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PubMed1978

Differentiation and aging of the rat intestinal mucosa. II. Morphological, enzyme histochemical and disc electrophoretic aspects of the aging of the small intestinal mucosa.

At different times of day (08.00, 12.00, 16.00 and 24.00) the small intestinal mucosa of four month (adult) and 30 month (senile) old rats was examined histologically, by scanning electron microscopy, autoradiography, enzyme histochemistry and disc electrophoresis. In senile rats a villous atrophy is found histologically and an irregular architecture is found in scanning electron microscopy. The changes are essentially restricted to the proximal small intestine. The enterocytes of adult and senile rats show an identical enzyme histochemical picture. In the proximal small intestine of adult and senile rats, synchronous statistically significant fluctuations of the activity of alkaline and acid phosphatase were revealed in the disc electropherograms. Likewise statistically significant are the at all times of day low enzyme activities in the intestinal mucosa of senile rats as compared to the findings in adult rats. The fall in activity of alkaline and acid phosphatase in old rats is attributed to the numerical reduction of the enterocytes which is caused by the age atrophy of the intestinal mucosa. These findings are discussed in connection with results of our own studies of proliferation kinetics and those of other authors.

Acid Phosphatase↗
PubMed1994

Eosinophils within the healthy or inflamed human intestine produce substance P and vasoactive intestinal peptide.

The purpose of this study was to show if inflammatory cells within healthy or diseased human intestinal mucosa produce some regulatory neuropeptides. First, inflammatory cells were isolated from the intestinal lamina propria of 11 patients with ulcerative colitis or Crohn's disease. Also collected were cells from anatomically normal intestine derived from five patients requiring bowel resection for diseases not related to inflammatory bowel disease. Extracts of these isolated cells contained authentic substance P (SP) and vasoactive intestinal peptide (VIP) as shown by RIA and their elution profiles on HPLC. Immunostaining of cells from nine of 13 additional patients localized immunoreactive SP and VIP to secretory granules within most mucosal eosinophils. No other cell types stained positive. Messenger RNA encoding SP and VIP was localized to lamina propria eosinophils by in situ hybridization. Mucosa inflammatory cells, from eight of nine more patients, cultured in vitro, released detectable amounts of VIP, but not SP. It is concluded that intestinal eosinophils produce SP and VIP. Since the eosinophils store and release more VIP than SP, it is possible that VIP is the preferred secretory product.

Adolescent↗
PubMed1985

Gastric and intestinal release of vasoactive intestinal polypeptide in the milk-fed lamb.

Vasoactive intestinal polypeptide (VIP) has been proposed as the neurotransmitter of the atropine-resistant relaxation of gastric structures in the lamb. To examine this proposal VIP concentrations in plasma from arterial, gastric venous and intestinal venous blood were measured in healthy conscious lambs before, during and after teasing with, and sucking of milk. Basal arterial plasma VIP concentrations were undetectable (less than 3 pmol/l) and remained so during and after feeding. Before feeding VIP was detected in only 2 of 12 gastric venous plasma samples (5 and 13 pmol/l). During teasing with food there were increments in VIP of 19 +/- 4 pmol/l and during feeding of 27 +/- 5 pmol/l. VIP concentration in gastric venous plasma rapidly returned to fasting levels after cessation of sucking. In contrast VIP in the intestinal venous plasma did not rise during teasing or upon commencement of sucking but a peak increment of 34 +/- 6 pmol/l occurred at 5 min after cessation of feeding. The results are consistent with the hypotheses that VIP is released in anticipation of and during sucking from inhibitory neurones involved in relaxation of gastric structures and that intestinal release of VIP is a consequence of entry of digesta into the small intestine.

Animals↗
PubMed1990

Purification and biological properties of an epithelial intestinal cell growth inhibitor from a human small intestine.

Endogenous mitotic inhibitors act as control-mechanisms in intestinal epithelium proliferation. The presence of an inhibitor of cultured intestinal epithelial cell from a villous extract of rat jejunum has been reported in one of our papers. The object of the study now reported was to find the presence of a growth inhibitor in the villous extract from man's small intestine and to purify and characterize this factor when found. Our results reveal that: (1) Such an inhibitor was found in a supernatant preparation obtained from human intestinal epithelial cells. The inhibition of the proliferation of epithelial cells (IRD-98) it induced was seem to be dose-dependent and non-cytotoxic. (2) After chromatography on hydroxylapatite, on DEAE and then on ACA 54 (gel permeation), a low-molecular-weight protein (15 kDa) called purified intestinal inhibitor (PII) was isolated (purification factor of approx. 50,000 with respect to the supernatant fraction). This fraction proved to inhibit the IRD-98 cells in a reversible manner. When cells are incubated with this protein, cells prove to be arrested in phase G1 of the cell cycle as is revealed by the flow cytometry studies. The results obtained support the hypothesis that regulation of cell proliferation is mediated by endogenous inhibitors at the epithelial level.

