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PubMed1988

[Experimental study on interdigestive migrating contractions with intestinal transection and injection of Ringer solution into intestine].

The occurrence and mechanism of IMC are still not completely elucidated. Base on the conjecture of that the region of intestine and its ingredients may be concerning with the conduction mechanism of IMC, following experiment was performed by author. Small intestine was cut into two parts. Anal side was closed as blind end, and the end of oral side was sutured to colon or anal part of intestine by end to side anastomosis. Gastric fistula and intestinal fistula of the blind ending intestine were also made, and six pieces of force transducers were sutured to the serosa of the intestine in order to observe the movement of intestine. Under non-anesthesia and non-restricted condition for whole day long, Ringer solution was injected into gastric or intestinal fistula by 50 ml one shot or continuous dripped infusion of 250 ml per hour. The result is: In upper part of intestine, the appearance of IMC in oral and anal side of intestine is continuously observed. However, in lower part of intestine, the IMC of oral and anal part of intestine appeared completely independent without any continuity. And, as one shot of 50 ml of Ringer solution was injected, the conduction of IMC was suppressed but still observable, while continuously infused of 250 ml/hr, the IMC was completely disappeared.

Anastomosis, Roux-en-Y↗
PubMed2004

Foxl1 null mice have abnormal intestinal epithelia, postnatal growth retardation, and defective intestinal glucose uptake.

Mice lacking the mesenchymal winged helix transcription factor Foxl1 exhibit markedly abnormal small intestinal epithelia and postnatal growth retardation. We investigated whether defects in intestinal nutrient uptake and specific transport processes exist in mice homozygous for a Foxl1 null allele (Foxl1-/-). Foxl1-/- mice and controls on a defined genetic background were weighed regularly and killed at 2, 4, and 12 wk of age. Intestinal uptake studies, quantitative real-time PCR, RNase protection assays, and Western blot analyses were performed. Foxl1-/- mice have dysmorphic small intestinal epithelia and postnatal growth retardation. Foxl1-/- mice demonstrate decreased small intestinal uptake of D-glucose in all age groups studied. Intestinal uptake of D-fructose and two amino acids, L-proline and L-leucine, is not altered. Consistent with these findings, Foxl1-/- mice show decreased levels of the intestinal D-glucose transporter SGLT1. Expression of sucrase-isomaltase, lactase, GLUT2, and Na+-K+ ATPase are not changed. Foxl1-/- mice demonstrate markedly abnormal intestinal epithelia, postnatal growth retardation, and decreased intestinal uptake of D-glucose. The specific effect of Foxl1 on intestinal d-glucose uptake is due to decreased production of SGLT1 protein in the small intestine. Thus we identified, for the first time, a link between a mesenchymal factor, Foxl1, and the regulation of a specific epithelial transport process.

Animals↗
PubMed2006

Intestinal insulin resistance and aberrant production of apolipoprotein B48 lipoproteins in an animal model of insulin resistance and metabolic dyslipidemia: evidence for activation of protein tyrosine phosphatase-1B, extracellular signal-related kinase, and sterol regulatory element-binding protein-1c in the fructose-fed hamster intestine.

Postprandial dyslipidemia is recognized as an important complication of insulin-resistant states, and recent evidence implicates intestinal lipoprotein overproduction as a causative factor. The mechanisms linking intestinal lipoprotein overproduction and aberrant insulin signaling in intestinal enterocytes are currently unknown. Intestinal insulin sensitivity and lipid metabolism were studied in a fructose-fed hamster model of insulin resistance and metabolic dyslipidemia. Intestinal lipoprotein production in chow-fed hamsters was responsive to the inhibitory effects of insulin, and a decrease in circulating levels of triglyceride-rich apolipoprotein (apo)B48-containing lipoproteins occurred 60 min after insulin administration. However, fructose-fed hamster intestine was not responsive to the insulin-induced downregulation of apoB48-lipoprotein production, suggesting insulin insensitivity at the level of the intestine. Enterocytes from the fructose-fed hamster exhibited normal activity of the insulin receptor but reduced levels of insulin receptor substrate-1 phosphorylation and mass and Akt protein mass. Conversely, the protein mass of the p110 subunit of phosphatidylinositol 3-kinase, protein tyrosine phosphatase-1B, and basal levels of phosphorylated extracellular signal-related kinase (ERK) were significantly increased in the fructose-fed hamster intestine. Modulating the ERK pathway through in vivo inhibition of mitogen-activated protein/ERK kinase 1/2, the upstream activator of ERK1/2, we observed a significant decrease in intestinal apoB48 synthesis and secretion. Interestingly, enhanced basal ERK activity in the fructose-fed hamster intestine was accompanied by an increased activation of sterol regulatory element-binding protein. In summary, these data suggest that insulin insensitivity at the level of the intestine and aberrant insulin signaling are important underlying factors in intestinal overproduction of highly atherogenic apoB48-containing lipoproteins in the insulin-resistant state. Basal activation of the ERK pathway may be an important contributor to the aberrant insulin signaling and lipoprotein overproduction in this model.

