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PubMedDate not supplied

Processing of vasoactive intestinal peptide and transferrin in human cancerous colonic cells.

Endocytosis of vasoactive intestinal peptide (VIP) and of transferrin (Tf) was comparatively studied in human cancerous colonic HT-29 cells. Cellular depletion in potassium inhibits the internalization of VIP (23%) and to a greater extent (42%) that of Tf. This indicates that clathrin-coated pits are also involved, at least in part, in VIP uptake. The distribution of 125I-Tf- or 125I-VIP-containing vesicles in sucrose gradients revealed low and high density vesicle subpopulations. The low density vesicle subpopulation represented a transient compartment from which incoming vesicles containing N-leucyl-beta naphthylamidase were recycled back to the membrane while those containing beta-hexosaminidase (HA) and ligand were mostly transferred into the high density compartment. Subsequent fusion of the latter with heavy vesicles was demonstrated by the shift of HA and ligand with vesicles that had been prelabeled with horseradish peroxidase (HRP). Simultaneous internalization of Tf-HRP and 125I-VIP showed that both the low and high density vesicle subpopulations comprised of two types of VIP-containing vesicle, as confirmed by the density shift reaction: two-thirds of VIP shifted with the Tf-HRP-containing vesicles to denser fractions and the remaining was found with unshifted vesicles. These findings indicate that the VIP-receptor complex processing in HT-29 cells follows two routes, the major route being common with Tf endocytosis.

Coated Pits, Cell-Membrane↗
PubMed1993

Regulated expression of an intestinal mucin gene in HT29 colonic carcinoma cells.

We have investigated the regulation of the intestinal mucin gene MUC2 in HT29 cells. Surprisingly, sodium butyrate, an effective inducer of aspects of colonic cell differentiation in HT29 cells, fails to induce MUC2 during short-term exposure, despite the fact that it has been used to select stably differentiated clones of HT29 that resemble goblet cells and produce mucin. However, 12-O-tetradecanoylphorbol-13-acetate and forskolin, which trigger the protein kinase C- and A-dependent signal transduction pathways, respectively, are potent inducers of MUC2 gene expression. 12-O-Tetradecanoylphorbol-13-acetate and forskolin operate through distinct mechanisms, with the former requiring de novo protein synthesis and the latter not. Experiments using specific protein kinase inhibitors suggest that both inducers operate by triggering their respective signal transduction pathways. Nuclear runoff analyses suggest that post-transcriptional (rather than transcriptional) mechanisms are important in the accumulation of MUC2 mRNA. Finally, we show that in several cell lines from human mucinous tumors, characterized by elevated levels of mucin production, MUC2 expression is very high and constitutive compared to forskolin-treated HT29 cells. Thus, the different regulation of MUC2 in HT29 cells and in mucinous tumor cell lines may reflect molecular pathways that characterize colon carcinomas of different histology and pathology.

1-Methyl-3-isobutylxanthine↗
PubMed1999

Chemopreventive effect of N-(2-cyclohexyloxy-4-nitrophenyl)methane sulfonamide (NS-398), a selective cyclooxygenase-2 inhibitor, in rat colon carcinogenesis induced by azoxymethane.

