SEARCH · PubMed Health

Results for “Intestinal Mucosa”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources

PubMed1981

[Biochemical and micromorphological investigation of lipids in small intestinal mucosa of patients with diabetes mellitus (author's transl)].

Hyperlipemia is a frequent finding in diabetes mellitus. As not only the liver, but intestinal mucosa as well synthesizes endogenous lipoproteins, we have investigated the small intestinal mucosal lipid content in 11 adult patients with juvenile onset diabetes and in 7 patients with maturity onset diabetes. Eleven non-diabetic patients served as controls. After a fasting period of 12-14 h blood was drawn for determination of glucose, lipids and glycosylated hemoglobin AI. Then several small bowel biopsies were performed by an hydraulic multiple biopsy tube or endoscopically and the specimens were processed immediately for further biochemical, histochemical and electronmicroscopical workup. Patients with juvenile and with maturity onset diabetes did not differ from controls with regard to serum lipids and to intestinal mucosal lipids determined biochemically. Surprisingly, patients with maturity onset diabetes exhibited a significantly (p less than 0,005) higher concentration of intestinal mucosal triglycerides than patients with juvenile onset diabetes. Fasting blood glucose and hemoglobin AI levels were slightly elevated in both groups of diabetic patients. Histochemically lipid particles were demonstrable in intestinal mucosa of diabetics and of controls with equal variability. The electronmicroscopical appearance of intestinal mucosa did not differ between diabetic patients and controls. Only in one patient with juvenile onset diabetes an accumulation of lipid particles within the cisternae of the Golgi apparatus was observed. In conclusion, neither biochemically, nor histochemically, nor electronmicroscopically an abnormal accumulation of lipids could be found in the small intestinal mucosa of patients with well controlled diabetes mellitus.

Adult↗

PubMed1994

Plasmenylethanolamine in human intestinal mucosa detected by an improved method for analysis of phospholipid.

Analysis of phospholipid and their fatty acid composition of human intestinal mucosa was performed by an method elaborated to analyze the limited amount of sample with 2-dimensional TLC followed by lipid-phosphorus determination. Using this method, plasmenylethanolamine was detected in human intestinal mucosa and accounted for about 7% of phospholipid in small and large intestinal mucosa. The amounts of polyunsaturated fatty acids of phosphatidylethanolamine were higher than those of other phosphoglycerides in intestinal mucosa, hence, inflammation-related eicosanoids may originate from ethanolamine containing phospholipid.

Arachidonic Acid↗

PubMed1982

Effect of spironolactone on bilirubin metabolism in rat liver and small intestinal mucosa.

In vitro and in vivo experimental models were designed for the study of the effect of spironolactone (SP) on bilirubin metabolism in rat liver and small intestinal mucosa. In vitro studies included uptake of bilirubin by liver slices and intestinal sheets, determination of glucuronyltransferase activity in mucosal homogenates, and the handling of bilirubin by the isolated perfused liver after bilirubin overload. In vitro studies were carried out to measure the plasma disappearance rate of bilirubin and to determine the extent of bilirubin conjugation and biliary excretion of the pigment infused intravenously. The results obtained suggested that the mechanisms involved in the uptake of bilirubin by tissues were not influenced by SP pretreatment. Glucuronyltransferase activity in the small intestinal mucosa was significantly induced by SP, as previously observed in rat liver. Isolated perfused livers from SP-treated rats, as well as treated living rats, exhibited a greater than normal capacity for bilirubin excretion into bile at the expense of bilirubin diglucuronide. Conjugated bilirubin in the small intestinal mucosa of rats infused with unconjugated pigment was also increased after SP pretreatment. The results favoured the conclusion that SP is an inducer of bilirubin conjugation in the livers as well as in extrahepatic tissues, such as the small intestinal mucosa.

Animals↗

PubMedDate not supplied

Portosystemic shunt prevents apoptosis in rat intestinal mucosa caused by total hepatic ischemia.