Administration, Oral↗
PubMed2004

Frog intestinal sac: a new in vitro method for the assessment of intestinal permeability.

The aim of this study was to evaluate a new experimental protocol utilizing isolated frog intestinal sacs for the assessment of intestinal drug permeability in humans. Segments of approximately 5.0 cm in length were used for these experiments. The intestinal sacs were filled with a solution of the appropriate drug in frog Ringer (FR) and immersed in a vial containing fresh FR. The transport was monitored for a period ranging from 2 to 5 h by moving the intestinal sac at each time point to a new vial containing fresh medium (Method A). Alternatively, according to Method B, at predetermined times aliquots of receiving mixture were taken up without removing the intestinal sac, and replaced with fresh drug-free FR. In all cases, the samples were analyzed by HPLC. A series of 20 noncongeneric drugs, predominantly absorbed by passive diffusion mechanism, was examined. The results indicate that drugs completely absorbed in humans had Papp values greater than 1 x 10(-6) cm/s, while drugs absorbed <90% had Papp values lower than 1 x 10(-6) cm/s. By plotting Log Papp values against percent human absorption, an approximately sigmoidal relationship was obtained. The frog intestinal sac method was evaluated as a permeability model to classify the 20 studied drugs into the Biopharmaceutics Classification System (BCS). By comparing the predictions made by this new approach with those reported in literature, it can be concluded that a satisfactory biopharmaceutical classification may be based on the Papp values determined by the frog intestinal permeability. Molecular properties relevant to passive intestinal permeability were considered to evaluate the correlation with the frog intestinal permeability rates recorded. Good relationships were observed when hydrogen-bonding parameters were expressed as a function of the Log Papp values. It can be concluded that the in vitro permeability coefficient deduced from isolated frog intestinal experiments can be used for predicting peroral absorption in humans for passively absorbed compounds. Computational methods for prediction of frog intestinal permeability may be applied in a highly simplified manner.

Animals↗
PubMed1986

Substance P, neurokinin A, vasoactive intestinal polypeptide and gastrin releasing peptide in the intestine and pancreas of spontaneously obese-diabetic mice.

The concentrations and contents of immunoreactive substance P (SP), neurokinin A (NKA), vasoactive intestinal polypeptide (VIP) and gastrin releasing peptide (GRP) were measured in acid-ethanol extracts of intestine (duodenum-jejunum-ileum) and pancreas of C57BL/KsJ diabetes-obese (db/db) mice, Aston obese-hyperglycaemic (ob/ob) mice, and their respective lean controls. The intestinal concentration of GRP and pancreatic concentrations of VIP and GRP were 36-57% lower in lean Aston mice than lean C57BL/KsJ mice, indicating the influence of genetic background in control mice. Intestinal concentrations of SP and NKA were reduced by 19-33% in the db/db and ob/ob mutants compared with their lean controls, but the intestinal contents of these peptides were normal or greater than normal due to intestinal hypertrophy of the mutant mice. The intestinal VIP concentration was not altered, but the content was increased by 87% and 25% respectively in db/db and ob/ob mice, whereas the intestinal GRP concentration was reduced by 51% in ob/ob mice. Pancreatic concentrations and contents of NKA, VIP and GRP were similar in lean and db/db C57BL/KsJ mice. However, pancreatic concentrations and contents of VIP and GRP were reduced by 51-55% in ob/ob mice compared with their lean controls. The sensitivity of the present assay did not permit accurate determination of the low pancreatic concentrations of SP. The results suggest that the spontaneous ob/ob and db/db syndromes of obesity and diabetes in mice are associated with reduced intestinal concentrations of SP and NKA. The ob/ob mouse also exhibited reductions of intestinal GRP and pancreatic GRP and VIP concentrations. These changes in regulatory peptides may relate to abnormalities of intestinal and possibly pancreatic function in obese and diabetic mutant mice.

