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At least 199 records · Page 11Linked to original sources
PubMed1996

Parenteral versus enteral nutrition: morphological changes in human adult intestinal mucosa.

In animal experiments total parenteral nutrition induces an atrophy of the small intestinal mucosa. In humans morphological data are few and controversial. Therefore, the aim of this study was to investigate the effect of parenteral nutrition on the intestinal mucosa of human adults. For this purpose samples of the proximal jejunum of a) patients with chronic pancreatitis receiving total parenteral nutrition as presurgical treatment, b) enterally nourished patients without (controls) and c) with chronic pancreatitis were compared using light and scanning electron microscopy. Statistical differences were assessed applying computer-assisted morphometry. The results demonstrated that the thickness of the jejunal mucosa decreased already in enterally nourished patients with chronic pancreatitis. However, after total parenteral nutrition the decrease (atrophy) was enhanced due to a strong reduction in villus height albeit the crypt length increased. In addition, scanning electron microscopy revealed distinctive changes in mucosal surface pattern, whereby finger-like villi were replaced by leaf-like villi and by long, winding bifurcating ridges. Cell shedding was absent. In conclusion, total parenteral nutrition in humans induces 1) an atrophy and 2) a remodelling of the intestinal mucosa (epithelium and lamina propria) with a decrease in the absorbing surface. These alterations involve both cell proliferation and cell shedding. The response of the mucosa to parenteral nutrition is immediate and the effect of the treatment in bringing about morphological alterations is more efficacious at the beginning than in the successive period. The basic disorder (chronic pancreatitis) of the patients nourished parenterally contributes to mucosal atrophy, but not to remodelling.

Adult↗
PubMed1992

Presence and properties of acyl coenzyme A synthetase for medium-chain fatty acids in rat intestinal mucosa.

A system was developed for assay of acyl coenzyme A (acyl CoA) activity on medium-chain fatty acids in rat intestinal mucosa. Using this system, we compared the characteristics of octanoyl (C8:0) CoA synthetase activity and palmitoyl (C16:0) CoA synthetase activity. Palmitoyl CoA synthetase activity as a function of palmitate concentration followed Michaelis-Menten kinetics, but octanoyl CoA synthetase activity as a function of octanoate concentration showed a biphasic reaction curve. The distributions of octanoyl CoA synthetase activity and palmitoyl CoA synthetase activity along the gastrointestinal tract were similar, both activities being present mainly in the middle portion of the small intestine. Incubation of octanoate with a homogenate of intestinal mucosa revealed that octnoate, like palmitate, is incorporated into phospholipids and triglycerides after its CoA activation. Oral administration of medium chain triglycerides induced a nearly 2-fold increase in octanoyl CoA synthetase activity in rat intestinal mucosa, whereas oral administration of long chain triglycerides did not affect the palmitoyl CoA synthetase activity. These results indicate that acyl CoA synthetase for medium-chain fatty acids in rat intestinal mucosa plays a key role in the utilization of medium-chain fatty acids for lipid synthesis, and that it is regulated in a different manner from acyl CoA synthetase for long-chain fatty acids.

Adenosine Triphosphate↗
PubMed1985

Ornithine transcarbamylase and disaccharidase activities in damaged intestinal mucosa of children--diagnosis of hereditary ornithine transcarbamylase deficiency in mucosa.

Ornithine transcarbamylase (OTC) and disaccharidase activities were measured in the intestinal mucosa from 182 children. Sixty-nine had normal mucosa, whereas the others had different degrees of mucosal damage. Brush border disaccharidases are significantly decreased in all degrees of villous atrophy. In contrast, OTC is not affected in moderate atrophy and only slightly decreased in severe atrophy. Consequently, the OTC-to-lactase ratio increases with the degree of atrophy and permits discrimination between normal and damaged mucosa. The assay of OTC activity in intestinal mucosa for the diagnosis of hereditary deficiency in male hemizygote patients generally provides nonambiguously low results, whereas in heterozygote females the amount of residual activity is in the range of the results found in damaged mucosa.

