Showing papers on "Small intestine published in 1986"

Limits to starch digestion in the ruminant small intestine.

Abstract: Site and extent of starch digestion by ruminant animals varies with species, grain type and processing method. Based on a review of 40 different experiments with cattle, between 18 and 42% of the dietary starch from corn and sorghum grains fed to cattle reaches the small intestine for digestion. With more extensive grain processing, a smaller quantity of starch reaches the small intestine. In the small intestine, from 47 to 88% of the presented starch is digested, while in the large intestine, 33 to 62% of the presented starch is digested. Though limits to digestion in and absorption from the small intestine can be demonstrated by infusing starch and glucose into the duodenum, enzymatic capacity does not appear to limit intestinal starch digestion since no plateau in the amount of starch disappearing from the small intestine is detected with typical diets. Yet, extent of digestion is incomplete. Other factors, such as time and surface exposure may limit small intestinal digestion of starch. Processing methods to reduce particle size or alter the protein matrix, which cements starch granules together, will increase the extent of digestion both in the rumen and in the small intestine. Performance data from growing cattle fed processed corn and sorghum grains indicate that starch was used 42% more efficiently if it was digested in the small intestine rather than in the rumen. Though total tract starch digestibility is of primary concern, results support the concept that energetic efficiency of growing ruminants is greater if starch is digested in the small intestine rather than in the rumen.

A new approach to the oral administration of insulin and other peptide drugs

Abstract: The oral administration of peptide drugs is well known to be precluded by their digestion in the stomach and small intestine. As a new approach to oral delivery, peptide drugs were coated with polymers cross-linked with azoaromatic groups to form an impervious film to protect orally administered drugs from digestion in the stomach and small intestine. When the azopolymer-coated drug reached the large intestine, the indigenous microflora reduced the azo bonds, broke the cross-links, and degraded the polymer film, thereby releasing the drug into the lumen of the colon for local action or for absorption. The ability of the azopolymer coating to protect and deliver orally administered peptide drugs was demonstrated in rats with the peptide hormones vasopressin and insulin.

Glucagon-Like Peptides GLP-1 and GLP-2, Predicted Products of the Glucagon Gene, Are Secreted Separately from Pig Small Intestine but Not Pancreas

Abstract: We developed specific antibodies and RIAs for glucagon-like peptides 1 and 2 (GLP-1 and GLP-2), two predicted products of the glucagon gene, and studied the occurrence, nature, and secretion of immunoreactive GLP-1 and GLP-2 in pig pancreas and small intestine Immunoreactive GLP-1 and GLP-2 were identified in glucagon-producing cells of the pancreatic islets, and in glicentin-producing cells of the small intestine Immunoreactive GLP-1 and 2 in intestinal extracts corresponded in molecular size to peptides synthesized according to the predicted structure By reverse phase HPLC, intestinal and synthetic GLP-1 behaved similarly, whereas synthetic and intestinal GLP-2 differed Pancreatic extracts contained a large peptide with both GLP-1 and GLP-2 immunoreactivity Secretion was studied using isolated perfused pig pancreas during arginine stimulation, and isolated perfused pig ileum during either luminal glucose stimulation or vascular administration of the neuropeptide, gastrin-releasing peptide (GRP) Im

Antigen presentation by epithelial cells of the rat small intestine. I. Kinetics, antigen specificity and blocking by anti-Ia antisera.

Abstract: Columnar epithelial cells (EC), isolated from the proximal small intestine of the rat, bind ovalbumin (OVA) by a non-specific, cold-inhibitable mechanism and continue to express Ia antigens after 24 hr culture in vitro. Lymph node T cells from rats immunized with OVA proliferate following 18 hr coculture with EC and OVA. This accessory cell function of EC is antigen-specific and is blocked by anti-Ia monoclonal antisera.

Effect of non-steroidal anti-inflammatory drugs and prostaglandins on the permeability of the human small intestine.