Animals↗
PubMed2003

Intestinal-type and liver-type fatty acid-binding protein in the intestine. Tissue distribution and clinical utility.

OBJECTIVES: Intestinal-type fatty acid-binding protein (I-FABP) has been proposed as plasma marker for the detection of acute intestinal injury. However, intestinal mucosa also expresses liver-type FABP (L-FABP). We have investigated the tissue distribution of I-FABP and L-FABP in segments of the human intestine along the duodenal to colonal axis and the potential of both proteins to serve as plasma marker for the diagnosis of intestinal injury. DESIGN AND METHODS: I-FABP and L-FABP were measured with specific immunoassays in autopsy samples of the intestine (duodenum, jejunum, ileum and colon) of 23 subjects and in plasma samples from patients (n = 51) with intestinal and/or hepatic disease. Plasma reference values were established in normal healthy individuals (n = 92). RESULTS: The I-FABP tissue contents in duodenum, jejunum, ileum, proximal colon and distal colon amounted to 2.22, 4.79, 1.04, 0.27 and 0.25 mug/g ww, respectively. L-FABP tissue contents were markedly higher, amounting to 124 and 198 mug/g ww in duodenum and jejunum, and to 58, 26 and 44 mug/g ww in ileum, proximal colon and distal colon, respectively. Elevated plasma levels of both I-FABP and L-FABP were found in patients suffering from intestinal diseases, while only L-FABP was increased in cases of purely hepatocellular injury. CONCLUSIONS: I-FABP and L-FABP show a similar pattern of tissue distribution along the duodenal to colonal axis with highest tissue contents found in the jejunum but in each intestinal segment a >40-fold higher content of L-FABP than of I-FABP. Accordingly, besides I-FABP, also L-FABP is a useful plasma marker for the detection of intestinal injury, especially in patients undergoing intestinal surgery.

Adult↗
PubMed1993

Intestinal adaptation during lactation in the mouse. II. Altered intestinal processing of a dietary protein.

We previously demonstrated in lactating mice a six- to eightfold increase in the intestinal uptake of the dietary protein, ovalbumin (OVA), administered by gavage. In this study, we tested the possibility that alterations in intestinal morphology, transit time, reduced luminal proteolysis, and enhanced association with the intestinal surface might account for the increased uptake of the protein observed in lactating mice. We found that these animals had a significant increase in length, wet weight, and surface area of the small intestine. No change in the number of Peyer's patches was noted. Intestinal transit was assessed by gavage administration of 125I-OVA and 10 mg OVA and localization of the peak of radioactivity 15, 30, and 60 min after feeding. Although motility (distance traveled per unit time) was not different in lactating and control mice at 15 and 30 min, the fraction of the small intestine traversed by the peak of radioactivity was less in lactating mice. Digestion of 125I-OVA administered by gavage with 10 mg unlabeled OVA was examined by trichloroacetic acid precipitation and gel permeation of the resulting fragments. Lactating and control mice did not show differences in digestion of 125I-OVA by either measurement. The association of 125I-OVA with small intestinal segments, however, was enhanced in lactating mice, especially in the second and third segments of the small intestine. Thus several factors including an increase in length and surface area of the small intestine, prolonged contact of protein with the small intestinal absorptive surface, and enhanced association of the protein with the intestinal surface contribute to increased uptake.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed2006

Intestinal permeability of metformin using single-pass intestinal perfusion in rats.