BACKGROUND: Prolonged splanchnic congestion due to total hepatic ischemia (THI) has been shown to induce damage to the intestinal mucosa. The present study was conducted to examine whether the protective effect of portosystemic shunt (PSS) can be seen on apoptosis of intestinal mucosa in a rat model of THI. METHODS: Adult male Wistar rats were divided into the following 3 groups: control group; the THI group underwent THI for 30 min, and the PSS group was subjected to THI for 30 min with PSS. Rats were killed after 1, 2, and 6 h of reperfusion. For each time point, levels of serum liver enzymes, intestinal morphology, malondialdehyde (MDA) contents and DNA fragmentation in intestinal tissue were determined. In addition, the 7-day survival rate was measured. RESULTS: The 7-day survival rate of THI group remained at 50%, whereas that of PSS group was significantly higher at 90% (p < 0.01). Serum AST and ALT levels of the THI and PSS groups rapidly increased after reperfusion, reaching peak values at 2 h. MDA levels after 1 and 2 h of reperfusion in the THI group were significantly increased as compared with the control group (p < 0.001). Increases in the percentage of fragmented DNA peaked 1 h after reperfusion in the THI group. PSS resulted in the reduction of DNA fragmentation and preserved the macroscopic and microscopic appearance of the intestinal mucosa. CONCLUSIONS: Splanchnic congestion due to portal occlusion increased apoptosis in the rat intestinal mucosa. PSS is very effective in counteracting the principal negative effects of total hepatic ischemia.

Alanine Transaminase↗

PubMed2000

Administration of bacterial lipopolysaccharide to rats induces heme oxygenase-1 and formation of antioxidant bilirubin in the intestinal mucosa.

Heme oxygenase (HO)-1, the rate-limiting enzyme in heme degradation, is induced by oxidative stress and its major end product, bilirubin, is a potent physiological antioxidant. We studied the induction of HO-1 and bilirubin production in intestinal mucosa using a rat model of sepsis. E. coli lipopolysaccharide was administered intraperitonealy to male Wistar rats and intestinal mucosa was harvested. Intestinal lipid peroxides increased significantly at 1 hr and peaked at 170% of the control value at 5 hr. GSH significantly decreased at 3 hr, reaching the nadir of 50% of the control value at 5 hr. HO-1 mRNA was maximally induced fivefold at 3 hr and HO-1 protein maximally increased to 10 times the control value at 7.5 hr. Both bilirubin and bilirubin oxidative metabolites were maximally increased at 10 hr, to 4.3 and 3.7 times the control value, respectively. These data suggest that oxidative stress in sepsis quickly induces HO-1 in intestinal mucosa and that subsequent production of bilirubin works as an antioxidant. The small intestinal mucosa is an active participant in the general response to sepsis.

Animals↗

PubMed2001

Suppression of apoptosis is responsible for increased thickness of intestinal mucosa in streptozotocin-induced diabetic rats.

Intestinal mucosal growth is a common, but uncharacterized, observation associated with diabetes mellitus. Epithelial homeostasis is balanced by regulation of cell proliferation and cell death. To determine the contribution of apoptosis to the overall maintenance of intestinal growth, we examined intestinal apoptosis in the well-characterized streptozotocin (STZ)-induced diabetes rat model. Rats were injected with STZ (75 mg/kg body weight), thereafter they were allowed free feeding or restricted feeding for 3 weeks. Food intake and intestinal mucosal height were evaluated. In a second experiment, additional groups of animals were injected with STZ and were fed ad libitum for 1 or 3 weeks. Ornithine decarboxylase (ODC) activity, ratio of fragmented DNA to total DNA, electrophoresis of fragmented DNA, and Western blot analysis of caspase-3 were examined. Food intake gradually increased in free-feeding rats after induction of diabetes. Intestinal mucosal height in free-feeding diabetic rats was approximately 25% longer than controls, but this increase in mucosal height was not observed in restricted-fed diabetic rats (25 g/d). ODC activity in intestinal mucosa in diabetic rats did not differ from that of control rats. Percent fragmented DNA of diabetic rats 1 week after STZ injection was significantly lower than that of control rats, and this decrease returned to the control level 3 weeks after STZ treatment. Active form of caspase-3 was attenuated 1 week after drug treatment. Attenuated effect of diabetic rats on intestinal apoptosis did not affect increased apoptosis after ischemia-reperfusion. Suppression of apoptosis in the early days of STZ-induced diabetes was responsible for the increased mucosal height in the small intestine in STZ-induced diabetic animals.

