Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The kinetics, mineral dependency, and pH dependency of phytate hydrolysis by preparations of chicken small intestinal brush border membrane vesicles were determined. Substantial phytate hydrolysis occurred over the pH range from 5 to 6.5 with a maximum hydrolysis at pH of 6. Inclusion of 25 mM MgCl2 in the media doubled the rate of phytate hydrolysis. The brush border was shown to have no nonspecific acid phosphatase activity and excess phytate had no effect on alkaline phosphatase activity at pH 11. Under optimal conditions of pH 6 plus 25 mM MgCl2, a kinetic model of a single Michaelis-Menten type of enzymatic activity with a Km of 0.160 +/- 0.008 mM and a Vmax of 42.5 +/- 1.0 nmol/mg vesicle protein per min plus a small unsaturable component converged to the data (P < 0.05). The specific and total activities of intestinal brush border phytase were highest in the duodenum (P < 0.05) and decreased progressively down the length of the gut. Intestinal brush border vesicles prepared from broiler chicks and mature laying hens had comparable specific phytase activity. However, the total activity of brush border phytase was 35% higher in the small intestine of laying hens (P < 0.05). Intestinal brush border phytase could contribute to phytate-phosphorus digestibility and may be subject to regulation in response to the dietary phosphorus and vitamin D status of the chicken.
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PMID:Phytase activity in the small intestinal brush border membrane of the chicken. 956 39

The temporospatial distribution of bovine primordial germ cells was studied in 34 embryos (18 to 39 days). For a reliable identification of bovine primordial germ cells in varying localizations and at different developmental stages the alkaline phosphatase reaction combined with the use of selected lectins was applied. The first potential primordial germ cells were identified in an 18-day-old trilaminar embryo in the caudal wall of the proximal yolk sac at a distance of less than 100 microm from the germ disc. These cells are alkaline phosphatase-positive. but do not yet react with lectins. From 18 through 23 days, morphogenetic folding converts the flat trilaminar disc into a cylindrical embryonic body. During this folding process primordial germ cells located in the proximal yolk sac area are incorporated into the embryo when this portion of the yolk sac becomes the hind- and mid-gut. Consequently, in 23- to 25-day-old embryos putative primordial germ cells (alkaline phosphatase- and lectin-positive) are situated predominantly in the axial body region at the level of the mesonephros. When the gonadal ridge develops in this region (about day 27) it contains a certain number of primordial germ cells present from the very beginning. Thus, the assumptions of a long-range chemoattraction of primordial germ cells by the gonadal ridge, of active immigration from an extraembryonic site. or of a passive transportation via the blood stream are not necessary to explain the initial settlement of bovine primordial germ cells in the gonadal ridge. Within the gonadal ridge (days 27-31) and later in the still sexually indifferent gonadal fold (32-39 days) the primordial germ cells are unevenly distributed. Extragonadal potential primordial germ cells (alkaline phosphatase-positive, but with reduced or no lectin staining) are regularly present in large numbers in bovine embryos with indifferent gonads. Such cells occur predominantly in the paraaortal tissue and in the liver, but also in the branchial arches. The different locations of extragonadal primordial germ cells are discussed in the light of recent evidence that germ cells and haematopoietic cells share common ancestors.
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PMID:Identification and temporospatial distribution of bovine primordial germ cells prior to gonadal sexual differentiation. 968 76

The lining of the gut, together with the pancreas, liver, gall bladder, and respiratory system, is formed from the endoderm. The gut also contains smooth muscle and connective tissue of mesodermal origin. The amphibian Xenopus laevis is potentially an excellent model organism for studying how the cells of the endoderm and mesoderm become programmed to produce these internal organs. However, the anatomical complexity of the coiled gut presents a problem in studying its development. In order to overcome this problem we here present a comprehensive guide to the anatomy and histology of the developing Xenopus gut. We use a simple dissection to display its anatomy and the expression of four endodermal markers (alkaline phosphatase, IFABP, XlHbox8, and endodermin). We present schematic diagrams that show how the gut is arranged in three dimensions and how this organisation changes during development. We also present drawings of histological sections of the gut which allow any region to be identified and so represent an atlas for working with sections. Finally, we describe the histology of the cells of the various organs of the gut. This histological identification may be necessary for the identification of parts following experiments in which the normal pattern is disturbed.
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PMID:Development of the gut in Xenopus laevis. 970 24

When Xenopus embryos from mid-tailbud to early tadpole stages were exposed to retinoic acid (RA), the gut developed with an uncoiled, straight intestinal tube, morphogenesis of the liver and stomach was affected and intestinal epithelial cells developed without a brush border and alkaline phosphatase activity. However, the temporal and spatial expression pattern of X1Hbox 8, the only homeobox gene expressed in the endoderm was unaffected. In lateral plate mesodermal cells the expression of alpha-smooth muscle (SM) actin was delayed. A similar syndrome has been reported in a study of embryos lacking functional FGF receptors in which it was proposed that the uncoiled intestinal tube and the delayed differentiation of the intestinal muscle cells are causally related. Our results support this proposition and further suggest that mesenchymal-epithelial interactions concerned with regional specification of the endoderm may be impaired resulting in other defects in the gut.
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PMID:Effects of retinoic acid on the endoderm in Xenopus embryos. 971 22

