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PubMed1997

Luminal antigliadin antibodies in small intestinal bacterial overgrowth.

OBJECTIVE: Elevated antigliadin antibody levels in small intestinal luminal secretions of subjects with normal or only mildly abnormal small intestinal histology are considered indicative of "latent" or "potential" celiac disease. The purpose of this study was to determine whether small intestinal bacterial overgrowth (SIBO) might provide an alternative explanation for positive luminal antigliadin antibodies in such subjects. METHODS: Twenty-six adult subjects without predisposition to disturbed mucosal immunity were investigated with culture of small intestinal luminal secretions. Luminal total IgA and IgA-antigliadin antibody concentrations were measured by radial immunodiffusion and indirect enzyme immunoassay, respectively. Local mucosal counts of IgA-plasma cells were determined by immunohistochemistry. Small intestinal histology and intraepithelial lymphocyte counts were assessed by light microscopy. Corresponding serum antigliadin antibody concentrations were determined. RESULTS: SIBO was present in 17/26 (65.4%) subjects. No subject with SIBO had villous atrophy. Luminal total IgA concentrations (p < 0.0005), mucosal IgA-plasma cell counts (p < 0.01), and intraepithelial lymphocyte counts (p < 0.01) were significantly increased in subjects with SIBO. Luminal IgA-antigliadin antibodies were detected in 6/17 (35.3%) subjects with SIBO and 0/9 (0%) subjects without SIBO. Luminal IgA-antigliadin antibody concentrations correlated significantly with luminal total IgA levels (p < 0.01) but not with serum values (p < 0.1). Serum IgG-antigliadin antibody concentrations were elevated in 2/6 (33.3%) subjects with SIBO and positive luminal antigliadin antibodies. CONCLUSIONS: SIBO may be an alternative explanation to "latent" or "potential" celiac disease for positive luminal antigliadin antibodies in subjects with either normal or only mildly abnormal small intestinal histology, even when serum antigliadin antibody concentrations are elevated. Positive luminal antigliadin antibodies in SIBO probably occur as epiphenomena in the context of a graded mucosal immune response to local bacterial antigens.

Adult↗
PubMed1979

[Spontaneous solubilization of mcuosal peptide hydrolases in rat small intestine].

In vitro incubations of small intestine preparation lead to the spontaneous release of mucosal enzymes into the incubation medium, due to superficial dissolution and membrane lesions. One-hour anaerobic incubation of everted small intestine segments produces the liberation of from 13% (leucine arylamidase) to 30% (Gly-L-Pro-splitting peptide hydrolase) of the mucosal enzyme activities. Under the conditions of in vivo perfusion, the solubilization rates are from 50 to 80% lower than these values. The tendency to solubilization is only in part reduced to a significant extent by the saturation of the incubation medium with oxygen, but it does not reach the in vivo level. The detectability of membrane-bound and intracellular marker enzymes in the incubation medium permits no conclusions concerning the physiological localization of the released peptidases.

Anaerobiosis↗
PubMed2005

Cytotoxic chemotherapy upregulates pro-apoptotic Bax and Bak in the small intestine of rats and humans.

AIMS: Small intestinal crypt cells rapidly undergo apoptosis in response to cytotoxic drug treatment that results in gastrointestinal toxicity. The Bcl-2 family have been implicated in both positive and negative regulation of intestinal cell apoptosis. The aim of this study was to examine the effect of cytotoxic treatment on Bcl-2 protein expression in patients and rats with tumours. METHODS: Four pro- and four anti-apoptotic members of the Bcl-2 family, caspase-3 and p53 were examined in small intestinal crypts before and after treatment in rats and humans. Immunohistochemistry identified changes in protein expression over time, while relative RT-PCR was used to investigate mRNA expression in rat small intestine. RESULTS: Cytotoxic treatment increased p53 and caspase-3 which coincided with elevated levels of apoptosis. Bax and Bak protein and mRNA expression also significantly increased at 6 hours following treatment in rats. Bax and Bak protein increased at day 1 after treatment in humans. Anti-apoptotic Mcl-1 protein decreased within 24hours. Other Bcl-2 family members showed only modest changes. CONCLUSION: Increased expression of Bax and Bak but not other Bcl-2 family members is associated with apoptosis in small intestinal crypts and may amplify the sensitivity and susceptibility of crypt cells to chemotherapy-induced enteropathy.

Animals↗
PubMed1991

Small intestinal length: a factor essential for gut adaptation.