Abstract: Intestinal permeability was estimated in healthy subjects after ingestion of aspirin (12+12 g), ibuprofen (400+400 mg) and indomethacin (75+50 mg) at midnight and an hour before starting a 51chromium labelled ethylenediaminetetraacetate absorption test Intestinal permeability increased significantly from control levels following each drug and the effect was related to drug potency to inhibit cyclooxygenase Intestinal permeability increased to a similar extent after oral and rectal administration of indomethacin showing that the effect is systemically mediated Prostaglandin E2 decreased intestinal permeability significantly but failed to prevent the indomethacin induced increased intestinal permeability These studies show that non-steroidal anti-inflammatory drugs disrupt the intestinal barrier function in man and suggest that the morphological correlates of the damage may reside at the level of the intercellular junctions

Immunohistochemical localization of epidermal growth factor in rat and man

Abstract: Epidermal growth factor (EGF) is a peptide which stimulates cell mitotic activity and differentiation, has a cytoprotective effect on the gastroduodenal mucosa, and inhibits gastric acid secretion. The immunohistochemical localization of EGF in the Brunner's glands and the submandibular glands is well documented. The localization of EGF in other tissues is still unclarified. In the present study, the immunohistochemical localization of EGF in tissues from rat, man and a 20 week human fetus were investigated. In man and rat, immunoreaction was found in the submandibular glands, the serous glands of the nasal cavity, Brunner's glands of the duodenum, the Paneth cells of the small intestine, and the tubular cells of the kidney. In the fetus EGF was found in the kidney and in the intestinal Paneth cells. Antisera raised against rat submandibular EGF did not recognize EGF in human tissues, whereas antisera against human urinary EGF worked in rat as well as man. EGF was found only in cells with an exocrine function.

Characterization and autoradiographic localization of multiple tachykinin binding sites in gastrointestinal tract and bladder.

Abstract: Binding sites for the [125I]Bolton-Hunter-labeled tachykinins substance K (BHSK), eledoisin (BHE) and substance P (BHSP) were investigated using crude membrane suspensions and autoradiography. In smooth muscle membranes from guinea-pig small intestine and rat duodenum, specific binding of BHSK was saturable and reversible, showing a single class of sites with a KD of 1 to 3 nM and maximum number of specific binding sites of 1 to 2 fmol/mg of wet weight tissue. Pharmacological characterization of this binding revealed a novel receptor site (K) with affinity for substance K greater than kassinin greater than or equal to eledoisin greater than neuromedin K greater than substance P greater than physalaemin. Inhibition of the binding of BHSK in membranes from mouse urinary bladder exhibited a similar K-type pattern. In rat duodenum and mouse bladder membranes, the binding of BHE was inhibited by substance K greater than kassinin greater than eledoisin greater than neuromedin K greater than substance P greater than physalaemin indicating the same receptor site as for BHSK. On the other hand, in rat cerebral cortex membranes BHE binding was inhibited by neuromedin K = kassinin = eledoisin greater than physalaemin greater than substance K greater than substance P indicating a definitive tachykinin E receptor site. The same displacement pattern of BHE binding was also detected in longitudinal muscle membranes from the guinea-pig small intestine. In mouse bladder membranes and in rat and guinea-pig intestine, the binding of BHSP was inhibited by substance P greater than physalaemin greater than substance K greater than or equal to eledoisin = kassinin greater than neuromedin K indicating a definitive tachykinin P receptor site. Autoradiographic binding sites for both BHSK and BHSP were seen in circular muscle of the rat stomach, small intestine and colon and in circular and longitudinal muscle of the guinea-pig small intestine and colon. Binding sites for BHSK, but not for BHSP, were seen in the muscularis mucosae of the gastric fundus and colon of the rat. Binding sites for BHSP, but not for BHSK, were seen in mucosa of guinea-pig colon and were densely clustered over ganglia of the myenteric and submucous plexuses in rat and guinea-pig colon. The guinea-pig intestine probably contains all three types of tachykinin binding sites whereas rat duodenum and mouse bladder contain only K and P sites. Some tissues classified previously as SP-P or SP-E may actually contain P and/or K sites.(ABSTRACT TRUNCATED AT 400 WORDS)

Amyloid A gene family expression in different mouse tissues.

