the duodenal circumference and measurements of neuronal and nuclear areas on equal numbers of cells. Number and size of the myenteric neurons stained with Giemsa were not significantly different between groups. On the other hand, the proportion of NADH-positive neurons increased from 18.54% on the controls to 39.33% on the diabetics. The authors discuss that this increased reactivity probably results from a greater NADH/NAD+ ratio, described in many tissues of diabetic animals, which has consequences on the modulation of the enzymes that use these cofactors and whose activity is detected by the NADH-diaphorase technique.

Acute Disease↗
PubMed1979

Trophic effect of tetragastrin on the stomach, duodenum and pancreas in rats.

Subcutaneous injections of a large dose of tetragastrin (2 mg/day) into a rat for 4 weeks caused hypertrophy of parietal cells of the stomach, intestinal glandular cells of the duodenum, and pancreatic acinar cells. Ths histometrical analysis revealed that these trophic effects of tetragastrin were produced in varying degrees in different sites.

Animals↗
PubMed1981

Mucosal secretion of the duodenum in peptic ulcer disease.

Mucosal secretin content of the duodenum was measured using bioptic specimen in healthy controls and patients of peptic ulcer. Immunoreactive secretin in the duodenal mucosa was found greater in healthy controls (7.73 +/- 2.71 ng/mg dry wt., mean +/- S.D.) than in gastric ulcer patients (5.76 +/- 3.51 ng/mg dry wt.) and duodenal ulcer patients (5.54 +/- 2.48 ng/mg dry wt.), but the difference was not significant. There was no significant relationship between mucosal secretin and acid output in these patients.

Adult↗