Changes in small intestinal structure, cytokinetics, and function are dynamic ways in which the gut adapts to diet, disease, and damage. Adequate length provides a static 'reserve' permitting an immediate response to pathophysiological changes. The length of the small intestine from conception to adulthood using data taken from eight published reports of necropsy measurement of 1010 guts is described. Mean length at 20 weeks' gestation was 125 cm, at 30 weeks' 200 cm, at term 275 cm, at 1 year 380 cm, at 5 years 450 cm, at 10 years 500 cm, and at 20 years 575 cm. Prenatal small intestinal growth exceeded that of body length according to the law: small intestinal length alpha body length to the power 4/3. After birth there was a noticeable deceleration: small intestinal length alpha body length to the power 1/2. The coefficient of variation of small intestinal length postnatally was 24%, sixfold greater than for body length. The rapid prenatal small intestinal growth rate ensures that the mature newborn has adequate small intestine to meet postnatal nutritional demands, but handicaps the preterm infant who undergoes intestinal resection. The wide variation in lengths suggests a 'surplus' surface area that is immediately available to respond, independent of dynamic mucosal changes, to fluctuations in food availability, local intestinal disease, damage, rapid transit, and resection.

Adaptation, Physiological↗
PubMed1991

Importance of local versus systemic effects of non-steroidal anti-inflammatory drugs in increasing small intestinal permeability in man.

Increased small intestinal permeability caused by non-steroidal anti-inflammatory drugs (NSAIDs) is probably a prerequisite for NSAID enteropathy, a source of morbidity in patients with rheumatoid arthritis. This increased small intestinal permeability may be a summation of a local effect during drug absorption, a systemic effect after absorption, and a local effect of the drug excreted in bile, but the relative contribution made by these factors is unknown. We assessed the effect of indomethacin and nabumetone on intestinal permeability. The principal active metabolite of nabumetone, 6-methoxy-2-naphthylacetic acid, is not subject to appreciable enterohepatic recirculation. Twelve volunteers were studied before and after one week's ingestion of indomethacin (150 mg/day) and nabumetone (1 g/day) with a combined absorption/permeability test. Neither drug had a significant effect on the permeation of 3-0-methyl-D-glucose, D-xylose, and L-rhamnose. Indomethacin increased the permeation of radioactive 51chromium ethylenediaminetetra-acetic acid (51Cr EDTA) significantly from baseline (mean (SEM) 0.63 (0.09)% v 1.20 (0.14)%, p less than 0.01) but nabumetone did not (0.70 (0.10)% p greater than 0.1). These results were supported by the 51Cr EDTA/L-rhamnose urine excretion ratios, which reflect changes in intestinal permeability. They suggest that NSAIDs increase intestinal permeability during absorption or after biliary excretion and that the systemic effect is of minor importance.

Adult↗
PubMedDate not supplied

Effect of energy substrates on protein degradation in isolated small intestinal enterocytes from rats.

BACKGROUND: Nutrients affect small intestinal protein mass and metabolism, but studies on the effect of nutrients on small intestinal protein degradation are very limited due to a lack of a proper method. The objectives of this study were to establish a method to directly estimate protein degradation in isolated enterocytes from rats and to test the effect of energy substrates on protein degradation. METHODS: Male Sprague-Dawley rats (150-200 g, n>or=8 per treatment) were used. Cell viability, tyrosine release as an indicator of protein degradation, and the effect of osmolarity, 50 mmol/L glucose, 20 mmol/L beta-hydroxybutyrate, 4.7 mmol/L butyrate, and 30 mmol/L glutamine on protein degradation were measured. RESULTS: The average viability of enterocytes at time 30 minutes was 85.8% (range, 81%-94%). Tyrosine release was linear over the course of experiments, indicating constant protein degradation (R2=0.9943; p<.05). Osmolarity, glucose, and glutamine had no effect on protein degradation in isolated enterocytes. Beta-hydroxybutyrate significantly decreased it (-16%; p<.05), whereas butyrate slightly increased it (+5%; p<.05). CONCLUSIONS: A high viability and constant protein degradation indicate a successful establishment of a method to estimate protein degradation in isolated small intestinal enterocytes from rats. The large effect of beta-hydroxybutyrate suggests a potential positive role for ketone bodies to limit the loss of small intestinal protein mass by decreasing protein degradation.

3-Hydroxybutyric Acid↗
PubMed1979

Ionic composition of small intestinal secretion induced by PGE2.