Abstract: Serum amyloid A (SAA) is a major acute-phase reactant and apoprotein of high density lipoprotein (HDL). SAA is encoded by a family of three active genes. We examined hepatic expression and searched for extrahepatic expression of the three SAA mRNAs after injection with casein or LPS. Studies using an SAA cDNA, which detects all three SAA mRNAs, revealed that after casein injection liver SAA mRNA was elevated approximately 1,000-fold. Adrenal gland expressed SAA mRNA at a low level (0.5% of hepatic level), and was the only extrahepatic tissue with elevated SAA mRNA after casein injection. The small intestine, primarily the ileum, and the large intestine of unstimulated control animals contained 5- and 15-fold higher SAA mRNA levels than control liver. LPS also elevated liver SAA mRNA approximately 1,000-fold. However, in contrast to casein injection, every extrahepatic tissue examined expressed SAA mRNA. Lung and kidney contained 2-5% and large intestine contained nearly 10% of SAA mRNA levels found in liver RNA. SAA mRNA levels were lower in the remaining tissues and ranged from 0.1% in the brain and pancreas to 1.0% in the small intestine, with the ileum containing 50-fold more than the duodenum. Analysis of liver with SAA1, SAA2, and SAA3 mRNA-specific oligonucleotide probes revealed that SAA1 and SAA2 mRNA were elevated approximately 50-fold higher than SAA3 mRNA after casein administration. LPS, however, induced all three SAA mRNAs equally. In extrahepatic tissues, SAA1, SAA2, and SAA3 mRNAs were expressed differentially and can be grouped into three general classes: tissues expressing all three genes, tissues expressing SAA1 and SAA3, and tissues expressing predominantly or only SAA3.

Apamin distinguishes two types of relaxation mediated by enteric nerves in the guinea-pig gastrointestinal tract

Abstract: Eight smooth muscle preparations from the stomach, small intestine and large intestine of the guinea-pig were used to compare apamin's actions in reducing the effectiveness of transmission from enteric inhibitory nerves and in reducing responses to inhibitory agonists alpha, beta-methylene ATP, VIP and isoprenaline. The effects of apamin on inhibitory reflexes in the ileum and colon were also evaluated. Apamin had little or no effect on responses to VIP and isoprenaline in any region, but consistently and substantially reduced responses to alpha, beta-methylene ATP. Responses to stimulation of enteric inhibitory neurons were substantially reduced by apamin in the antrum circular muscle, ileum longitudinal and circular muscle, taenia coli and distal colon longitudinal muscle, but it was ineffective in the fundus circular muscle, proximal colon longitudinal muscle and distal colon circular muscle. It caused a small reduction of the relaxation of the ileal circular muscle caused reflexly by distension, but did not modify the similar descending inhibitory reflex in the circular muscle of the colon. It is concluded that apamin can be used to distinguish two types of non-noradrenergic transmission from enteric inhibitory nerves to gastrointestinal muscle. Furthermore, neither VIP nor ATP can be the sole transmitter chemical released from enteric inhibitory neurons throughout the gastrointestinal tract.

Angiotensin I converting enzyme in human intestine and kidney. Ultrastructural immunohistochemical localization.

Abstract: The localization of immunoreactive angiotensin I-converting enzyme (ACE) has been investigated at the optical and ultrastructural level with anti-human ACE antibodies in the human kidney and small intestine. In both tissues ACE was found in blood vessels and in extravascular situation in the absorptive epithelial cells of intestinal mucosa and renal proximal tubules. Ultrastructural immunohistochemistry showed that in intestinal and renal proximal tubular cells ACE was prominent in microvilli and brush borders. In the kidney ACE was also present on the basolateral part of the plasmalemmal membrane, where it may contribute to the regulation of angiotensin II-dependant absorption processes. Intracellular positivities were also observed inside the renal vascular endothelial and proximal tubular cell in endoplasmic reticulum and nuclear envelope reflecting the synthesis and the cellular processing of ACE. The intestinal microvascular endothelium was strongly labeled suggesting that the mesenteric circulation is an important site for the production of angiotensin II. Vascular endothelial ACE was also detected in the peritubular but not glomerular capillaries of the kidney.

Fate of pancreatic enzymes during small intestinal aboral transit in humans.