Animals↗

PubMed2003

Effects of antioxidative agents on apoptosis induced by ischaemia-reperfusion in rat intestinal mucosa.

BACKGROUND AND AIM: We have previously demonstrated that ischaemia-reperfusion induces apoptosis in the intestinal mucosa. To evaluate that reactive oxygen species enhanced intestinal apoptosis after ischaemia-reperfusion, we examined whether antioxidants reduced apoptosis. METHODS: Rats were infused through a duodenal tube with antioxidative agents, glutathione, rebamipide and dymethylsulfoxide during 2 h before an ischaemic insult. The superior mesenteric artery was occluded for 60 min, followed by 60 min reperfusion. Apoptosis was evaluated by percentage fragmented DNA (fragmented DNA/total DNA) and immunochemical staining. RESULTS: Increase in apoptosis in the intestinal mucosa after ischaemia-reperfusion was attenuated by intraduodenal infusion of antioxidative agents, but was not completely abolished. CONCLUSION: Scavenging effects of the antioxidative agents attenuated increases in intestinal apoptosis, indicating that oxidative stress after ischaemia-reperfusion plays an important role in induction of apoptosis in the intestinal mucosa.

Alanine↗

PubMedDate not supplied

[Study of hydrolase activity of rat small intestine mucosa with vitamin A deficiency].

The activity of amylase, alkaline phosphatase and lipase in the pancreas, in the mucosa and on the surface of small intestine (turned out segments) was studied for elucidating the effect of vitamin A deficiency on the synthesis of the studied enzymes and their translocation to the surface of glycocalix cell membranes. The activity of amylase is established to increase in the homogenate of the pancreas, intestine mucosa and on the surface of cell membranes. The activity of alkaline phosphatase and lipase in the homogenate of small intestine mucosa and in the pancreas lowers. The results obtained evidence for a disturbance in the intestine digestive function with vitamin A deficiency, the may be connected with the damage of the mucosa membrane structures as well as with a disturbance in the biosynthesis of the protein playing a decisive role in formation of secretory products in cells.

Alkaline Phosphatase↗

PubMed1972

Stages of uptake and incorporation of micellar palmitic acid by hamster proximal intestinal mucosa.

The stages of uptake and incorporation of micellar palmitic acid by hamster proximal intestinal mucosa were investigated by incubation of everted sacs at 4 degrees C and 37 degrees C for 2, 5, 10, and 15 min in a micellar solution (10 micro moles of [1-(14)C]palmitic acid, 10 micro moles of monoolein, and 100 micro moles of sodium taurodeoxycholate) and subsequent serial rinsing of the sacs in ice-cold solutions as follows: one 20-sec rinse in unlabeled micellar solution, five 1-min rinses in Krebs-Ringer buffer (0.15 m, pH 6.3), and ten 2-min rinses in 2.5% albumin solution. The fatty acid-solubilizing capacity of all the rinsing solutions was always in excess of the amounts of radioactive palmitic acid released during each rinse. Radioactivity was determined in the tissue homogenates, rinsing solutions, and serosal fluids. The results indicate that a significant proportion of radioactive palmitic acid taken up by the sacs during the short incubation was released into the rinsing solutions. Rinsing in Krebs-Ringer buffer resulted in release of 15.5 +/- 2.4% of the labeled fatty acid, and this fraction was independent of the temperature of incubation. In contrast, the amounts of palmitic acid released in albumin were significantly greater and were markedly dependent on the temperature of incubation; a total of 48.6 +/- 7.0% and 26.3 +/- 5.1% was released from sacs incubated at 4 degrees C and 37 degrees C, respectively. While the proportion of radioactive palmitic acid in the free fatty acid fraction of the tissue after the rinsing sequence remained reasonably constant regardless of the temperature and duration of incubation, the radioactivity of the esterified palmitic acid in the tissue was much greater in the sacs incubated at 37 degrees C and tended to increase linearly up to 10 min of incubation. A highly significant inverse relationship was found between the fraction of radioactive palmitic acid released by rinsing in albumin and the fraction of the label in the tissue esterified fatty acids. The results suggest that the initial uptake of micellar fatty acid by intestinal mucosa may involve reversible binding to superficial sites with at least two strengths of binding: a weak, temperature-independent binding which could be easily dissociated by rinsing in Krebs-Ringer buffer, and a stronger, temperature-dependent binding which could be dissociated by rinsing in albumin, but not in Krebs-Ringer buffer. Analogous binding of micellar palmitic acid occurred in a brush border preparation of proximal intestine which was devoid of any fatty acid esterifying activity. This suggested that the reversible binding of fatty acid by the intestinal mucosa may be a property of its superficial components, namely the glycocalyx or microvillous membranes, and that it may be independent of the esterifying capacity of the tissue.