Small intestinal fluid secretion induced by oral prostaglandin E2 in fasted rats was analyzed for various ionic components. Rat intestinal fluid had elevated calcium and potassium as well as decreased sodium and chloride concentrations relative to plasma electrolytes. Either low dose prostaglandin (0.15 mg/kg) or 1 ml of intragastric mannitol (5%) induced accumulation in the small intestine of fluid that had elevated chloride and depressed calcium and sodium concentrations compared to vehicle-treated controls. Higher doses of prostaglandin (1.0 mg/kg) led to secretions with increased sodium and chloride concentrations with respect to mannitol-induced fluid. Electrolyte concentrations in fluid induced by low dose prostaglandin appear to be similar to those in fluid caused by osmotically-induced changes. Higher doses of prostaglandin E2 induce additional electrolyte alterations which may result from modified gut transport of water and ions.

Animals↗
PubMed2001

Permanent jejunal fistula: promising method for obtaining small intestinal chyme without disturbing intestinal function.

Accurate information on changes in small intestinal microflora in dogs is rather limited because of difficulties in obtaining samples of small intestinal chyme. In the study reported here, intussuscepted nipple valves were surgically placed into the jejunum of seven laboratory beagles to obtain intestinal juice samples. The influence of the fistula on intestinal motility was determined by use of barium-impregnated polyethylene spheres (BIPS) and on microflora by use of bacterial culturing. The BIPS were fed two weeks before surgery and again five weeks after surgery. Bacterial samples were collected before (fecal samples), during (small intestinal samples) and 11 weeks after surgery. There were no surgical complications, and the animals tolerated the fistula well. Mean orocolic transit percentage was 93% before and 83% after surgery, and notable changes in gastrointestinal motility were not seen, except in one dog. The surgery did not markedly alter the bacterial flora in feces. Microflora did change in small intestinal samples; however, methodologic factors may explain most of these differences. In conclusion, the nipple valve is a promising method that creates easy and safe long-term access to the jejunum and appears not to have an influence on intestinal function.

Animals↗
PubMed1975

[Multilocular tumors of small intestine (author's transl)].

Tumors of small intestine can be recognized in time and evaluated histologically by means of roentgenographic and endoscopical-bioptic methods, respectively. Among radiologic techniques, the double contrast examination of the small intestine has especially high diagnostic value. On the other hand, selective angiography reveals bleeding of accompanying small intestinal tumors. Out of 23 patients with these tumors -- diagnosed in the Medical Department of the Erlangen University from 1968 to July 1974 -- there was one case with multilocular occurrence; the diagnostic efficiency of double contrast technique proved to be particularly suitable in this patient.

Adenocarcinoma↗
PubMed1998

Evaluation of damaged small intestine of mouse following methotrexate administration.

PURPOSE: Methotrexate (MTX) treatment causes damage to the small intestine, resulting in malabsorption and diarrhea. The active and passive transport capacities of the small intestine are decreased by the treatment. The purpose of this study was to evaluate the damage to the small intestine of mice caused by MTX administration by examining the permeability of the paracellular pathway of the small intestinal epithelium. METHODS: MTX was administered orally to male ddY mice once daily for 1-6 days. The permeability of the small intestine to the nonabsorbable markers phenol red (PR) and fluorescein isothiocyanate (FITC) dextrans was examined using everted segments of the intestine. RESULTS: PR and FITC dextran permeation through the small intestine increased significantly in parallel with changes in body weight of the mice, wet weight of the small intestine and chemical composition of the small intestinal epithelium. CONCLUSIONS: In addition to changes in permeation through the transcellular pathway reported previously, this study revealed that MTX treatment disorders the paracellular barrier function of the small intestinal epithelium, resulting in increased permeation of nonabsorbable markers via the paracellular pathway of the small intestinal mucosa. The present approach to the examination of the barrier function of the intestinal epithelium could be of great use in evaluating the damage to the small intestine and malabsorption.

Administration, Oral↗
PubMed1996

Association between H. pylori, duodenal mechanosensory thresholds, and small intestinal motility in chronic unexplained dyspepsia.