Child↗
PubMed1986

Gluconeogenesis from lactate in the small intestinal mucosa of suckling rats.

Glucose formation from uniformly labeled 14C-lactate was studied in the small intestinal mucosa of rats and rabbits. It was found to occur in infant but not in adult (weaned) animals and to be increased by the presence of dibutyryl cyclic AMP or tetradecyl glycidic acid. Similarly the formation of glyceride glycerol was enhanced by tetradecyl glycidic acid but not by glucagon or cyclic AMP. The glycogen content of the intestinal mucosa was always low, but increased significantly at the time of weaning. It is suggested that gluconeogenesis occurs in the small intestinal mucosa of infant rodents to supply glucose to the muscular part of the small intestine.

Aging↗
PubMed2001

Mycobacterium avium invades the intestinal mucosa primarily by interacting with enterocytes.

Previous studies have demonstrated that Mycobacterium avium can invade intestinal epithelial cells both in vitro and in vivo. When given to mice orally, M. avium preferentially interacts with the intestinal mucosa at the terminal ileum. We evaluated the mechanism(s) of M. avium binding and invasion of the intestinal mucosa using three different systems: (i) electron microscopy following administration of M. avium into an intestinal loop in mice, (ii) quantitative comparison of the bacterial load in Peyer's patch areas of the terminal ileum versus areas that do not contain Peyer's patches, and (iii) investigation of the ability of M. avium to cause disseminated infection following oral administration using B-cell-deficient mice, lacking Peyer's patches, in comparison with C57BL/6 black mice. By all approaches, M. avium was found to invade the intestinal mucosa by interacting primarily with enterocytes and not with M cells.

Animals↗
PubMed1985

Exogenous uridine diphosphoglucuronic acid breakdown in rat small intestinal mucosa preparations. Effect of other nucleotides.

Breakdown of UDPGA incorporated in a mixture containing rat liver or small intestinal mucosa preparations was investigated in the absence of exogenous sugar acceptor. A rapid UDPGA breakdown was seen with intestinal mucosa preparations in such a way that UDPGA decreased to about 1% or less of the initial value after 15 min of incubation. It was estimated that 60 to 70% of total products derived from UDPGA at the end of the incubation with intestinal tissue was in the form of uridine (90%) and uracil (10%). The addition of UDPG, ATP or UDP-N-acetylglucosamine protected UDPGA against degradation by tissue. The results indicated that care must be taken during the incubation of exogenous UDPGA for glucuronyltransferase assay in the intestinal mucosa due to the predominance in this tissue of enzyme systems involved in UDPGA breakdown.

Animals↗
PubMed1975

Triacylglycerol biosynthesis in everted sacs of rat intestinal mucosa.

The molecular specificity of the biosynthesis of triacylglycerols by rat intestinal mucosa was examined by means of radioactive and mass tracers, and thin-layer chromatography with silver nitrate and gas-liquid chromatography with radioactivity monitoring. Bile salt micelles of alternately labeled monoacylglycerols and free fatty acids were incubated with everted sacs of intestinal mucosa for various periods of time and the triacylglycerols isolated by solvent extraction and thin-layer chromatography. Analyses of the molecular species of the triacylglycerols labeled from monoacylglycerols showed that the 2-monoacylglycerol pathway was responsible for the biosynthesis of a maximum of 90% and the X-1-monoacylglycerol pathway for about 10% of the total radioactive triacylglycerols. Detailed analyses of the molecular species of triacylglycerols labeled fro free fatty acids showed that the phosphatidic acid pathway contributed a minimum of 20-30% of the total labeled triacylglycerol formed. There was a preferential utilization in triacylglycerol biosynthesis of the more unsaturated diacylglycerols arising from the monoacylglycerol pathway and of the more saturated diacylglycerols originating from the phosphatidic acid pathway. The above experiments do not allow a demonstration of the utilization of the sn-2,3-diacylglycerols in triacylglycerol biosynthesis but are not inconsistent with it.