Non-steroidal anti-inflammatory drugs (NSAIDs) such as sulindac and indomethacin inhibit colon carcinogenesis, and selective cyclooxygenase (COX)-2 inhibitors are considered to be potential chemopreventive agents without the side effects of usual NSAIDs. We reported that NS-398, N-(2-cyclohexyloxy-4-nitrophenyl)methane sulfonamide, suppressed the formation of preneoplastic lesions, aberrant crypt foci (ACF), induced by azoxymethane (AOM) in a short-term assay of rat colon carcinogenesis. In this study, we examined the effects of long-term NS-398 administration on rat colon carcinogenesis. After three AOM treatments at weekly intervals, a dose of 10 mg/kg of NS-398 in 5% Arabic gum solution was administered by gavage three times per week in group 2 until the termination of the experiment. Rats in group 1 were fed in a basal diet and given 5% Arabic gum solution alone after AOM treatment. At 40 weeks after the first AOM treatment, all rats were killed and the whole intestines including colon were examined. While the incidences of whole intestinal and colon neoplasms in group 1 were 84.6% and 80.8%, respectively, those in group 2 (given NS-398) were 51.9% and 44.4% respectively (P=0.0177 and P=0.0103 by Fisher's exact test, respectively). The multiplicities in group 2 (0.67+/-0.78 and 0.48+/-0.58) were also decreased significantly compared with those (1.39+/-1.10 and 1.08+/-0.74) in group 1 (P<0.01 by Welch's method and P<0.002 by Student's t test, respectively). In immunohistochemistry for proliferative cell nuclear antigen (PCNA), the PCNA-stained cell index (7.40+/-0.5) in group 2 was significantly decreased from that in group 1 (14.03+/-0.82) (P<0.001 by Welch's method). The results suggest that NS-398, a selective COX inhibitor, has a chemopreventive activity against colon carcinogenesis without side-effects such as gastric ulceration.

Animals↗
PubMed1978

[Characterization of radioactivity distribution in the organism during constant intravenous infusion of tracer amino acids and calculation of the rate of tissue protein synthesis in rats].

Male wistar rats (100 g live mass) were given infusions into the tail vein of 14C-leucine and 14C-lysine simultaneously for 0.5; 1.0; 2.0; 3.0; 4.5; 6.0 and 7.0 hours. At the end of the infusion the specific radioactivity of the free leucine and lysine in the blood plasma, liver, M. gastrocnemius, small intestines and colon were ascertained as well as after the 6-and-7-hour infusion that of the protein-bound leucine and lysine. In all tested tissues the specific radioactivity of the free amino acids attained a plateau during the 6-and-7-hour infusion. The rate constants for the increase were calculated for each organ tested. The two amino acids used are suitable for the calculation of the fractional rate of protein synthesis in tissues. The values of the fractional rate of protein synthesis calculated on the basis of the 6-and-7-hour infusion were: 54 +/- 7.7%/day for the liver, 9.4 +/- 1.2%/day for muscles, 89 +/- 12.2%/day for the small intestines and 42 +/- 5.9%/day for the colon. The simultaneous application of two tracer amino acids is recommendable for the estimation of the precursor pool for protein synthesis and the more accurate calculation of the rate of protein synthesis.

Amino Acids↗
PubMed1990

[The development of an aerobic intestinal microflora in newborn infants].

The microbial colonization of the intestinal tract was studied in 60 newborn babies from three hospitals, with special regard to the typical hospital "problem" strains. Escherichia coli was the predominant initial colonizing species. Opportunistic pathogens were repeatedly detected. Some 30% of E. coli strains showed beta-hemolysis. Distinct differences between the three clinics were noted with respect to the detection frequency of the species isolated, hemolytic bacteria, the predominating E. coli strains, the occurrence of Candida albicans, and the time course of colonization of the gut by E coli. The microbial environment of the respective neonatal unit has a great influence on the initial intestinal colonization by aerobic microorganisms.

Bacteria, Aerobic↗
PubMed1996

Protein and lipid refeeding changes protein metabolism and colonic but not small intestinal morphology in protein-depleted rats.