Abstract: To determine survival of pancreatic enzymes during small intestinal aboral transit in humans, seven healthy volunteers were intubated with an oroileal tube. By using nonabsorbable markers we measured the cumulative amount of lipase, trypsin, and amylase activities and lipase and trypsin immunoreactivities delivered postprandially to the duodenum, midjejunum, and terminal ileum. We found that as the enzymes moved from duodenum to ileum, 74% of amylase activity, 22% of trypsin activity, and 1% of lipase activity survived transit. Enzymatic activity and immunoreactivity of trypsin and lipase disappeared at different rates, suggesting that for these enzymes the sites of enzymatic activity and immunorecognition are not identical. Since tryptic activity is present even in the absence of immunorecognizable trypsin, complete structural integrity of the trypsin molecule may not be essential for its enzymatic activity. The short intraluminal survival of lipolytic activity may partially explain why patients with progressive exocrine pancreatic insufficiency malabsorb fat earlier than other nutrients.

Tissue-specific expression and developmental regulation of the rat apolipoprotein B gene.

Abstract: Expression of the apolipoprotein B (apoB) gene was examined in a variety of fetal, neonatal, and adult rat tissues by probing RNA blots with a cloned rat apoB cDNA. Among 10 adult male tissues surveyed, small intestine had the highest concentration of apoB mRNA. Its abundance in liver and adrenal gland was 40% and 0.5%, respectively, of that in small bowel, while none was detected in colon, kidney, testes, spleen, lung, heart, or brain. ApoB mRNA is as abundant in 18-day fetal liver as at any subsequent period of hepatic development. In contrast, the concentration of apoB mRNA remains low in fetal intestine until the last (21st) day of gestation, when it increases sharply to levels that are several-fold higher than in the liver. ApoB mRNA levels in fetal membranes harvested during this late gestational period were 10 times greater than in fetal liver. Since the major lipoprotein species in 19-day fetal plasma is low density lipoprotein, these observations suggest that fetal liver, and particularly its functional homologue, the yolk sac, are the principal sites of fetal lipoprotein synthesis at this stage of development. A 20-fold increase in placental apoB mRNA concentrations during the last 48 hr of pregnancy (to a level that is 50% of that encountered in fetal membrane RNA) suggests a specific role for this organ in maternal-fetal lipid transport immediately prior to parturition. Pulse-labeling experiments using 21-day fetal tissue slices showed that the liver synthesizes both apoB-100 (B-PI) and apoB-48 (B-PIII) albeit in somewhat different ratios than the adult organ. Fetal intestine produces almost exclusively the smaller apoB species, while fetal membranes and placenta synthesize only the larger peptide. The postnatal pattern of apoB mRNA accumulation is similar in liver and intestine. Profound decreases were observed during the late suckling and weaning periods, followed by an increase to adult levels. These final concentrations were similar to those encountered at birth. Analysis of these developmental changes offers an opportunity to generate testable hypotheses about the factors that modulate apoB synthesis.

Ca2+ and Cyclic AMP in Regulation of Intestinal Na, K, and Cl Transport

Abstract: This review is an update of the current understanding of how Ca2+ and cAMP regulate mammalian small intestinal and colonic electrolyte transport. We review the transport processes present in plasma membranes of absorptive and secretory epithelial cells and the way these processes are affected by Ca2+ and cAMP. Studies of intestinal electrolyte transport are complicated by several factors, including the presence, and often simultaneous function, of both absorptive and secretory processes, and by the presence of multiple cell types. A cultured cell line that retains the electrolyte transport properties of the intact tissue would greatly simplify investigation. However, to date neither a transporting small intestinal nor an intestinal absorptive cell line has been developed. A CI­ secreting human colonic epithelial cell line, named T-84, has been reported (1 �-17), but these studies must be interpreted with the realization that such cells do not represent the normal colon, but a cancer cell line. It is generally believed that electrolyte absorption and secretion are carried out by two separate epithelial cell types (38). The absorptive cells are thought to be present only on the villus of small intestine and on the surface of the colon, while the secretory cells are mostly present in the crypts.

Vagal receptors sensitive to lipids in the small intestine of the cat.