Animals↗
PubMedDate not supplied

Autoradiographic distribution of vasoactive intestinal polypeptide receptors in rabbit and rat small intestine.

Vasoactive intestinal peptide (VIP) is found in the enteric nervous system of all layers of the small intestine. In the gastrointestinal tract, VIP receptors coupled to adenylate cyclase are present on epithelial, smooth muscle and possibly mononuclear cells. This study analyzes the distribution of VIP binding using in vitro autoradiographic techniques. VIP binding was present in high density in the mucosal layer of rabbit duodenum, jejunum and ileum. Low VIP binding was noted over the smooth muscle layers or the lymphoid follicles. Similar results were obtained in rat small intestine. The density of VIP binding was greatest in duodenal mucosa but was present in lower density in jejunal and ileal mucosa. Again, low VIP binding was noted in the smooth muscle layers or lymphoid follicles. Thus, autoradiographic maps of small intestine indicate that VIP receptors are found primarily in the small intestinal mucosa.

Animals↗
PubMed2005

Intestinal metabolism of PAH: in vitro demonstration and study of its impact on PAH transfer through the intestinal epithelium.

Food would seem to be one of the main ways of animal and human contamination with polycyclic aromatic hydrocarbons (PAHs). In vivo studies suggest a transfer in intestinal epithelium by diffusion, which appears extensively governed by the physicochemical properties of PAHs, particularly lipophilicity. However, other mechanisms, such as metabolism, are considered to intervene. Our work aimed at testing in vitro intestinal metabolism and defining its impact on transepithelial transport of PAHs. Caco-2 cells were cultivated on permeable filters and incubated with 14C-labeled benzo[a]pyrene (BaP), pyrene (Pyr), and phenanthrene (Phe), which differ in their physicochemical properties. The results showed that the cells were able to metabolize the compounds. In basal media, Phe appeared to be the least hydroxylated molecule (45% after a 6-h exposure), followed by Pyr (65%) and finally BaP (96%). Inhibition of PAH metabolism showed a determinant effect on kinetics profiles. Transfer in the basal compartment of BaP, Pyr, and Phe radioactivities was, respectively, 26, 4, and 2 times lower with inhibitors, corroborating that intestinal metabolism of PAHs would have a positive impact on their transfer, an impact that increased with their lipophilicity. Furthermore, after a 6-h incubation, metabolites were also detected in apical medium. These findings suggested that intestinal metabolism might play a key role in intestinal barrier permeability and thus in the bioavailability of tested micropollutants.

Benzo(a)pyrene↗
PubMed2000

Improvement of intestinal absorption of peptides: adsorption of B1-Phe monoglucosylated insulin to rat intestinal brush-border membrane vesicles.

In a previous study we glycosylated insulin to improve its intestinal absorption. When the glycosylated product, p-(succinylamido)-phenyl-alpha-D-glucopyranoside (SAPG)-substituted insulin (SAPG-INS), was administered intra-intestinally to rats, it showed a greater hypoglycemic effect than native bovine insulin. The enhanced hypoglycemic effect of SAPG-INS was considered to be due to an increase in membrane permeability as well as an increase in resistance to enzymatic degradation. In particular, membrane permeability may be related to an interaction with the Na(+)-dependent D-glucose transporter (SGLT-1) which is located in the brush-border membrane of epithelial cells. The insulin product used in the previous study, however, comprised a mixture of mono-, di- and tri-SAPG-substituted insulin. In this study SAPG-INS with a defined substitution number and position was synthesized to examine the interaction between the transporter and glycosylated insulin in more detail. The new product was mono-SAPG-substituted insulin substituted at the B1-phenylalanine position (B1-SAPG-INS) and was selectively synthesized after protection of the A1-glycine and varepsilonB29-lysine amino acids. The hypoglycemic effect of B1-SAPG-INS in rats after an intravenous dose of 71 microg/kg was almost the same as that of native bovine insulin at a dose of 1 U/kg and B1-SAPG-INS retained about 60% of the immunoreactivity of native bovine insulin. The interaction of B1-SAPG-INS with the intestinal transporter was examined by a rapid filtration technique using (125)I-labeled B1-SAPG-INS and brush-border membrane vesicles (BBMVs) which were prepared from rat small intestine by the Mg-precipitation method. The amount of B1-SAPG-INS adsorbed or absorbed by BBMVs in the presence of an inward Na(+)-gradient into BBMVs was greater than that of native bovine insulin. This adsorption/absorption was significantly inhibited by the presence of 1 mM phloridzin. A similar inhibition was observed when Na(+) was replaced with K(+) and when B1-SAPG-INS was incubated with BBMVs at 4 degrees C. From the effect of osmolarity on the extent of adsorption/absorption, it was considered that B1-SAPG-INS was not taken up into the intravesicular space but adsorbed onto the external membrane surface of BBMVs. These findings suggested that B1-SAPG-INS was adsorbed specifically onto the transporter. The hypoglycemic effect of insulin was enhanced by glycosylation at the B1 position in in situ experiments using normal and diabetic rats. Consequently, it is suggested that B1-SAPG-INS was adsorbed specifically onto the glucose transporter of intestinal BBM. This specific adsorption may be involved in the mechanism of the enhanced hypoglycemic effect of B1-SAPG-INS both in normal and diabetic rats.