In this study, we fed rats a 2% casein AIN 76 diet for 2 wk to produce protein malnutrition. We determined in these animals the effects of different concentrations of dietary protein refeeding (2% and 20% casein) on recovery and gut mucosal repletion and the potential role of type of dietary fat in the regulation of protein metabolism and mucosal growth by providing conventional long-chain triglyceride (LCT), a structured lipid composed of long-, medium- and short-chain fatty acids (SC/SL), or a physical mixture of the same components present in the structured lipid given as individual pure triglycerides (SC/PM) along with adequate amounts of protein and energy. The results confirmed that protein malnutrition can be reversed rapidly by protein refeeding, as indicated by an increase in body weight, positive nitrogen balance, liver growth and elevations in plasma concentrations of insulin-like growth factor-1, leucine and albumin. In the colon, crypt cell number, crypt depth and number of crypt cells in the rapidly proliferating fraction of the colon were greater in rats fed the higher protein diet. However, the general architecture of small intestinal mucosa, including duodenum, jejunum and ileum, was not affected by protein malnutrition. Although the number of colonic cells was similar with fat refeeding, there were significantly fewer displaying the proliferating cell nuclear antigen in the colonic epithelium when rats were fed SC/PM compared with SC/SL. Therefore, changes in colonic mucosal proliferation were only seen with repletion by adequate protein and by SC/SL feeding.

Absorption↗
PubMed2003

Human gastrointestinal sulfotransferases: identification and distribution.

Sulfotransferases (STs) catalyze the sulfation of many structurally diverse molecules. Enzymatic assays and Western blots have been used to identify and characterize STs in the human gastrointestinal tract. Sulfation activities for 2-naphthol, dopamine, estradiol, and dehydroepiandrosterone (DHEA) from 23 donors were measured in cytosol prepared from stomach, duodenum, segments of small intestine, and colon and were compared to levels in human liver cytosol. Stomach and colon had low 2-naphthol and dopamine sulfation activities and almost no estradiol and DHEA sulfation activity. For all four substrates, small intestine has higher activities than both stomach and colon. Human small intestine 2-naphthol sulfation specific activity is approximately half that of human liver. Human small intestine dopamine sulfation activity is three times as high as that of human liver. While estrogen sulfation activity is about the same for both human intestine and human liver, human liver DHEA sulfation activity is about five times as high as that of human small intestine. The distribution of ST activities along the length of the small intestine was very different among different donors. Some donors had higher activity in the proximal segments of the small intestine, whereas other donors had higher activity in the distal segments of the small intestine. Our results also demonstrated high variation of small intestine sulfation activities compared with human liver activities among different donors. The Western blot results agreed with the enzymatic assay results. These results suggest that xenobiotics may regulate human small intestinal STs.

Adolescent↗
PubMed2006

Investigation of the absorption mechanisms of baicalin and baicalein in rats.

To characterize and compare the absorption mechanisms of baicalin (BG) and baicalein (B), either of them was perfused in situ in rats with ligation of the bile duct as well as without it. Two RP-HPLC methods were developed to determine the drugs' concentrations in the gastric and intestinal perfusates, respectively. The result showed that BG was moderately absorbed in stomach but poorly in small intestine and colon, while B was well absorbed in stomach and small intestine but relatively less in colon. It also indicated that bile could excrete BG and significantly promote the absorption of B. When BG or B was perfused alone in the small intestine after ligation of the bile duct, there came out to be increasing B or BG in the perfusate, respectively. In addition, when B was intravenously administered to rats after ligation of the bile duct, there came out to be BG in the intestinal perfusate. In conclusion, B was more suitable to be administered orally than BG, which was absorbed as B and then restored to BG in the body. Part of the BG formed from the absorbed or intravenously administered B could be excreted back into the gut.

Administration, Oral↗
PubMed2004

Vitamin A deficiency aggravates rotavirus infection in CD-1 mice through extensive involvement of the gut.