Abstract: In anesthetized cats, the unitary activity of 53 sensory vagal neurons was recorded in nodose ganglia by means of extracellular glass microelectrodes. All the neurons had non-modullated fibres, with conduction velocities ranging from 0.8 to 1.2 m/s. Forty of these cells were stimulated by perfusion of the small intestine with lipids. Two types of receptors were identified: (1) 21 endings were activated by glycerol and short chain lipids, and (2) 19 endings were activated by long chain lipids. These receptors did not respond to either mechanical or osmotic stimulation. The discharge frequency generally increased with the concentration. The short latency suggested that they were located close to the enterocyte. The role of vagal intestinal receptors sensitive to lipids is discussed. Their functional characteristics along with previous experimental data suggest that they may be involved in the regulation of gastric emptying and alimentary behaviour, particularly satiety mechanisms.

Experimental disease in infant goats induced by a Mycobacterium isolated from a patient with Crohn's disease. A preliminary report.

Abstract: Pilot studies were done to assess the pathogenicity of aMycobacterium which had been recovered from the diseased ileum of a patient with Crohn's disease. In four separate studies, pairs of infant goats served as subjects. One of each pair received an oral inoculum of freshly harvestedMycobacterium species strain Linda suspended in cream. A littermate or stablemate which received only cream served as control. Necropsies were done at three, five, six, and 10 months postinoculation. Each of the four inoculated animals developed segmental granulomatous disease of the ileum or ileum and more proximal segments of small intestine, and regional lymph nodes. The earliest lesion occurred in Peyer's patches of the ileum and consisted of granulomatous clusters of epithelioid cells and giant cells, without caseation, which often occurred in a mantle of lymphocytes between the germinal centers and the muscularis mucosae. Nine of 10 such granulomas were free of acid-fast bacilli. In more advanced lesions, there was confluence of granulomas and ulceration of the mucosal surface. Two of the four inoculated animals also had lymphocytic lymphangitis in affected segments. Although theMycobacterium Linda was recovered from intestinal segments of all four animals, acid-fast bacteria were not demonstrable in the intestines in two of them. Control animals remained free of lesions and acid-fast bacilli and were negative by bacteriologic culture. TheMycobacterium species strain Linda represents an enteric pathogen capable of inducing granulomas of the distal small intestine of susceptible species. The lesions produced have distinct similarities to those occurring in Crohn's disease.

Vagal control of canine postprandial upper gastrointestinal motility

Abstract: The role of the vagus nerves in the control of postprandial motility in the upper gastrointestinal tract was investigated in four dogs by use of a bilateral cervical cooling blockade technique. On administration of food, the fasting migrating motor complex (MMC) was replaced by the postprandial (feeding) pattern. Feeding pattern duration varied in a dose-dependent manner with either total volume or calories of food. During the feeding pattern, oscillations in lower esophageal sphincter (LES) pressure occurred at time intervals equivalent to the MMC cycle period. Twenty-one control feeding experiments and 17 postprandial vagal blockade experiments were performed, with a minimum of three of each type in each dog. Vagal blockade, initiated at times ranging from 15 min to 4 h after feeding and maintained for up to 5 h, abolished the postprandial activity in the upper gastrointestinal tract. During postprandial vagal blockade, LES pressure was abolished and bursts of contractions were observed only in the upper small bowel, a pattern resembling that observed during vagal blockade in the fasted state. These bursts occurred at the expected times relative to, and their cycle period was not significantly different from, that of the MMCs recorded prior to feeding. Vagal blockade started prior to feeding prevented initiation of the fed pattern, which appeared immediately on termination of the blockade. We conclude that initiation and maintenance of the postprandial pattern in the upper gastrointestinal tract with concurrent inhibition of the fasting MMC normally require vagal integrity. The "clock" controlling the MMC cycle period is not reset by feeding, but its effect on motility is suppressed.

Immunoelectron microscopic localization of HLA-DR antigen in control small intestine and colon and in inflammatory bowel disease.