Adsorption↗
PubMed1996

A vasoactive intestinal polypeptide-like protein excreted/secreted by Nippostrongylus brasiliensis and its effect on contraction of uninfected rat intestine.

The 50-30 kDa fraction isolated from the excretory/secretory products (E/S) of the nematode Nippostrongylus brasiliensis significantly decreased the amplitude of contraction of segments of uninfected rat intestine when injected into the lumen of the segments maintained in an organ bath. Dot blot analysis of the fraction suggested that it was similar in immunoreactivity to porcine vasoactive intestinal polypeptide (VIP). When antiserum to porcine VIP was mixed with N. brasiliensis E/S and the mixtures were injected into the lumen of segments of rat intestine, the inhibitory effect of the E/S on amplitude of contraction decreased. When physiological concentrations of porcine VIP (12.9 pmol/ml) were injected into the lumen of segments of uninfected rat intestine the amplitude of contraction decreased significantly. Western blot analysis of the E/S, using antiserum to porcine VIP, recognized a 30 kDa protein in the E/S and also in whole worm homogenate suggesting that synthesis of the peptide occurs inside the nematode. Peptide histidine isoleucine (PHI)-like immunoreactivity was detected in a 68 kDa fraction of the E/S and the homogenate but this fraction did not affect the amplitude of contractions of the intestine.

Animals↗
PubMed2004

Intestinal barrier function and secretion in methotrexate-induced rat intestinal mucositis.

Chemotherapy-induced mucositis is an important dose-limiting and costly side effect for which there is no definitive prophylaxis or treatment. This is due in part to the lack of understanding of its pathophysiology and impact on intestinal function. The objectives of this study were to investigate the small intestine barrier function and electrolyte and water transport in an experimental model of methotrexate-induced mucositis, and to correlate these alterations with histological damage. Wistar rats were treated with methotrexate (1.5-3.5 mg/kg) for 3 days to induce mucositis. Intestinal permeability was measured by the urinary excretion rate of lactulose and mannitol following administration by gavage. Intestinal perfusion was performed in vivo for evaluation of water and electrolyte transports. Methotrexate-treated rats lost a significant amount of weight and presented a marked reduction in food intake. Methotrexate induced significant and dose-dependent villous atrophy and elongation of crypts in duodenum, jejunum, and ileum. Methotrexate also induced an increase in sodium and potassium secretion and an important reduction of the mucosa absorptive surface area, shown by the decrease in the mannitol excretion ratio. In conclusion, methotrexate caused major changes in small bowel function by disrupting intestinal permeability and inducing electrolyte secretion in parallel with substantial histological damage.

Animals↗
PubMed2001

Intestinal transit of an orally administered streptomycin-rifampicin-resistant variant of Bifidobacterium longum SBT2928: its long-term survival and effect on the intestinal microflora and metabolism.

AIMS: The objectives of this study are to investigate the fate of a streptomycin-rifampicin-resistant variant of Bifidobacterium longum SBT2928 (BL2928SR) and the influence of its oral administration on the composition and metabolism of the intestinal microflora. METHODS AND RESULTS: Intestinal passage of BL2928SR was monitored by a combination of selection with antibiotics and identification by a randomly amplified polymorphic DNA (RAPD)-PCR method. Intestinal microflora was analysed by the method developed by Mitsuoka et al. (1965, 1974). Long-term survival of orally administered BL2928SR in the human intestine was confirmed. BL2928SR ingestion specifically lowered faecal populations of Enterobacteriaceae and clostridia, including lecithinase-positive Clostridium spp. CONCLUSION: BL2928SR and its parent strain, BL2928, are considered to be appropriate candidates for probiotics. SIGNIFICANCE AND IMPACT OF THE STUDY: It is clarified that BL2928SR has the ability for long-term survival in the human gastrointestinal tract, and alters the composition and metabolism of the intestinal microflora.

