Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.26 (invertase)
 4,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatostatin is a widely distributed hormone localized in the central nervous system, pancreas and gastrointestinal tract. We have investigated the possible influence of somatostatin and a synthetic analogue, (D-Trp8,D-Cys14)-somatostatin, on the intestinal absorption 'in vivo' of D(+)-glucose and D(+)-galactose and also the effect on disaccharidase intestinal activities in hamster. Somatostatin, or its analogue, (12 micrograms/100 g body wt) was administered intraperitoneally 4 or 14 h prior to experiments. The results are compared to control animals. Animals treated with somatostatin and the synthetic analogue showed that there were no significant difference from control animals with respect to intestinal absorption of carbohydrates. Somatostatin produced inhibition of brush-border lactase activity in females only, whereas brush-border sucrase was increased 14 h after treatment in males and females, and brush-border maltase was inhibited in females only 4 h after hormone administration.
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PMID:Somatostatin and its analogue (D-Trp8,D-Cys14)-somatostatin do not modify intestinal absorption in vivo of carbohydrates in hamster intestine, but they do modify some disaccharidases. 251 89

The influence of somatostatin injection on intestinal disaccharidase and alkaline phosphatase activity in rat and chick was investigated. Disaccharidase and alkaline phosphatase activities of rat and chick homogenates were not modified. In rat the activities of mucosal brush-border maltase and sucrase were significantly increased. In chick brush-border a significant increase of duodenal mucosal activity and duodenal and jejunal sucrase activity is observed.
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PMID:Effect of somatostatin on small intestine enzyme activities in rat and chick. 285 90

Fractions of isolated epithelial cells were harvested from a segment of porcine jejunum by ten successive incubations with a chelating buffer. The cell fractions showed a progressive decrease in the activity of the brush-border enzymes, alkaline phosphatase and sucrase, with increasing incubation number but a progressive increase in the ability to incorporate labelled thymidine into DNA. Fractions enriched in cells from the crypt region (fractions 9 and 10) contained higher concentrations per mg protein of somatostatin-like immunoreactivity (1.8-fold), glucagon-like immunoreactivity (5.3-fold) and serotonin (3.0-fold) than fractions enriched in cells from the villus tip (fractions 1 and 2). Analysis of extracts of the fractions by gel filtration/radioimmunoassay showed that somatostatin-28 represented the predominant molecular form of somatostatin-like immunoreactivity in all cell fractions but the relative proportion of somatostatin-14 (and related metabolites) to somatostatin-28 was significantly higher (P less than 0.05) in fractions enriched in villus cells (fraction 1 and 2) than in fractions enriched in crypt cells (fractions 5-10). This result suggests that metabolism of somatostatin-28 to somatostatin-14 takes place during migration of the D cell from the crypt base to the villus tip. Heterogeneity in the somatostatin-14 region of the chromatograms indicates that the peptide may be further metabolized by the action of aminopeptidases.
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PMID:Conversion of somatostatin-28 to somatostatin-14 during maturation of epithelial cells in the porcine jejunum. 286 59

The effects of somatostatin on cholera toxin-induced secretory diarrhea and the appearance of glycoenzymes in the intestinal lumen and intestinal lymph were investigated in rat small intestine. After exposure to cholera toxin, marked fluid accumulation in the small intestinal tract and elevation of the jejunal mucosal cyclic AMP (cAMP) concentration were observed. The activity of alkaline phosphatase, aminopeptidase and sucrase increased in the intestinal lumen after toxin exposure. In intestinal lymph, alkaline phosphatase activity was increased after cholera toxin administration, while aminopeptidase activity remained unchanged. Somatostatin suppressed cholera toxin-induced secretory diarrhea, but it did not affect the elevated mucosal cAMP concentration. This peptide also inhibited the appearance of glycoenzymes in the intestinal lumen and lymph induced by cholera toxin administration. These results suggest that somatostatin exerts its inhibitory effects on cholera toxin-induced secretory diarrhea and on the appearance of glycoenzymes in the intestinal lumen and lymph by affecting processes beyond cAMP formation.
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PMID:Inhibitory effect of somatostatin on cholera toxin-induced diarrhea and glycoenzyme secretion in rat intestine. 288 40