Animals↗

PubMed1982

Bile acid uptake by isolated intestinal mucosa cells of guinea pig.

Isolated intestinal mucosa cells of the guinea pig were employed to study intestinal transport of bile acids. Chenodeoxycholate and lithocholate were rapidly taken up into jejunal and ileal cells by diffusion. Taurocholate and cholate however showed only a minor diffusion rate and were preferentially taken up by the ileal bile acid carrier. This uptake was saturable with an apparent Km of 231 microM and V of 7 nmol/mg protein per min for taurocholate; this bile acid was accumulated 90-fold. Its uptake was strongly inhibited by antimycin A, FCCP, ouabain or Na+ -deficiency in the medium. Sugars or amino acids did not interfere with uptake. Experimental conditions were optimized with regard to incubation medium, cell amount, cell age and length of preincubation. It is concluded that ileal cells of the guinea pig are superior to other experimental models for characterizing the ileal bile acid carrier, because they allow us to determine initial rates of uptake and have a very efficient energetic coupling.

Animals↗

PubMed2000

[Effects of different nutritional support routes on the intestinal mucosa mucosainjury and renovation in burned rats].

OBJECTIVE: To compare the effects of different nutritional support routes on the intestinal mucosa in burned rats. METHODS: Wistar rats inflicted with 30% TBSA full thickness burns were employed as the model and randomly divided into three groups: burn with enteral nutrition (EN), burn with parenteral nutrition (PN), and normal control (C). Solutions for intravenous and oral application with same volume, calorie, nitrogen and other nutrients were administered to rats in PN and EN groups, respectively. The plasma diamine oxidase (DAO) activity, the intestinal mucosa change of proliferating cell nuclear antigen (PCNA), of transmembrane electric potential difference (PD), of intestinal trefoil factor and their correlation analysis (ITF) were observed. RESULTS: Plasma DAO activity increased obviously and PD, PCNA values, ITF content were much lower in EN, PN groups than those in C group. The ITF content, the values of PD and PCNA in EN were much higher than those in PN group, while DAO activity in EN group was obviously lower than that in PN group. In addition, ITF content was significantly negatively correlated to plasma DAO activity, and obviously positively correlated to PCNA and PD values. It is suggested that intestinal mucosa injury was much more severe in PN group than that in EN group. CONCLUSION: Postburn intestine mucosa mucosal structural injury was related to the evident decrease of synthesis and secretion of ITF. Enteral nutrition might slow down the decrement of ITF, which could explain why EN was superior to PN in terms of decreasing intestinal mucosal injury and enhancing intestinal renovation.

Amine Oxidase (Copper-Containing)↗

PubMed2004

Binding of Vibrio anguillarum to neutral glycosphingolipids from intestinal mucosa of rainbow trout (Oncorhynchus mykiss).