Actinomycetales Infections↗
PubMed1995

Microcolon-intestinal hypoperistalsis without megacystis: uncommon form of neonatal intestinal pseudoobstruction.

Two cases of microcolon-intestinal hypoperistalsis without megacystis are reported. They had dilated proximal small bowel and narrowed distal small bowel and malrotated microcolon. No organic obstructive intestinal lesion was found and double-barrel ileostomy was performed. The biopsy specimens showed ganglion cells to be normal in number and appearance in the entire intestinal wall. The ileostomy did not function postoperatively and drugs stimulating bowel movement failed to induce peristalsis. We have suggested that microcolon-intestinal hypoperistalsis without megacystis may be the cause of functional intestinal obstruction in neonates and it is a variant of megacystis-microcolon-hypoperistalsis syndrome.

Colon↗
PubMed1998

A method for assaying intestinal brush-border sucrase in an intact intestinal preparation.

Small intestinal brush-border hydrolases usually are assayed in intestinal mucosal homogenates resuspended in solutions of unphysiological ionic composition. Thus, extrapolation of measured Vmax values (maximal reaction rates at high substrate concentrations) to in vivo conditions, hence comparison with physiological substrate loads, is uncertain. We therefore have developed a sucrase assay in an intact preparation of mouse small intestine, an everted intestinal sleeve incubated in a physiological Ringer's solution. As in homogenate studies, sucrase is assayed by glucose production measured colorimetrically, but uptake of liberated glucose into the intestinal sleeve is prevented by the transport inhibitor phlorizin. The coefficient of variation of Vmax is 16% for sleeves from the same mouse and 8% for mean values from different mice. Sleeve sucrase activity is abolished by the inhibitor castanospermine. Activity in sleeves and homogenates proves to be the same when measured under identical solution conditions, but variations in assay conditions cause large activity changes from values measured in physiological solutions.

Animals↗
PubMed2001

A new hypothesis on the pathogenesis of intestinal pseudo-obstruction by intestinal neuronal dysplasia (IND).

Using morphometry and image analysis, we investigated 17 patients showing intestinal pseudo-obstruction secondary to intestinal neuronal dysplasia (IND) and 20 controls. In addition to an increase in the number and size of the ganglia and the ganglionic cells, we also noted a significant increase in NO synthase-containing ganglionic cells. We found that this enzyme, responsible for the synthesis of nitrous oxide caused by oxidation of L-argynine aminoacid, is a neurotransmitter able to induce smooth muscle relaxation by activating cyclic AMP. If the increase in NO synthase-producing ganglionic cells is responsible for the increase in nitrous oxide production, one can hypothesize that an overproduction of nitrous oxide plays a role in the pathogenesis of intestinal pseudo-obstruction secondary to neuronal dysplasia. As NO synthase can be blocked, as was demonstrated by giving L-methil-arginine or N-G-nitro-L-argynine, it might be possible to treat intestinal pseudo-obstruction caused by intestinal neuronal dysplasia at the pharmacological level.

Adolescent↗
PubMed1986

Studies on the secretion of amino acids and of urea into the gastro intestinal tract of pigs. 2. Net secretion of leucine into the small and large intestines.

The experiment was carried out on 3 pigs of 34 kg body weight equipped with re-entrant cannulas both in the duodenum and terminal ileum. Furthermore, catheters were inserted into the external jugular vein and into the carotid artery. During a preliminary period digesta from both cannulas were collected and stored. This digesta was than reintroduced during a 12 hours period of intravenous infusion of 14C-leucine while outflowing digesta from the proximal parts of the cannulas were collected, stored and analyzed for leucine content, 14C-radioactivity and specific radioactivity of leucine. This paper reports the net secretion of 14C-activity and of 14C-leucine by the small intestine and the recovery of both in the content of the digestive tract at the end of the infusion. It was concluded that endogenous leucine enters the lumen of the small intestine through the intestinal wall mainly in a protein bound form. Free leucine is secreted, however, only in small amounts. Metabolites of leucine were also secreted into or formed in the lumen of the small intestine. A proportion of endogenous leucine was reabsorbed during the passage of digesta along the small intestine.