Alterations of small intestinal sensory thresholds and small intestinal dysmotility are associated with functional dyspepsia. Because gastric and duodenal afferents partly project to the same areas, we postulated that patients with functional dyspepsia and H. pylori infection would be characterized by lower duodenal sensory thresholds. We evaluated 16 patients with functional dyspepsia and 16 age- and sex-matched controls. All patients had undergone an extensive diagnostic work-up to exclude organic lesions. Mechanosensitive function was tested in the third portion of duodenum utilizing a barostat device, and small intestinal motility was assessed before and during duodenal nutrient infusion with a five-channel low-compliance perfusion system. H. pylori status was assessed by a validated serological test. Small intestinal sensory thresholds (first perception and maximal tolerated pressure) were significantly lower in patients (21.1 +/- 2.1 and 30.9 +/- 1.8 mm Hg) compared to controls (33.0 +/- 2.2 and 38.8 +/- 0.9 mm Hg, all P < 0.003). Nine of 16 patients compared with five of 16 controls were H. pylori positive (P = 0.15). Thresholds for H. pylori-negative (28.7 +/- 2.8 and 36.5 +/- 1.1 mm Hg) or -positive subjects (25.0 +/- 3.0 and 32.7 +/- 2.4 mm Hg) were overall not significantly different (P > 0.3). However, in patients with defined high H. pylori titers (>50 units/ml) defined a priori, thresholds for first perception were significantly lower (14.7 +/- 2.9 mm Hg, N = 5) compared to patients with H. pylori titers below this threshold (24.3 +/- 2.9 mm Hg, N = 4) or without H. pylori infection (23.8 +/- 3.4 mm Hg, P < 0.05). During duodenal nutrient infusion, the duodenal motility index increased (P < 0.03). This increase was not significantly different in patients and controls or in H. pylori-negative or -positive subjects. Sensory abnormalities are present in patients with functional dyspepsia. In a small subgroup of patients with high H. pylori titers, sensory abnormalities may be linked to H. pylori infection.

Adult↗
PubMed2001

[Diagnosis and treatment of acute adhesive small intestine obstruction].

Experience of treatment of 162 patients with acute adhesive intestinal obstruction (AAIO) is described. These patients had most often (23.3%) appendectomy in anamnesis. Conservative treatment was effective in 23 (14.2%) patients only. Surgical treatment was performed in 139 (85.8%) patients including traditional open operation in 79 (56.8%) patients, laparoscopic and laparoscopy-assisted in 60 (43.2%). Advanced adhesive process with formation of single intestinal conglomerate, neglected forms of AAIO with paralytic ileus were indications to open operations; lethality in these operations was 17.7%. Laparoscopic operation was indicated in AAIO due to isolated commissure as well as in early adhesive obstruction; lethality was 1.7%. If diagnostic laparoscopy showed that AAIO is caused by intestinal deformation in small intestinal conglomerate or intestinal resection is required, laparoscopy-assisted operations were performed.

Acute Disease↗
PubMed2001

[Small intestine obstruction caused by primary malignant neoplasms].

The authors presented 4 cases of primary malignant neoplasm of the intestine caused by small intestine obstruction. These patients underwent emergency surgery. In all cases, a segmental resection of the intestine was performed. There were two cases of adenocarcinoma and two cases of carcinoid. Three patients were complementarily treated using chemotherapeutics. One of them died two years post operation. The last three patients survived 0.5-5 years post operation.

Adenocarcinoma↗
PubMed1981

Biosynthesis of plasma apolipoproteins by rat small intestine without dietary or biliary fat.

Using two complementary methods developed and applied earlier in rats absorbing triacylglycerols, we have now determined the intestinal contribution of individual plasma apolipoproteins when the rate of intestinal lipid absorption is very low. After all dietary fat was withheld for 16-20 h, the intestine produced approximately 50% of the plasma apolipoprotein A-I (apo-A-I) and apo-A-IV, similar to its contribution during fat absorption. When rats were fed a fat-free diet for 12 days and, in addition, biliary fat was diverted from the intestine for 16 h, the intestine still produced approximately 50% of the apo-A-I and only slightly less of the apo-A-IV. Under both conditions of reduced fat absorption, a larger proportion of the intestinally-derived apo-A-I and apo-A-IV bypassed the mesenteric lymph and was released directly into intestinal venous blood. The intestinal apo-B contribution, 16% of the total in fat-fed rats, was reduced to approximately 5% when dietary fat was withheld. Intestinal apo-B was released entirely into the lymph. Intestine produced only small amounts of apo-C and little or no apo-E under all conditions. The results indicate that production of apo-A-I and apo-A-IV by the small intestine is not regulated by the rate of intestinal triacylglycerol transport.

Animals↗
PubMed1984

Enumeration and presumptive identification of bacteria from the small intestine of sheep.