Rotavirus (RV) is one of the leading causes of life-threatening viral gastroenteritis in infants and animals. More than 100 million children live in endemic areas where they are at risk of rotavirus infection. In the western world, rotavirus is usually a self-limiting disease that involves no major sequelae; however, in the developing world it often leads to morbidity and mortality. One of the major components influencing the prognosis of rotavirus-infected children is their nutritional status. The prevalence of vitamin A deficiency in developing countries, where RV infection can be fatal, encompasses up to 40% of preschool children. We hypothesized, therefore, that vitamin A deficiency in an animal model would aggravate the course of rotavirus disease. CD-1 mice were infected with RV and fed either vitamin A-sufficient or vitamin A-deficient diets. Histological components of the small intestine and colon, stool samples from which rotavirus was recovered, and vitamin A levels were examined. Flattening of the villi along the duodenum was observed in both rotavirus-infected and non-infected vitamin A-deficient mice. Maximal effect was obtained with a combination of vitamin A deficiency and RV infection. The colon of vitamin A-deficient, infected mice displayed a significantly (p < 0.05) smaller glandular area and higher level of mucin, and viral excretion in the stool became significantly (p < 0.01) increased and lasted longer than in controls. We conclude that vitamin A deficiency aggravates the course of RV infection through both small intestinal and colonic damage.

Animals↗
PubMed1999

Expression and localization of aquaporins in rat gastrointestinal tract.

A family of water-selective channels, aquaporins (AQP), has been demonstrated in various organs and tissues. However, the localization and expression of the AQP family members in the gastrointestinal tract have not been entirely elucidated. This study aimed to demonstrate the expression and distribution of several types of the AQP family and to speculate on their role in water transport in the rat gastrointestinal tract. By RNase protection assay, expression of AQP1-5 and AQP8 was examined in various portions through the gastrointestinal tract. AQP1 and AQP3 mRNAs were diffusely expressed from esophagus to colon, and their expression was relatively intense in the small intestine and colon. In contrast, AQP4 mRNA was selectively expressed in the stomach and small intestine and AQP8 mRNA in the jejunum and colon. Immunohistochemistry and in situ hybridization demonstrated cellular localization of these AQP in these portions. AQP1 was localized on endothelial cells of lymphatic vessels in the submucosa and lamina propria throughout the gastrointestinal tract. AQP3 was detected on the circumferential plasma membranes of stratified squamous epithelial cells in the esophagus and basolateral membranes of cardiac gland epithelia in the lower stomach and of surface columnar epithelia in the colon. However, AQP3 was not apparently detected in the small intestine. AQP4 was present on the basolateral membrane of the parietal cells in the lower stomach and selectively in the basolateral membranes of deep intestinal gland cells in the small intestine. AQP8 mRNA expression was demonstrated in the absorptive columnar epithelial cells of the jejunum and colon by in situ hybridization. These findings may indicate that water crosses the epithelial layer through these water channels, suggesting a possible role of the transcellular route for water intake or outlet in the gastrointestinal tract.

Animals↗
PubMed1999

Urocortin mRNA is expressed in the enteric nervous system of the rat.

The expression of the urocortin gene in the gastrointestinal tract was investigated using reverse transcription polymerase chain reaction (RT-PCR) and in situ hybridization histochemistry. PCR demonstrated the presence of urocortin mRNA in the rat brain, duodenum, small intestine, and colon. By in situ hybridization, urocortin-containing cells were exclusively localized to the submucosal plexus and myenteric plexus in the duodenum, small intestine and colon. These results suggest that urocortin may play an important role in the regulation of gastrointestinal motor function throughout the enteric nervous system.

Animals↗
PubMed2006

Modulatory influence of dietary resveratrol during different phases of 1,2-dimethylhydrazine induced mucosal lipid-peroxidation, antioxidant status and aberrant crypt foci development in rat colon carcinogenesis.