Animals↗
PubMed1972

HMG CoA reductase of intestinal mucosa and liver of the rat.

Methods were developed for the determination of HMG CoA (3-hydroxy-3-methylglutaryl CoA) reductase activity in subcellular fractions of intestinal mucosa and liver of Wistar strain rats. In the liver, reductase activity was located exclusively in the microsomal fraction. In the intestinal mucosa, activity was found in both mitochondrial and microsomal fractions of crypt cells but not of villi. The microsomal HMG CoA reductases of liver and intestinal mucosa had similar kinetic characteristics and pH optima. However, the activity of the hepatic enzyme differed with age and sex of the experimental animals while that of the intestinal crypt cells did not. Cholestyramine treatment enhanced the activity of the microsomal HMG CoA reductase in both liver and intestinal mucosa. Reductase activity of the intestinal crypt cells was elevated in both jejunum and ileum. The greatest stimulation, both relatively and absolutely, was observed in the distal half of the jejunum.

Aging↗
PubMed1984

Energy level in large intestinal mucosa in patients with ulcerative colitis.

In 7 patients with ulcerative colitis, the energy level in the large intestinal mucosa was investigated. ATP and energy charge in the intestinal mucosa in ulcerative colitis showed lower levels than those of control subjects. Therefore, energy-deficit may exist in the large intestinal mucosa in ulcerative colitis.

Adenine Nucleotides↗
PubMed1989

Binding of cholera toxin to pig intestinal mucosa glycosphingolipids: relationship with the ABO blood group system.

A search for compounds from intestinal mucosa of pigs carrying and not carrying blood group A-active substances (A+ and A- pigs, respectively) capable of binding cholera toxin (CT) was performed. Glycolipid extracts from a pool of pig intestinal mucosa resolved in thin-layer chromatography (TLC) revealed the presence of six to eight compounds capable of binding 125I-CT, two of them running as the ganglioside standards GM1 and GD1b. When intestinal mucosa glycolipids from single pigs were assayed by TLC for CT-binding capacity, two different patterns of labeling were observed. The main difference was at the level of compounds running below GD1b. The A+ pigs but not the A- pigs showed CT binding at this level. The major CT-binding compound detected only in A+ pigs was purified and some properties were determined. After TLC developed with different solvent systems, the purified compound bound CT and also immunoreacted with anti-A and anti-AB antisera but not with anti-B antiserum. The compound was also able to inhibit the hemagglutination of human A erythrocytes caused by anti-A antiserum, but inhibition was not observed with the B-anti-B or O (H)-Ulex europaeus lectin systems. A partial chemical characterization indicated that the active compound is a neutral glycosphingolipid containing glucose, fucose, galactose, and hexosamine. The existence of a blood group-active substance(s) able to interact with CT may help to explain the relationship between ABO blood groups and the diarrheal disease caused by infection with Vibrio cholerae.

ABO Blood-Group System↗
PubMed1986

Some properties of the fatty alcohol oxidation system and reconstitution of microsomal oxidation activity in intestinal mucosa.

This paper describes the metabolism of fatty alcohols by microsomal and cytosolic fractions from intestinal mucosa. Microsomes of rabbit intestinal mucosa had a high activity of [1-14C]dodecanol oxidation as did those of liver. The intestinal cytosolic fraction also exhibited oxidation activity to a lesser extent than the microsomes did. The reaction product was determined as lauric acid using thin-layer chromatography. Laurylaldehyde was detected as another product, when semicarbazide was added to the incubation system. Cyclodextrins exhibited a stimulation effect similarly to bovine serum albumin on the microsomal activity. We have compared the stimulatory effects of dimethyl-beta-cyclodextrin, beta-cyclodextrin, gamma-cyclodextrin and alpha-cyclodextrin, which decrease in that order. Effects of NAD+ and dodecanol concentrations, pH and pyrazole on microsomal activity were compared with those on cytosolic activity. Dodecanol oxidation activity was solubilized and reconstituted with a fatty alcohol dehydrogenase and a fatty aldehyde dehydrogenase separated from the intestinal microsomes. These findings indicate that both the dehydrogenases participate in microsomal oxidation of fatty alcohols to fatty acids with fatty aldehydes as intermediates in the reaction.