Microflora of the small intestine of sheep was examined. Samples of tissue and digesta were taken from four sites along the small intestine (3, 8, 13, and 18 m from the pylorus) and maintained under anaerobic conditions. The pH of the digesta taken at the 3rd, 8th, 13th, and 18th m sections were 5.44, 6.37, 7.24, and 6.79. Digesta and tissue samples were diluted serially and plated within the anaerobic glove box on complex medium containing rumen fluid. In addition, each sample was plated on the same medium and incubated aerobically. As determined by growth under anaerobic conditions, viable counts of the digesta ranged from 5 X 10(4) to 7 X 10(6) cells/g, whereas counts for the tissue ranged from 2 X 10(2) to 4 X 10(4) cells/g. Viable counts determined aerobically for the digesta ranged from 1 X 10(4) to 5 X 10(6) cells/g, whereas the counts for the tissue ranged from 5 X 10 to 6 X 10(4) cells/g. Tentative identification of 50 isolates from samples of tissue and digesta in the 13th m section revealed a predominance of streptococcal organisms and rod shaped organism morphologically similar to Propionibacterium. An indigenous population of acid-tolerant bacteria with the ability to ferment simple sugars and starch was in the small intestine.

Animals↗
PubMed1981

Fecal intestinal alkaline phosphatase: a parameter for toxic damage of the small intestinal mucosa.

An immunoprecipitation procedure is presented for the measurement of rat intestinal alkaline phosphatase (I-AP) in feces. Controls exhibit a logarithmic normal distribution of fecal I-AP. Single administration of an agent toxic for small intestinal mucosa like bleomycin or triparanol induces an increase of fecal I-AP on the 1st day and a marked reduction of I-AP activity on the following 3 days. After the 5th day, abnormal high fecal I-AP activities were observed during regeneration. In parallel, morphometry and measurements of I-AP activity in the homogenate of small intestinal mucosa were performed. Rat fecal I-AP excretion proved to be a simple, non-invasive, sensitive marker for toxic damage of the small intestinal mucosa.

Alkaline Phosphatase↗
PubMed1991

Alcohol and the small intestine.

Several alterations of the small-intestinal morphology and function have been documented after alcohol ingestion. There are morphologic changes macroscopically and microscopically after acute alcohol administration in the proximal part of the small intestine, which are quickly reversible. There are no macroscopic changes and, in most patients, very discrete light microscopic changes in the small intestine after chronic alcohol ingestion. The ultrastructural changes are, however, profound, as seen by both transmission and scanning electron microscopy. The permeability is probably increased, permitting entrance of possible noxious agents, which may explain some of the extraintestinal tissue damage observed in chronic alcoholism. The transit is increased, at least after acute alcohol administration, perhaps contributing to the diarrhea commonly seen after heavy drinking. Several of the enzymes located in the brush border are affected; lactase activity can be depressed and perhaps result in a transient milk intolerance in predisposed individuals. The activity of GGT is increased and may partly account for the GGT elevation in serum after heavy drinking. Other enzymes, such as Na(+)-K(+)-ATPase, can be inhibited and result in a decreased absorption of substances that require active, energy-dependent transport mechanisms. The secretion of water and electrolytes may be increased (an effect on cAMP?). The absorption of several nutrients, vitamins, and other elements is disturbed. The bacterial flora is increased and changed, which may give rise to symptoms and also increase the production of acetaldehyde by bacterial metabolism of ethanol. Acetaldehyde is more toxic than ethanol, and an increased concentration of acetaldehyde can possibly accentuate the damage to the liver and other organs. The bacterial overgrowth can possibly cause endotoxinemia. Although studies on alcohol-related intestinal alterations have been relatively sparse, the acute and chronic effects of alcohol thus seem to be considerable. From available results it is, however, difficult to draw any definite conclusions about the clinical importance of many of the findings. Future research will need to study the relationship between, for example, the chronic morphologic changes, the absorptive dysfunction, and permeability alterations, on the one hand, and the gastrointestinal symptoms, the extraintestinal damage, and various deficiencies, on the other hand.

Animals↗
PubMedDate not supplied

[Relation between blood hydrolases and small-intestinal contents].

Absorption of enzymes in the small intestine and some mechanisms providing the enzymatic homeostasis in the body were studied in isolated portions of the small intestine of rats in chronic experiments on rats and dogs, and in clinically observed subjects. A conclusion has been made that under normal conditions the level of enzyme resorption is low, and it is localized in the distal portions of the small intestine. Changes in the hydrolytic activity of blood and urine are the result of not only the resorption of pancreatic enzymes from the small intestine, but also of the shifts in their incretion by the pancreas when enzymes are introduced into the duodenum, and the secretion of enzymes in the pancreatic juice is lowered, while their incretion by the pancreas into the blood flow is increased.

Amylases↗