The effects of the energy and purine content in the diet on mucosal cell mitosis, function, and apoptosis in the small intestine of pigs were investigated in two experiments. In experiment I, three groups of five pigs were first fed a commercial diet that contained 9.1 MJ metabolizable energy (ME) per kilogram dry matter (DM) and 16.4% crude protein. It was followed by the experimental diets for 5 days each starting with an energy deficit (5.8 MJ ME/kg DM; 7% crude protein) followed by a high-energy diet with low purine content (14.1 MJ ME/kg DM; 13.6% crude protein; 460 mg purines/kg), or alternatively an isocaloric high-purine diet (2,160 mg purines/kg). During experimental periods, blood samples were drawn daily through catheters for insulin-like growth factor-I (IGF-I) determination. The animals were killed at the end of the corresponding feeding period and gut tissue samples were collected. In tissue samples, IGF-I and parameters for the characterization of mitosis (thymidine kinase [TK], proliferating-cell nuclear antigen [PCNA]) and differentiation (RNA content, alkaline phosphatase, sucrase) were measured. The degree of apoptosis was determined histologically. In experiment II, five pigs were fitted with simple T-cannula at the distal jejunum. They were fed the three experimental diets consecutively for 7 days each and sucrase and alkaline phosphatase were measured in digesta (four samples daily). IGF-I in blood but not in tissue clearly responded to the energy content of the diet with a decrease during the deficit and an increase in the two high-energy groups. However, purines had no additional effect on IGF-I. TK, PCNA, and gut weight showed an energy effect on mitosis, which was paralleled by increased peripheral IGF-I. Purines led to a further increase of mitosis, but IGF-I and gut weight were not increased. The degree of mitosis was correlated with higher activities of sucrase and alkaline phosphatase and also with the number of apoptotic cells. The enzyme activity increased from the deficit to the high-energy group and was further elevated due to purines. The results from experiment II also confirm these effects of energy and purines, because the activities of the enzymes in digesta decreased during energy deficit, but increased due to energy and in addition to purines.
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PMID:Effects of energy and purines in the diet on proliferation, differentiation, and apoptosis in the small intestine of the pig. 975 Dec 40

Although both lipopolysaccharide (LPS) and sodium butyrate are major bacterial products and bioactive chemicals with multiple functions on mucosal cells in the gut, their interaction effects on epithelial cells are not well understood. The purpose of the present study was to investigate whether LPS modulates butyrate-induced and retinoic acid-mediated alkaline phosphatase (ALP) activity of IEC-6 cells - a rat nontransformed small intestinal epithelial cell line. When cells reached confluency, various combinations of sodium butyrate, retinoic acid and LPS were added to the cultures. Cells were then harvested for the measurement of ALP activities. Sodium butyrate, but not retinoic acid or LPS alone, enhanced ALP activity. When LPS was additionally used with butyrate or retinoic acid, synergistic induction of ALP activities was demonstrated. No additive effect for ALP activity was observed when muramyl peptides or N-formylmethionyl-leucyl-phenylalanine was used with these acids. The present study clearly demonstrated that the specific combination of butyrate and LPS synergistically increased ALP activity, an epithelial differentiation-associated marker, of an intestinal epithelial cell line.
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PMID:Lipopolysaccharide exhibits synergistic enhancement of butyrate-induced and retinoic acid-mediated alkaline phosphatase activity on small intestinal epithelial cell line, IEC-6. 981 94

Several lines of evidence suggest an important role for insulin in the regulatory mechanism of rodent small intestinal development. To investigate its potential implication in human gut, the immunofluorescent localization of insulin receptors (IR) and the influence of insulin (30 microU or 3 mU/ml) on [3H]-thymidine incorporation and on lactase and alkaline phosphatase activities were studied in fetal jejunum and colon (14-19 weeks). We demonstrate the early presence of IR, mainly detected in the basolateral portion of enterocytes and colonocytes along the crypt-villus axis. Insulin increased [3H]-thymidine incorporation as well as epithelial labeling indices in cultured explants from jejunum and colon without affecting enzymic activities. This study establishes, for the first time, that insulin stimulates proliferation of epithelial cells expressing IR in both segments without affecting brush border hydrolases in the developing human gut.
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PMID:Insulin modulates cellular proliferation in developing human jejunum and colon. 992 1