To shed light on the association of lipid peroxidation and antioxidant status with the development of aberrant crypt foci (ACF), we studied the modulatory influence of resveratrol, supplemented in three dietary regimens (initiation, post-initiation and entire period) on 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis. Rats were administered DMH (20 mg/kg body weight, s.c.) for 15 weeks and were supplemented with resveratrol (8 mg/kg body weight, p.o. everyday) in three dietary regimens. Intestines and colons were analyzed for the levels of diene conjugates (DC), lipid hydroperoxides (LOOHs) and thiobarbituric acid reactive substances (TBARS). Enzymic antioxidants (superoxide dismutase, SOD; catalase, CAT; glutathione peroxidase, GPX; glutathione S-transferase, GST; and glutathione reductase, GR) and non-enzymic reserve (reduced glutathione, GSH; ascorbate; and alpha-tocopherol) were also assessed in the intestine and colon. Unsupplemented DMH exposed rats showed significantly decreased levels/activities of tissue DC, LOOHs, TBARS, SOD, CAT, GSH, GR and significantly elevated (P<0.05) GPX, GST, alpha-tocopherol and ascorbate as compared to control rats. Resveratrol supplementation during the entire period of the study resulted in significant (P<0.01) modulation of lipid peroxidation markers and antioxidants status, which were paralleled with ACF suppression, as compared to DMH-alone treated rats. These results indicate that resveratrol effectively inhibits DMH-induced ACF and colonic tumor development.

1,2-Dimethylhydrazine↗
PubMed1975

Binding of cholera toxin by various tissues.

Under certain conditions, it is possible to confirm the observation by Peterson (1974) that the cholera toxin-binding capacities of tissues from brain and colon mucosa, and from liver and small intestine mucosa, are comparable. Binding of toxin by all tissues except brain is very variable, but is roughtly proportional to their content of the toxin-binding ganglioside galactosyl-N-acetylgalactosaminyl (sialosyl) lactosyl ceramide. It appears that some toxin-binding sites of the mucosa of the small intestin and colon may be masked. It has also been confirmed that there may be some solubilization of toxin-binding material from brain on standing a few days at 4 C, but this is comparatively slight. Some disadvantages of measuring toxin binding by adding small amounts of radioactive toxin to compartively large amounts of tissue are discussed.

Animals↗
PubMed2005

Isolated crypts form spheres prior to full intestinal differentiation when grown as xenografts: an in vivo model for the study of intestinal differentiation and crypt neogenesis, and for the abnormal crypt architecture of juvenile polyposis coli.

We describe a model system in which single crypts, isolated from newborn rats, were embedded in a type I collagen gel and subcutaneously grafted to the flanks of nude mice, whereupon they underwent full intestinal morphogenesis. Small fragments of small intestine and colon were incubated with the divalent cation chelator EDTA, resulting in the release of crypts and villi. Released crypts were then suspended sparsely in type I collagen gel. Segments of gel containing a single crypt were grafted subcutaneously into a nude mouse. Grafts were harvested at weekly intervals. By 2 days, the mouth of the crypts had joined to seal the crypt and, within 1 week, the structure ballooned to form a spherical cystic structure lined by flattened epithelial cells showing no evidence of cytodifferentiation. After 2 weeks, host stromal cells had invaded the collagen and settled around this spherical crypt. At points where stromal cells appeared in contact with the crypt, the epithelium exhibited a more columnar phenotype. By 4 weeks, the 'crypt sphere' was surrounded by stroma expressing alpha-smooth muscle actin and, at this time, multiple buds appeared that gave rise to new crypts. By 5 weeks, villi had formed and cell lineages associated with the small intestine and colon were present; the original single crypt had transformed into a functional intestinal unit. Therefore, we have shown that a single crypt has the potential to grow, give rise to other crypts and dependent structures such as villi. This model has considerable potential for use in gene transfer experiments in the study of intestinal differentiation, and for the analysis of crypt neogenesis via crypt fission. Moreover, the appearances showed a close resemblance to those seen in juvenile polyposis syndrome (JPS), where the budding and fission of single crypts isolated by stromal overgrowth offers an alternative explanation for the histogenesis of JPS.

Adenomatous Polyposis Coli↗
PubMed2000

Cellular distribution of prostanoid EP receptors mRNA in the rat gastrointestinal tract.