Amino Acids↗
PubMed2006

Conditional deletion of beta1 integrins in the intestinal epithelium causes a loss of Hedgehog expression, intestinal hyperplasia, and early postnatal lethality.

Conditional deletion of beta1 integrins in the intestinal epithelium, unlike in epidermal and mammary epithelia, of mice does not result in decreased cell adhesion and proliferation, but instead causes a profound increase in epithelial proliferation with dysplasia and polypoid structures. The increased epithelial proliferation inhibited epithelial differentiation that caused severe malnutrition and early postnatal lethality. The striking similarities between beta1 integrin-deleted mice and neonatal mice with defective Hedgehog signaling led to the discovery that Hedgehog expression was markedly reduced in the former mice. beta1 integrins were found to drive the expression of Hedgehogs in intestinal epithelial cells in an HNF-3beta (Foxa2)-dependent fashion. The expression of Tcf-4, a transcription factor known to be required for intestinal epithelial stem cell proliferation, was increased and mislocalized in the intestinal epithelia of the beta1 integrin-deleted mice and in newborn mice treated with the Hedgehog signaling inhibitor cyclopamine. This study shows that beta1 integrins are key regulators of proliferation and homeostasis in the intestine and achieve this not through anchorage-dependent effects but by generating Hh expression and signaling.

Animals↗
PubMed1996

Type II TGF(beta) receptor expression in intestinal cell lines and in the intestinal tract.

The recent identification and cloning of mammalian transforming growth factor beta (TGFbeta) receptors permits further analysis of the importance of the TGFbeta family in intestinal biology. Expression of the type II TGFbeta receptor was examined in gastrointestinal cell lines and tissues. The 5.5 kb type II mRNA species was detected in poly-(A) mRNA isolated from the rat small bowel and colon. Northern blot analysis of RNA isolated from epithelial and non-epithelial small intestinal cell fractions showed the majority of receptor mRNA localized in the non-epithelial compartment. Immunohistochemical localization in the small intestine and colon supported the RNA findings; that is, expression was greatest in the lamina propria and muscularis. Staining was also detectable in the epithelium, where it was most prominent in the villus tip cells and absent in crypt cells. These findings mirror expression of TGFbeta in the epithelial compartment. The IEC-6, IPEC and RIE-1 cell lines, all of which are non-transformed, were growth inhibited by TGFbeta and expressed type II receptor mRNA and protein. By contrast, the ras-transfected RIE-1, HT-29, Caco-2 and SW-620 transformed lines were not growth inhibited by TGFbeta and all demonstrated a marked reduction in type II TGFbeta receptor mRNA expression and protein abundance by cross-linking. In conclusion, (i) colocalization of both ligand and receptor establishes the existence of potential autocrine and/or paracrine pathways for TGFbeta in the normal intestine and (ii) down-regulation of the type II TGFbeta receptor occurs in association with cellular transformation and may contribute to intestinal carcinogenesis.

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↗
PubMed1992

Cysteine-rich intestinal protein and intestinal metallothionein: an inverse relationship as a conceptual model for zinc absorption in rats.

Dietary zinc may regulate zinc absorption in part via the inhibitory effect of intestinal metallothionein, but the mechanism is unknown. We recently showed that cysteine-rich intestinal protein (CRIP) binds zinc during transmucosal zinc transport, and that CRIP may function as an intracellular zinc carrier. The present experiments examine the interaction of CRIP and metallothionein with zinc to evaluate their potential roles in the mechanism of zinc absorption. Intestinal metallothionein concentrations were lower and zinc absorption rates from isolated intestinal loops were higher in rats fed a low zinc diet compared with those fed a high zinc diet or given parenteral zinc to induce metallothionein synthesis. Zinc status did not affect the apparent CRIP concentration, but markedly altered the distribution of 65Zn in intestinal cytosol as determined by gel filtration HPLC. More 65Zn was associated with CRIP (40 vs. 14%) and less was bound to metallothionein (4 vs. 52-59%) in rats fed the low zinc diet compared with rats of high zinc status. Luminal zinc concentration also affected the distribution of 65Zn in the cytosol. CRIP bound progressively less (from 42 to 25%) of the 65Zn taken up from the lumen as the luminal zinc concentration was increased from 5 to 300 mumol/L. Collectively these data suggest that CRIP is a saturable, intracellular zinc transport protein, and that metallothionein inhibits zinc absorption by binding zinc in competition with CRIP. A hypothetical model for the mechanism of transcellular zinc absorption involving metallothionein and CRIP is presented and discussed.

Animals↗