In this study we aimed to elucidate the physiological role of gammadelta intraepithelial lymphocytes (IEL) in the mouse intestine. For this purpose, we used T-cell receptor (TCR) Vgamma4/Vdelta5 transgenic mice (KN 6 Tg: BALB/c background, H-2d), and compared the immunological and physiological characteristics of the intestinal tracts of KN 6 Tg and non-transgenic (non-Tg) littermates. In KN 6 Tg littermates, 95% of small intestinal (SI) and large intestinal (LI) IEL expressed gammadelta TCR, and their TCR was replaced by Tg gammadelta TCR. In these mice, class II major histocompatibility complex (MHC) expression was up-regulated in the SI epithelium, compared with the non-Tg littermates, under specific pathogen-free (SPF) conditions. Competitive reverse transcription-polymerase chain reaction (RT-PCR) analysis showed that the mRNAs of the I-Ealpha chain on the SI epithelial cells was higher in KN 6 Tg than in non-Tg littermates. However, in the LI, class II MHC molecules were not expressed in either KN 6 Tg or non-Tg littermates. The epithelial cell mitotic index in the SI, but not in the LI, was higher in KN 6 Tg than in non-Tg littermates under SPF conditions. However, differentiation markers for SI epithelial cells, such as alkaline phosphatase and disaccharidase (lactase, maltase and sucrase) activities, were similar in KN 6 Tg and non-Tg littermates. MHC class II molecule expression on the SI epithelium was absent in germ-free (GF) Tg mice, but was induced under SPF conditions, coinciding with the increase of interferon-gamma (IFN-gamma) mRNA in gammadelta TCR SI-IEL. These findings suggest that gammadelta TCR IEL regulate epithelial cell regeneration and class II MHC expression, but not cell differentiation in the SI. However, these functions were not observed in the gammadelta TCR IEL in the LI. In addition, the activation step in the gammadelta TCR SI-IEL is dependent on the presence of gut microflora.
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PMID:Physiological roles of gammadelta T-cell receptor intraepithelial lymphocytes in cytoproliferation and differentiation of mouse intestinal epithelial cells. 1044 10

The localization of hyaluronan has been determined in tailbud stage embryos of Xenopus laevis using a neurocan-alkaline phosphatase fusion protein. This polysaccharide was located between the germ layers and enriched in mesenchyme, the lumen of the neural tube, the embryonic gut, the hepatic cavity and the heart. A full-length cDNA for a hyaluronan synthase, Xhas2 has been cloned. The expression pattern of Xhas1 and 2 is closely similar to the distribution of hyaluronan in the embryo. Xhas1 produces hyaluronan with a molecular mass of around 40-200 kDa, while the product formed by Xhas2 has a molecular mass above 1 million Da.
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PMID:Synthesis of hyaluronan of distinctly different chain length is regulated by differential expression of Xhas1 and 2 during early development of Xenopus laevis. 1064 Jul 11

The effect of segregated early weaning (SEW) on postweaning small intestinal development was investigated in SEW and control (CON) pigs. Small intestines were collected from a total of 15 pigs killed at 11 (preweaning), 15 (3 d postweaning), and 34 d of age. At 3 d postweaning, the SEW and CON pigs had shorter villi (P<.01), deeper crypts (P<.01), and reduced (P<.01) ratios of villus height:crypt depth (V:C) compared with preweaning. Weaning also reduced specific activities of lactase (P<.01) in duodenum and ileum and alkaline phosphatase (ALP) (P<.05) in duodenum and jejunum. Sucrase activity in the three regions of the small intestine marginally decreased in both groups at 3 d postweaning. The mucosal protein:DNA ratio in duodenum and jejunum increased (P<.05) in SEW and CON pigs at 3 d postweaning compared with preweaning pigs. The SEW and CON treatments resulted in differences in postweaning gut development. At 15 d of age in SEW pigs, the mucosal protein:DNA ratio in duodenum and jejunum were 20 and 25.5% (P<.05) less, respectively, than those in CON pigs. However, at 34 d, these ratios in duodenum, jejunum, and ileum were 43.5 (P<.05), 24.3, and 32.9% (P<.05) greater, respectively, in SEW pigs than in CON pigs. Longer villi, shorter crypts (P<.01), and higher V:C ratios (P<.01) in jejunum and ileum were observed in SEW pigs vs CON pigs at 34 d of age. The specific activities of lactase in duodenum (P<.01) and jejunum (P<.05) and of ALP in duodenum (P<.01) were higher in SEW pigs. Sucrase activity in duodenum, jejunum, and ileum was 21.7, 46.3 (P<.05), and 11.2% greater in SEW pigs at 34 d of age. These results demonstrate differences in postweaning gut development between SEW and CON pigs. Furthermore, the number of intraepithelial lymphocytes in jejunum was greater (P<.001) in 34-d-old SEW pigs compared with CON pigs. Microscopy revealed a thick mucus coating over epithelial cells in the ileum of 34-d-old CON pigs that was not apparent in the SEW pigs. These observations are consistent with reduced pathogen exposure associated with SEW. We suggest that segregated early weaning advances postweaning gut maturation, which is consistent with improved growth and feed efficiency observed in SEW pigs.
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PMID:Effect of segregated early weaning on postweaning small intestinal development in pigs. 1064 63


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