The inhibition of PGE(2) synthesis resulting from sustained NSAIDs therapy has been linked to gastrointestinal irritations and ulceration. The multiple physiological effects of PGE(2) in the gut are mediated through the activation of four receptors termed EP(1-4). The aim of the study was to determine the precise distribution of the four prostaglandin E(2) receptors in the rat stomach, small intestine, and colon. We used non-radioactive in situ hybridization techniques on paraffin-embedded tissue. Mucous cells of the stomach and goblet cells of the small intestine and colon were found to express mRNA for all four EP subtypes. A positive hybridization signal for EP(1), EP(3), and EP(4) was detected in the parietal cells of the stomach whereas the chief cells expressed low levels of EP(1) and EP(3). The EP(1) and EP(3) receptor mRNA could also be detected in the muscularis mucosa, longitudinal muscle and enteric ganglias of the stomach and small intestine. However, close examination of the enteric ganglias indicated that most of the positive labeling was localized to the glial cells, although some neurons did express EP(3). In conclusion, we have detailed the distribution of prostanoid EP receptors in the gut at the cellular level, giving new insights to the role of prostaglandins in gastrointestinal functions.

Animals↗
PubMed2004

The use of formulation technology to assess regional gastrointestinal drug absorption in humans.

The aim of this study was to assess the feasibility of using oral modified-release formulations for the purposes of site-specific targeting and regional drug absorption assessment in man. An immediate release pellet formulation containing ranitidine as the model drug of choice for the study was fabricated by extrusion-spheronisation, and then film coated with either the enteric polymer polyvinyl acetate phthalate or the bacteria-degradable polymer amylose, in combination with ethylcellulose, to effect drug release within the small intestine and colon, respectively. Optimised formulations were evaluated in vivo in ten healthy volunteers, who each received, on four separate occasions, the immediate release, small intestinal release and colonic release formulations (each equivalent to 150mg ranitidine), and an intravenous injection of ranitidine (equivalent to 50mg ranitidine). Blood samples were collected and assessed for ranitidine concentration, and radiolabelled placebo pellets were co-administered with the coated ranitidine pellets to monitor their gastrointestinal transit using a gamma camera. Ranitidine was rapidly released and absorbed from the immediate release formulation, whereas the enteric formulation (10% coat weight gain) delayed drug release until some or all of the pellets had emptied into the small intestine. The amylose-ethylcellulose coated formulation (coat ratio 1:3, coat weight gain 25%) retarded ranitidine release until the pellets had reached the colon. The mean absolute bioavailability of ranitidine from the immediate release, small intestinal release and colonic release formulations were 50.6, 46.1 and 5.5%, respectively. These data are in general agreement to those obtained from a previous regional intubation study. The present study therefore demonstrates the practical potential of utilising a non-invasive, formulation-based approach to assess drug absorption from different regions of the human gastrointestinal tract.

Administration, Oral↗
PubMed1991

Tissue distribution of the 1,25-dihydroxyvitamin D3 receptor in the male rat.

Tissue distribution of 1,25-dihydroxyvitamin D3 receptors was studied in male rats using a quantitative immunoradiometric assay. Extracts were prepared from 16 different rat tissues and assayed for 1,25-dihydroxyvitamin D3 receptor. Measurable levels of receptor were detected in intestine, stomach, kidney, bone thyroid/parathyroid, skin, liver, spleen, heart and lung. The highest levels were found in the proximal small intestine and colon, containing over 1000 fmol/mg total protein, while ileum and kidney contained one-half and one-fourth of this amount, respectively. Other parts of the vitamin D endocrine system, including bone, thyroid/parathyroid and skin, contained moderate levels of receptor of 40 to 80 fmol/mg, while lung, heart, stomach, spleen and liver had levels at or below 20 fmol/mg. No 1,25-dihydroxyvitamin D3 receptor was detected in cerebrum, cerebellum or skeletal muscle. The data support a wide-spread role for 1,25-dihydroxyvitamin D3 on cellular processes and suggest a more important role for vitamin D in colon.

Animals↗