To test whether glycosphingolipids (GSLs) on the intestinal mucosa of rainbow trout (Oncorhynchus mykiss) serve as a binding receptor for Vibrio anguillarum, we analyzed neutral GSLs from rainbow trout intestinal mucosa and investigated the binding of bacteria to neutral GSLs. Two kinds of neutral GSLs, designated N-1 and N-2, were identified on high-performance thin-layer chromatography (TLC) plates. In TLC immunostaining tests, V. anguillarum bound only to galactosylceramide (GalCer), lactosylceramide and N-1 having the same TLC mobility as GalCer, but neither to glucosylceramide nor to N-2. These results suggest that N-1 is GalCer (Gal beta 1-1Cer) and also that N-1 (GalCer) on rainbow trout intestinal mucosa act as a receptor for V. anguillarum.

Animals↗

PubMed1991

[Dehydrogenase activity in small intestine mucosa in experimental coccidiosis in suckling pigs].

The activities of 3-beta-hydroxybutyrate dehydrogenase (EC. 1.1.1.30.; HBD) and isocitrate dehydrogenase (EC. 1.1.1.41; ICD) were evaluated microdensitometrically in the mucosa of duodenum, jejunum and ileum of 19 conventional piglets infected on the first day after parturition (DAP) with oocysts of Eimeria debliecki coccidium (infection dose of 200,000 oocysts). The two investigated enzymes are deposited in mitochondria which are dispersed in the supra-, para- and infranuclear region of absorption cells (Fig. 1). The synthesis of the two dehydrogenases was investigated in the small intestine mucosa in the period of 1st to 10th day after infection (DAI). The HBD and ICD activities were also followed in the small intestine of four control conventional piglets at the age of 2-5 days (Tab. I). The two dehydrogenases could be characterized by a topographic gradient; it means that their activity was increasing in the small intestine mucosa through duodenum in an aboral direction. The ICD activity is higher in the intestinal mucosa of healthy piglets (Figs. 2 and 3), where its topic concentration was more marked while the HBD activity is dispersed in enterocytes (Fig. 4). In infected piglets the density of the two enzymes was demonstrated to decrease already in the starting period of experimental infection, and it reaches the lowest values for the first time on DAI 5-6 (Fig. 5, Tab. II), then on DAIs 9 (HBD; Fig. 6, graph 11)) or 8 (ICD, Fig. 7 and 10). In the period of experimental infection no statistically significant predisposition to the hypoactivity of target dehydrogenases nor its marked shift were observed. Somewhat rapid resumption of synthesis was demonstrated as soon as on DAI 8 in ICD (Fig. 8); its activity on DAI 10 in the intestinal mucosa corresponded to the 93% activity of this dehydrogenase recorded in the small intestine of control piglets. The density of HBD to the same day (DAI 10) reached in the intestinal mucosa of infected piglets the values making only 44.7% of those demonstrated in the intestinal mucosa of the control group of animals.

Animals↗

PubMed1989

Glutathione and its related enzymes in the small intestinal mucosa of rats: effects of starvation and diet.

Starvation for 24 h causes a striking fall in glutathione content from 3.19 +/- 0.27 to 1.88 +/- 0.14 (X +/- SEM) mumol/g tissue and of GGT activity from 31.75 +/- 4.17 to 19.49 +/- 3.13 (X +/- SEM) nmol/min/mg protein in the homogenate from whole mucosa of the upper small intestinal segments. This was associated with a significant increase in GSH-Px activity and the content of lipid peroxides (measured by the thiobarbituric assay). On semi-synthetic iron-supplemented diet the activities of GSH-T and GGT were significantly decreased as compared with crude diet. On semisynthetic iron-depleted diet GSH-T and GGT activities were further depressed, but this was accompanied with an additional depression of GSH, glutathione reductase (GSSG-R), and glutathione peroxidase (GSH-Px) activities and lipid peroxide concentrations. Food deprivation significantly lowers the mucosal GSH-content and could lead to a destabilization of this system presumably by increased oxidative stress. As compared to normal "crude" diet, semisynthetic diets and oral iron depletion have been shown to cause a depression of the intestinal GSH system. As a consequence of these effects, the resistance of the small intestinal mucosa toward exogeneous dietary toxins might be reduced.

Animals↗

PubMed1986

In vitro activation of adenylate cyclase of atrophic celiac intestinal mucosa by wheat gliadin-derived peptides.