Alcohol Oxidoreductases↗
PubMed2006

Lactobacilli binding human A-antigen expressed in intestinal mucosa.

Adherent lactic acid bacteria (LAB) in the human intestine were investigated using the surface plasmon resonance technique with the biosensor BIACORE-1000. Ninety-three LAB strains were isolated from human feces and evaluated for binding to human blood type-A antigen [GalNAcalpha1-3 (Fucalpha1-2) Gal-: A-trisaccharide] expressed in the intestinal mucosa. Eleven strains showed strong adherence to an A-trisaccharide biotinyl polymer (BP) probe, and slightly or no adherence to a B-trisaccharide BP probe. Four strains with high adherence (high A/B ratio) were selected and their surface layer proteins (SLPs) were evaluated for A-antigen ligand binding using BIACORE. The SLP from L. brevis strain OLL2772 showed a single band at ca. 48 kDa by SDS-PAGE analysis and it had a very strong adherence to the human A-antigen, as shown using an anti-A lectin blocking technique. A partial N-terminal sequence of the band showed strong homology to an S-layer protein of L. brevis ATCC8287T. The probiotic LAB binds to human blood type-A antigen expressed in the intestinal mucosa which may aid in colonization of the gut.

ABO Blood-Group System↗
PubMed1996

Interleukin-11 prevents apoptosis and accelerates recovery of small intestinal mucosa in mice treated with combined chemotherapy and radiation.

Previous studies have shown that acute injury to rodent small intestinal mucosa as a result of either chemotherapy or radiation is caused by a combination of high-frequency cell death caused by apoptosis, continued migration of epithelial cells from the intestinal crypts toward the villi, and absence of adequate compensatory mitotic activity in the crypt bases. Recently, we have shown that IL-11, a novel multifunctional bone marrow stromal-derived growth factor, could stimulate rapid repair of small intestinal villous structures in mice treated with combined radiation and chemotherapy by increasing the mitotic index of crypt cells. To further clarify the biological mechanism responsible for its protective action, we used a similar experimental model to evaluate whether IL-11 could reduce the high frequency of apoptosis observed after cytoablative treatment. In the present study, 78 C3H/HeJ mice received 5-fluorouracil at 150 mg/kg body weight intraperitoneal injection 3 days before 7.0-Gy total body irradiation. The animals received IL-11 250 microg/kg body weight/day divided into two equal doses or vehicle control by subcutaneous injections beginning on the same day of irradiation within 1 hour of the end of the dose. The mice killed on Days 1, 2, and 5 after cytoablative treatment were autopsied, the small intestine was processed for histologic examination, and the mitotic index and other parameters were measured, including the expression of the proliferating cell nuclear antigen and of the p53 protein. Apoptosis was detected by a nonisotopic in situ DNA end-labeling technique applied to the same histologic sections. The cytoablative treatment caused marked degenerative changes in the small intestinal mucosa, including shortening of the villi and damage to the crypt cells. The degenerative changes, which included nuclear fragmentation with formation of apoptotic bodies, increased expression of proliferating cell nuclear antigen, and strong expression of p53 was seen in mice killed on Days 1 and 2 after cytotoxic treatment. IL-11 administration resulted in a partial suppression of apoptosis, as shown by a reduced number of crypt cells stained with in situ DNA end-labeling for fragmented DNA. In addition, IL-11 treatment was associated with an increase in the frequency of mitosis and proliferating cell nuclear antigen expression in crypt cells as compared with the vehicle treated mice. Morphometric analysis of intestinal villi and crypt depth showed increased villus length and decreased crypt to villus ratio after IL-11 treatment. These results indicate that IL-11 can exert a potent effect on the recovery of the small intestinal mucosa of mice by its combined effects on proliferation and apoptosis of crypt cells. IL-11 may thus have potential clinical applications in limiting the intestinal toxicity that is associated with cytotoxic therapies.