Abstract: We have elucidated the distribution of I2 (HLA-DR) antigen in control and inflammatory bowel disease specimens, using immunoelectron microscopic methods Control small intestinal epithelium and inflammatory bowel disease epithelium expressed I2 antigen, while control colonic epithelium did not I2 expression by enterocytes was more frequent on the lateral and basal surface than on the microvillus surface Two of three M cells in control ileum expressed I2 antigen I2-positive intraepithelial lymphocytes were rarely detected in both control and disease specimens I2-positive lamina propria lymphocytes were significantly increased in inflammatory bowel disease, while I2-positive lamina propria lymphocytes were virtually absent in control specimens I2-positive mononuclear cells in the intestinal lamina propria were largely macrophages and monocytes in both control and inflammatory bowel disease specimens I2-positive mononuclear cells resembling dendritic cells were not detected in control or disease specimens Furthermore, there were no significant morphological differences in I2-positive or-negative macrophages and monocytes in control and disease specimens The expression of I2 antigen on Schwann cells was detected more frequently in disease specimens than in control specimens Capillary endothelia of both control and disease specimens expressed I2 antigen We demonstrate that I2 expression is present on surface membranes of both immune and nonimmune cells of the intestine and colon and show that this expression is more prominent in inflammatory bowel disease than in control intestine and colon Further studies are required to determine whether this finding is meaningful in terms of antigen presentation and whether this apparent “immune activation” is involved in the pathogenesis of inflammatory bowel disease

T cell subclasses in fetal human ileum.

Abstract: Lymphocytes within fetal human ileum were studied by immunocytochemistry to determine the appearance of T cells in human small intestine and the role of enteric antigen in the accumulation of cells of the suppressor/cytotoxic phenotype in the gut epithelium. In fetal human gut epithelium, cells bearing the pan T cell marker UCHT1 (CD3) were present in all of the specimens studied (11-19 weeks gestation). Of these, UCHT4+ (CD8, suppressor/cytotoxic phenotype) predominated over the leu3a+ (CD4, helper/inducer phenotype), although the differences were not as marked as in postnatal gut. UCHT1+ cells were also present in the lamina propria, frequently as small aggregates beneath the epithelium.

Kinetics, tissue specificity and pathological changes in murine rotavirus infection of mice.

Abstract: Mice that did not contain antibodies to rotavirus were orally infected with murine rotavirus (EDIM strain) and observed over 7 days. As judged by ELISA, only the small intestine was infected, not the colon. The infection was biphasic, viral antigen peaks being observed at 48 h and approximately 120 h post-infection. Clinically evident diarrhoea was maximal at 72 h. Virus in the upper, middle and lower regions of the small intestine was mainly tissue-associated; most virus was found in the middle small intestine. Two peaks (48 h and 120 h post-infection) of virus antigen were observed in the colon, but these corresponded to luminal, not tissue-associated viral antigen. Only enterocytes in the upper two-thirds of villus epithelia were infected as judged by fluorescent-antibody analysis and transmission electron microscopy. Scanning electron microscopy revealed morphological appearances not hitherto correlated with the progress of the infection: villus tips were convoluted, corresponding to the shedding of virus-infected cells but the lower regions of infected villi were shrunken and considerably narrowed compared to tips.

Release of leukotriene C4 by isolated, perfused rat small intestine in response to platelet-activating factor.

Abstract: We reported a rat model of necrotizing enterocolitis by injecting platelet-activating factor (PAF) into the mesenteric vascular bed, and suggested that leukotrienes (LT) are secondary mediators. The present study, using isolated, buffer-perfused rat small intestine, shows: Isolated, perfused small intestine synthesizes LTs in response to PAF. Leukotriene C4 (LTC4) was the predominant LT released. The initial vasoconstriction after PAF injection was due to a transient release of LTC4 since FPL 55712 pretreatment abolished the vasoconstriction. The sustained rise in perfusion pressure was also blocked by FPL 55712, which suggests that other vasoconstrictors released are regulated by LTs. The vasoconstrictor(s) responsible for sustained rise in perfusion pressure is unknown, but is not thromboxane. Most of the LT was released from intestinal tissue rather than mesenteric arteries. Vasodilating prostaglandins (PGs) were also released, probably secondary to LTs. The complex interaction of these lipid mediators (PAF, LTs, and PGs) and their subtle balance may affect the course of the disease.