In order to demonstrate that gliadin peptides may interact with cell membranes of celiac small intestinal mucosa, the capacity of these peptides to activate the cell membrane enzyme adenylate cyclase was tested. The addition of peptides from bread wheat purified A-gliadin and whole gliadin (proteins that are toxic for celiac patients) enhanced the adenylate cyclase activity of crude cell membrane preparations obtained from atrophic small intestinal mucosa of celiac patients. No activation of adenylate cyclase of this tissue was observed with peptides from proteins nontoxic for celiac patients (bread wheat albumin and maize prolamin). Gliadin peptides did not activate adenylate cyclase of morphologically normal small intestinal mucosa from normal subjects or from celiac patients in remission. These results, therefore, suggest that peptides from bread wheat gliadin may interact with cell membrane of atrophic small intestinal mucosa of celiac patients.

Adenylyl Cyclases↗

PubMed1978

Separation and purification of phospholipid exchange proteins in rat small intestinal mucosa.

The cytosol fraction of rat small intestinal mucosa stimulated the transfer of [32P]phosphatidylcholine and [32P]phosphatidylinositol from donor liposomes to acceptor liposomes. The proteins which catalyzed the exchanges were separated into three fractions by gel filtration on a Sephadex G-75 column and chromatography on DEAE-cellulose and CM-cellulose. One of the fractions was purified 340-fold and stimulated phosphatidylcholine exchange but not phosphatidylinositol exchange. The other two fractions were active in the stimulation of phosphatidylcholine exchange as well as phosphatidylinositol exchange. These two fractions were purified 35-fold and 44-fold over the cytosol fraction with respect to the phosphatidylinositol exchange activity.

Animals↗

PubMed1975

Effects of diets containing dried whey on the lactase activity of the small intestinal mucosa and the contents of the small intestine and cecum of the pig.

Two studies were conducted to establish the effects of dietary lactose supplied from dried whey on the lactase activity in the contents of the small intestine and cecum as well as the mucosa of the small intestine. In the first study, feeding 0, 10, 25, or 40% dried whey for 120 days did not alter the mucosal lactase specific activity (mumoles galactose released/mg protein) in the duodenum, upper jejunum, or lower ileum. In the second study, total lactase activity in the small intestine was estimated from the total activity found in 10-cm segments of each meter of small intestine. Feeding a diet containing 40% whey continuously from weaning at 5 weeks of age or from 12 weeks of age did not alter the total lactase activity of pigs killed at 21 weeks of age. Dietary lactose tended to increase the lactase activity in the contents of the cecum and small intestine, but the increases were not always statistically significant. In the second study, Chester White pigs had approximately threefold greater mucosal lactase activities than that of Hampshires. These two breeds may be suitable models for detailed studies into the relationships between lactase deficiency and lactose intolerance.

Animals↗

PubMed1984

Isolation and characterization of pteroylpolyglutamate hydrolase from rat intestinal mucosa.

Pteroylpolyglutamate hydrolase was isolated from rat intestinal mucosa and purified with the aid of affinity chromatography. The affinity ligand was poly-gamma-glutamic acid (Mr approximately 12,000) derived from Bacillus subtilis. The specific enzymatic activity was increased 2,000-fold over the 100,000 X g supernatant of the mucosal homogenate with a yield of 20%. Sephadex G-200 gel filtration yielded an estimated molecular mass of 80,000 daltons. The isoelectric point was pH 8.2. The pH optimum in acetate buffer containing 1 mM zinc was 4.5. The KM values for pteroylheptaglutamate and pteroyltriglutamate were 0.21 and 0.67 microM, respectively. Polyanionic compounds, poly-gamma-glutamic acid, dextran sulfate, and heparin were noncompetitive inhibitors. Studies of the time course of hydrolysis of synthetic [3H]pteroylheptaglutamate by three separate techniques demonstrated the appearance of [3H]pteroylmonoglutamate, synchronous with substrate cleavage. Intermediate pteroyloligoglutamates were not detected. An endopeptidase-like mode of hydrolysis was further established by identification of a hexaglutamyl peptide as the other reaction product.

Animals↗