AIM: To characterize the intestinal transport and mechanism of metformin in rats and to investigate whether or not metformin is a substrate for P-glycoprotein (P-gp). METHODS: The effective intestinal permeability of metformin was investigated using single-pass intestinal perfusion (SPIP) technique in male Waster rats. SPIP was performed in three isolated intestinal segments (duodenum, jejunum and ileum) at the same concentration of metformin (50 microg/mL) to test if the intestinal transport of metformin exhibited site-dependent changes, and in a same isolated intestinal segment (duodenal segment) at three different concentrations of metformin (10, 50, 200 microg/mL) to test if the intestinal transport of metformin exhibited concentration-dependent changes. Besides, P-gp inhibitor verapamil (400 microg/mL) was co-perfused with metformin (50 microg/mL) in the duodenum segment to find out if the intestinal absorption of metformin was affected by P-gp exiting along the gastrointestinal track. Stability studies were conducted to ensure that the loss of metformin could be attributed to intestinal absorption. RESULTS: The effective permeability values (P(eff)) of metformin in the jejunum and ileum at 50 microg/mL were significantly lower than those in the duodenum at the same concentration. Besides, P(eff) values in the duodenum at high concentration (200 microg/mL) were found to be significantly lower than those at low and medium concentrations (10 and 50 microg/mL). Moreover the co-perfusion with verapamil did not increase the P(eff) value of metformin at 50 microg/mL in the duodenum. CONCLUSION: Metformin could be absorbed from the whole intestine, with the main absorption site at duodenum. This concentration-dependent permeability behavior in the duodenum indicates that metformin is transported by both passive and active carrier-mediated saturable mechanism. The P(eff) value can not be increased by co-perfusion with verapamil, indicating that absorption of metformin is not efficiently transported by P-gp in the gut wall. Furthermore metformin is neither a substrate nor an inducer of P-gp. Based on the P(eff) values obtained in the present study and using established relationships, the human fraction dose absorbed for metformin is estimated to be 74%-90% along human intestine.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1983

Effect of cimetidine on intestinal adaptation following massive resection of the small intestine.

Gastric acid hypersecretion follows massive resection of the small intestine. Steatorrhea as well as other metabolic imbalances is a challenging management problem associated with massive resection of the small intestine. In the literature, it has been suggested that the empiric use of cimetidine controls gastric acid hypersecretion following massive resection of the small intestine. In this study, an 80 per cent resection of the small intestine was performed upon 12 mongrel dogs. Ileal pH measurements, fecal fat content and serial intestinal biopsies were obtained for morphometric measurements. Steatorrhea was reduced by approximately 40 per cent in the cimetidine treated dogs. Ileal pH measurements declined immediately following intestinal resection. The cimetidine treated dogs demonstrated a return to normal levels within ten days following intestinal resection, p less than 0.05. Intestinal adaptation morphometric parameters revealed an accelerated adaptational response in the cimetidine treated dogs, p less than 0.05. Results of this study colaborates with the empiric and clinical indication for the use of cimetidine in the short gut syndrome clinical situation. In addition, the data suggest an intestinal adaptation accelerated response during the first phase of intestinal adaptation following massive resection of the small intestine in the dog.

Adaptation, Physiological↗
PubMed1990

The effect of intestinal resection and urogastrone on intestinal regeneration.

Intestinal regeneration in patched intestinal defects is enhanced by both intestinal resection and urogastrone. Our aim was to determine if these two stimuli have synergistic effects. Ileal defects were patched with colon serosa in 45 rabbits. Group 1 (n = 11) were control subjects; group 2 (n = 12) underwent 50% intestinal resection; group 3 (n = 11) received urogastrone (1.5 micrograms/kg per hour subcutaneously); and group 4 (n = 11) underwent intestinal resection and received urogastrone. Animals were killed at 7 and 14 days. Intestinal resection had the greater effect on epithelialization. Urogastrone inhibited contraction and intestinal resection did not. Both intestinal resection and urogastrone increased proliferative activity. Combining intestinal resection and urogastrone did not have a synergistic effect on epithelialization and diminished the effect of urogastrone on proliferation and contraction. These findings suggest that intestinal resection and urogastrone stimulate epithelialization via similar mechanisms and that urogastrone would not enhance regeneration during intestinal adaptation.

Animals↗
PubMed1995

Vasoactive intestinal polypeptide and other preprovasoactive intestinal polypeptide-derived peptides in the female and male genital tract: localization, biosynthesis, and functional and clinical significance.