Animals↗
PubMed1989

Trophic effect of Efamol on the rat small-intestinal mucosa.

1. The hypothesis that triacylglycerols are trophic to the small-intestinal mucosa of the rat was tested by comparing the action of the essential fatty acid-rich oil Efamol with that of glucose. 2. Two groups of nine female Wistar rats were pair-fed Vivonex HN with 50% calorie substitution by glucose or Efamol for 21 days. 3. Body weight gain was greater with glucose than with Efamol, but, despite this, whole gut weight, mucosal weight and mucosal protein were increased by Efamol in all small-intestinal segments. Total mucosal DNA was also increased with a significant change in the middle small-intestinal segment. These changes were associated with an increased crypt cell production rate. 4. Fasting plasma levels of peptidyltyrosyltyrosine ('peptide YY'), but not of enteroglucagon, were significantly elevated in the Efamol-fed group. 5. The data show a trophic effect of Efamol on the rat small-intestinal mucosa. Possible mechanisms are discussed.

Animals↗
PubMed1998

Nuclear factor-kappaB is activated in intestinal mucosa during endotoxemia.

BACKGROUND: The transcription factor nuclear factor-kappaB (NF-kappaB) regulates a large number of genes involved in the inflammatory response to critical illness. The intestinal mucosa plays an active role in the inflammatory and metabolic response to sepsis and endotoxemia, but it is not known if NF-kappaB is activated in the mucosa during these conditions. OBJECTIVE: To test the hypothesis that endotoxemia in mice activates NF-kappaB in intestinal mucosa. METHODS: Mice were injected subcutaneously with lipopolysaccharide, 12.5 mg/kg, or a corresponding volume of saline. At various intervals following injection, jejunal mucosa was harvested and nuclear and cytoplasmic fractions were prepared. The nuclear fractions were analyzed by electrophoretic mobility shift assay for NF-kappaB activation and by Western blot analysis for the NF-kappaB subunits p50 and p65. Cytoplasmic fractions were analyzed by Western blotting for the NF-kappaB inhibitory proteins IkappaB-alpha and IkappaB-beta. RESULTS: Electrophoretic mobility shift assay showed that NF-kappaB was activated in jejunal mucosa 1 hour after injection of lipopolysaccharide and persisted for at least 4 hours. The NF-kappaB subunits p50 and p65 were present in nuclear fractions of mucosa from endotoxemic mice at the corresponding time points. Cytoplasmic levels of the inhibitory proteins IkappaB-alpha and IkappaB-beta decreased during endotoxemia, and the proteins were nearly absent 60 minutes after injection of lipopolysaccharide. CONCLUSIONS: The results suggest that IkappaB is degraded and NF-kappaB is activated in intestinal mucosa during endotoxemia. The findings support the concept that the intestinal mucosa is an important component of the inflammatory response to sepsis and endotoxemia.

Animals↗
PubMed1975

Enzymes of fructose metabolism in human small intestine mucosa.

The enzyme activities involved in fructose metabolism were measured in human intestine mucosa. Mucosa of the following gut sections were used: duodenum, jejunum, jejunum in the region of the flexura duodenojejunalis, jejunum distal region, ileum middle region and ileum in the region of the valvula ileo coecalis. Ketohexokinase, aldolase, alcohol dehydrogenases NAD- and NADP- dependent were found in all gut sections. The activity of aldehyde dehydrogenase was low in all sections tested. Triokinase could be found only in the duodenum and jejunum region and was absent in the ileum. Glycerate kinase was not present in the human intestine mucosa.

Alcohol Oxidoreductases↗