Vasoactive intestinal polypeptide, a neuropeptide with wide distribution in the central and peripheral nervous system, has a broad spectrum of biologic actions. The demonstration of vasoactive intestinal polypeptide containing nerve fibers within the female and male genital tract 17 years ago indicated a putative role for this peptide in the local nervous control of reproductive functions. The genes encoding the preprovasoactive intestinal polypeptide precursor molecule and the vasoactive intestinal polypeptide receptor have been identified. The gene expression has been studied by the use of specific antibodies against the functional domains of the vasoactive intestinal polypeptide precursor and the biologic action elucidated by both in vivo and in vitro methods. Evidence has been provided to support vasoactive intestinal polypeptide as a neurotransmitter in several physiologic events in the genital tracts (i.e., blood flow and nonvascular smooth muscle relaxation). In the ovary vasoactive intestinal polypeptide seems to play an important role as regulator and/or modulator of folliculogenesis and steroidogenesis. In the male genital tract vasoactive intestinal polypeptide seems to participate in the control of erection. Vasoactive intestinal polypeptide has been suggested as a causative factor in some diseases of the genital organs (e.g., it may play a pathophysiologic role in male impotence and the peptide is currently used in the treatment of this condition). Vasoactive intestinal polypeptide may be important for control of the low resistance in the fetomaternal vascular bed and is therefore a putative factor involved in the development of preeclampsia. The therapeutic potential of vasoactive intestinal polypeptide and future agonists and antagonists will be revealed by ongoing and forthcoming studies.

Amino Acid Sequence↗
PubMed2001

Analysis of patients with longitudinal intestinal lengthening procedure referred for intestinal transplantation.

BACKGROUND/PURPOSE: Longitudinal intestinal lengthening procedures (LILP) in patients with short gut syndrome (SGS) enhances small intestinal peristalsis and decreases bacterial overgrowth without reducing absorptive surface. Therefore, patients theoretically may be easily weaned off TPN. The aim of this study was to evaluate the impact of failed LILP in SGS patients referred for intestinal transplantation. METHODS: Twenty-seven (11%) of 230 children with SGS and total parenteral nutrition (TPN) dependency evaluated for intestinal transplantation at our institution had undergone LILP. This was performed at a mean age of 1.7 years (range, 1 day to 14.7 years); the mean age at the time of evaluation was 3.3 years (range, 0.4 to 17 years). Two patients underwent LILP immediately after birth. The principle diagnoses producing SGS were gastroschisis (n = 8), intestinal atresia (n = 11), neonatal volvulus (n = 7) and necrotizing enterocolitis (n = 1). Before LILP, the mean length of intestine was 32 cm (range, 8 to 70 cm). Fifteen (56%) patients had jaundice at the time of evaluation. RESULTS: All but one child were considered candidates for intestinal transplantation. The mean intestinal length achieved after LILP was 48 cm (range, 16 to 100). The mean follow-up from the date of LILP was 876 days (range, 109 to 4,109 days). After LILP, only 9 (33%) patients increased their caloric intake through the enteral route by > or =50%, and only 1 patient could be weaned off TPN. In the patients with liver dysfunction at the time of LILP, none recovered. Most of the patients had multiple episodes of sepsis after LILP. Fourteen (52%) of 27 patients underwent intestinal transplantation, 7 combined with a liver allograft because of TPN-induced end-stage liver disease. Six of the transplanted patients are alive and TPN free. Of the remaining 13 (48%) nontransplanted patients, 9 patients died. The main cause of death was TPN-induced liver failure. Three patients are on partial TPN, and only 1 patient was weaned off TPN. The presence of an ileocecal valve did not impact on outcome. Surprisingly, patients with > or =50% of colon at the time of LILP had poorer survival than those with less. Twelve (44%) of 27 patients had surgical complications, and in both patients with LILP performed in the neonatal period it failed immediately with acute complications. There were no differences in patient survival rate for patients with SGS without LILP (n = 203) and those with LILP (n = 27). CONCLUSION: Based on patients with unsuccessful LILP referred for intestinal transplantation, we believe this procedure should be avoided in the neonatal period, in those patients with liver dysfunction, and when intestinal length is <50 cm.

Adolescent↗
PubMed1996

cis-Acting elements and transcription factors involved in the intestinal specific expression of the rat calbindin-D9K gene: binding of the intestine-specific transcription factor Cdx-2 to the TATA box.

The calbindin-D9K (CaBP9k) gene is mainly expressed in differentiated duodenal epithelial cells and is used as a model for studying the molecular mechanisms of intestine-specific transcription. The gene has been cloned, two major DNase-I-hypersensitive sites in the duodenum have been described, and a vitamin-D-response element has been identified. We have now analysed the transcription factors and regulatory sequences involved in the transcription of the CaBP9k gene in the intestine in ex vivo and in vitro experiments. Transfection experiments in intestinal (CaCo-2) and non-intestinal (HeLa) cell lines defined two regions in the 5'-flanking sequences of the rat CaBP9k gene. A minimal proximal region (-117 to +20) promoted transcription in both intestinal expressing and non-expressing cell lines. Tissue specificity was conferred by the sequences situated further upstream, which are responsible for complete repression in the non-intestinal cells. Intestinal transcription was specified by the proximal region, containing a specialized TATA box, and a distal region, which contains a previously described intestinal DNase-I-hypersensitive site. In vitro DNase I footprinting, electrophoretic mobility shift assays and antibody supershift assays were used to examine the factors bound to the proximal promoter region (-800 to +80 bp). Rat duodenal nuclear extracts protected 12 sites. Some of them appear to be binding sites for ubiquitous (nuclear factor 1) or hepatic-enriched sites (hepatocyte nuclear factors 1 and 4, enhancer binding protein alpha and beta factors. DNA binding studies and transfection experiments indicated that an intestine-specific transcription factor, caudal homeobox-2, binds to the TATA box of the rat CaBP9k gene. These data contribute to our understanding of the control of the intestinal transcription of the CaBP9k gene and demonstrate that several trans-acting factors, other than the vitamin D receptor, may be factors for intestine-specific CaBP9k gene expression.

Animals↗
PubMed2001

Shigella infection in a SCID mouse-human intestinal xenograft model: role for neutrophils in containing bacterial dissemination in human intestine.

Shigellae infect human intestine and cause intense inflammation and destruction of colonic and rectal mucosa. To model the interactions of shigella with human intestine in vivo, we have studied shigella infection in human intestinal xenografts in severe combined immunodeficient mice (SCID-HU-INT mice). Inoculation of shigella into human intestinal xenografts caused severe inflammation and mucosal damage, which was apparent as soon as 4 h following infection. Shigella infection was associated with human intestinal production of interleukin-1B (IL-1B) and IL-8 and a marked neutrophil influx into the graft. Depletion of neutrophils from SCID-HU-INT mice reduced inflammation in the human intestinal xenograft in response to shigella infection but failed to significantly alter tissue damage. However, the number of intracellular bacteria was more than 20-fold higher in the human intestinal xenografts from neutrophil-depleted SCID-HU-INT mice. Infection of human intestinal xenografts with an attenuated vaccine strain of shigella (CVD1203) induced lower levels of IL-1B and IL-8 than wild-type shigella and caused only moderate damage to the intestinal permeability barrier. Our studies establish the SCID-HU-INT mouse as a viable model for studying the interactions between shigella and human intestine and indicate that neutrophils are important for controlling the invasion of human intestine by shigella.

Animals↗
PubMed1987

Effect of intestinal denervation on intestinal vascular response to severe arterial hypoxia in newborn swine.

We examined the effects of alpha-adrenergic blockade (phentolamine) and intestinal denervation on the circulatory response of the newborn swine intestine to severe arterial hypoxia. Intestinal vascular resistance significantly increased during severe arterial hypoxia in the control group, whereas no change in intestinal vascular resistance was observed in the phentolamine or denervation groups at this time. Intestinal perfusion pressure increased in the control group but decreased in the phentolamine and denervation groups during severe arterial hypoxia. Despite the difference in intestinal vascular resistance, intestinal blood flow decreased in a similar manner in all groups during severe arterial hypoxia. Intestinal arteriovenous O2 content difference [(a-v)O2] and O2 uptake were greater during severe arterial hypoxia in the phentolamine and denervation groups than in the control group. We speculate that the sympathetic stimulation mediates the increase in intestinal vascular resistance in newborn swine during severe arterial hypoxia; and sympathetic stimulation limits the increase in intestinal (a-v)O2, which occurs during severe arterial hypoxia in the newborn swine intestine.

Animals↗
PubMed2007

Effects of butyrate on intestinal barrier function in a Caco-2 cell monolayer model of intestinal barrier.

Production of short-chain fatty acids (SCFA) in the intestinal lumen may play an important role in the maintenance of the intestinal barrier. However, overproduction/accumulation of SCFA in the bowel may be toxic to the intestinal mucosa and has been hypothesized to play a role in the pathogenesis of neonatal necrotizing enterocolitis (NEC). By using a Caco-2 cell monolayer model of intestinal barrier, we report here that the effect of butyrate on the intestinal barrier is paradoxical. Butyrate at a low concentration (2 mM) promotes intestinal barrier function as measured by a significant increase in transepithelial electrical resistance (TER) and a significant decrease in inulin permeability. Butyrate at a high concentration (8 mM) reduces TER and increases inulin permeability significantly. Butyrate induces apoptosis and reduces the number of viable Caco-2 cells in a dose-dependent manner. Intestinal barrier function impairment induced by high concentrations of butyrate is most likely related to butyrate-induced cytotoxicity due to apoptosis. We conclude that the effect of butyrate on the intestinal barrier is paradoxical; i.e. whereas low concentrations of butyrate may be beneficial in promoting intestinal barrier function, excessive butyrate may induce severe intestinal epithelial cell apoptosis and disrupt intestinal barrier.

Apoptosis↗
PubMedDate not supplied

Systemic intestinal metabolism of 1-naphthol. A study in the isolated vascularly perfused rat small intestine.

Using a vascularly and luminally perfused rat small intestine, we studied the systemic intestinal metabolism of the model substrate 1-naphthol (1-N) to 1-naphthol-beta-D-glucuronide (1-NG). An intestinal extraction ratio of 0.30 +/- 0.02 was found for 1-N. This implies that intestinal metabolism represents up to 14% of the total plasma clearance of 1-N in the rat in vivo. The formed 1-NG was preferentially released into the vascular perfusate, suggesting specialized transport carriers for 1-NG in brushborder and basolateral membrane. When the vascular flow rate was decreased from 10 to 0.5 ml/min, the clearance of 1-N appeared to be completely flow dependent. The apparent conflict between a low extraction ratio (0.30 +/- 0.02 at all flows investigated) and a flow rate-limited 1-N clearance can be explained by the presence of an intestinal vascular bed with a high extraction ratio. We suggest that 1-N is completely extracted from the mucosal blood flow. This view was confirmed by the results of experiments in which the capillary flow of the intestinal mucosa was decreased by infusion of noradrenaline. As a result a temporary decrease in the 1-N extraction ratio was observed. The contribution of the intestine to the total clearance can be masked by the hepatic clearance, because the blood supply to the intestine and liver is coupled in series. An equation was derived to describe the relative contribution of the intestine to the mesenteric clearance of the intestine-liver system. It appears that the effective contribution of the intestine to the mesenteric clearance is of little interest for high extraction drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

Distribution of marker enzymes and mucin in intestinal metaplasia in human stomach and relation to complete and incomplete types of intestinal metaplasia to minute gastric carcinomas.

Intestinal metaplasia of the human stomach was classified into two types, complete and incomplete. The complete type was associated with the intestinal marker enzymes sucrose alpha-D-glucohydrolase, alpha, alpha-trehalase, aminopeptidase (microsomal) (APM), and alkaline phosphatase (ALP). Tissue of this type contained goblet cells and Paneth's cells but not high-iron diamine (HID)-positive mucin staining with HID-Alcian blue. The incomplete type of intestinal metaplasia was associated with sucrose alpha-D-glucohydrolase, APM, goblet cells, and HID-positive mucin but not with alpha, alpha-trehalase, ALP, or Paneth's cells. For the examination of the distribution of the complete and incomplete types in 84, 27, and 16 resected specimens of human stomach with gastric carcinoma, gastric ulcer, and duodenal ulcer, respectively, disaccharidases were located with Tes-Tape. Specimens with intestinal metaplasia were divided into three classes: complete type only (class I), incomplete type only (class II), and a mixture of areas of the complete and incomplete types (class III). Of the 84 specimens from patients with gastric carcinoma, intestinal metaplasia was found in 76 (01%), and the percentages of specimens of classes I, II, and III were 32, 22, and 46, respectively. In these specimens, the percent incidence of class I increased and that of class II decreased with age. Of the 27 specimens from patients with gastric ulcer, 16 (59%) shopwed intestinal metaplasia and 10 of the 16 (63%) specimens were of class II. Of the 16 specimens from patients with duodenal ulcer, only 3 (19%) specimens showed intestinal metaplasia and all of them were of class II. The relationships of the complete and incomplete types of intestinal metaplasia to gastric carcinoma wre studied in 26 foci of minute carcinoma of the stomach less than 5 mm in largest diameter. Nineteen of 20 (05%) foci of the intestinal type of minute carcinoma were surrounded by intestinal metaplasia and 16 foci (80%) were surrounded by the incomplete type of intestinal metaplasia.

Adult↗