Intestinal adaptation has been studied in rats with pancreatic atrophy induced by feeding a copper-deficient diet and penicillamine and in rats with carbohydrate maldigestion induced by feeding of an alpha-glucosidase inhibitor (acarbose). Pancreatic atrophy led to a significant increase of weight, protein, and DNA content as well as specific activities and total amounts of the enzymes sucrase and maltase in the distal but not in the proximal part of the small intestine. Plasma levels of CCK and GIP were significantly higher in rats with pancreatic atrophy, whereas plasma levels of gastrin and insulin were lower. Tissue concentrations of gastrin in the antrum and GIP in duodenum and jejunum were unchanged. Duodenal CCK and jejunal substance P, somatostatin, and VIP and ileal substance P and somatostatin were significantly decreased in rats with acinar atrophy. Glucosidase inhibition by acarbose feeding led to weight increase of the small intestine and cecum. This was more marked when acarbose was fed together with a fiber-free diet. Under these conditions the protein and DNA content also increased significantly in both gut segments and maltase and sucrase content predominantly in the distal part. Insulin plasma concentration decreased significantly in the acarbose-fed groups, whereas GIP, gastrin, and CCK plasma concentrations remained unchanged. After fiber-rich diet tissue concentrations of gastrin in the antrum and insulin in the pancreas were significantly higher and GIP concentrations in the duodenum and jejunum significantly lower than after fiber-free diet. Acarbose increased the pancreatic insulin concentration only in the fiber-free group and did not influence gastrin and GIP concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adaptation of the small intestine to induced maldigestion in rats. Experimental pancreatic atrophy and acarbose feeding. 389 54

The effect of somatostatin on mucosal DNA, protein and brush border enzymes was studied in organ cultured rabbit jejunum and ileum. Compared to control cultures, somatostatin reduced the biopsy DNA and protein content in parallel in the jejunum, but was ineffective in the ileum. This was probably due to a direct growth inhibition, since DNA and brush border enzyme activity from desquamated cells in the postculture medium were unaffected. In addition, a direct inhibition of jejunal villous cell differentiation by somatostatin was reflected in a significant decrease of sucrase, maltase and alkaline phosphatase activity. In the ileum, only the specific activity of alkaline phosphatase was reduced. The key enzyme of cholesterol synthesis, HMG-CoA-reductase, was measured as an intracellular enzyme control and was not influenced by the hormone. The high somatostatin concentrations necessary to achieve the effects are not an artefact of hormone degradation during culture, as shown by radioimmunoassay, and suggest a local or "paracrine" rather than systemic, inhibitory action of somatostatin on intestinal growth and differentiation.
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PMID:Inhibitory effects of somatostatin on growth and differentiation in cultured intestinal mucosa. 614 52

The aim of this study was to determine the effects of a model of intestinal extrinsic denervation on mucosal structure and function. Six dogs underwent in situ neural isolation of the jejunoileum (Group 2); six other dogs served as operated controls (Group 1), and five nonoperated dogs were naive controls (Group 3). Thirty-centimeter segments of proximal jejunum and distal ileum were excised before (time zero) and at 2 weeks and 8 weeks postoperatively in Groups 1 and 2, while similar regions were removed at time zero in Group 3. Tissues were analyzed for morphology with quantitative morphometry, mucosal disaccharidase activities (sucrase, maltase, and lactase), and tissue content of selected regulatory peptides in transmural, mucosa/submucosa, and muscularis regions. In situ neural isolation had no significant or consistent effects on morphology/morphometry or on mucosal disaccharidase activities. Tissue content of neuropeptide Y decreased markedly (P < 0.002) in all layers of the jejunal and ileal walls, but tissue content of vasoactive inhibitory polypeptide, substance P, cholecystokinin, neurotensin, met-enkephalin, neurokinin A, somatostatin, and calcitonin gene-related peptide demonstrated only minor changes. The physiologic effects of intestinal transplantation (extrinsic denervation and disruption of intrinsic, enteric neural continuity, and lymphatic drainage) have little effect on morphology, mucosal disaccharidase activity, and tissue content of most regulatory peptides. How these minor alterations might affect enteric function, however, needs to be investigated.
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PMID:Neural isolation of the jejunoileum. Effect on tissue morphometry, mucosal disaccharidase activity, and tissue peptide content. 865 18

In this study we investigated whether brain-gut peptides are implicated in the activation of the hypophysial-adrenal axis (HAA) in suckling rats treated orally with spermine. The first group of rats received i.p. injections of bombesin, vasoactive intestinal polypeptide (VIP), somatostatin or neurotensin, starting on day 11 of life, and killed on day 14. The small intestine was removed and analysed for its content of proteins, DNA, polyamines and for its specific activity (SA) of disaccharidases. The second group of rats received one of the hormones cited above and was killed 45 min after the treatment for determination of corticosterone plasma concentration. Rats of the third group were adrenalectomised then treated with bombesin as the first group. The fourth group of rats was orally treated with spermine and sacrificed 2, 3, 4, 6 and 8 h thereafter for analysis of plasma and intestinal concentrations of bombesin. The i.p. injection of bombesin increased the sucrase and maltase SA in the whole small intestine, while it decreased the lactase SA in the distal part. Intestinal weight and length, contents of DNA, protein, spermidine and spermine, and corticosterone plasma levels were enhanced by bombesin treatment. Somatostatin, neurotensin and VIP were ineffective on all the parameters studied. Adrenalectomy, in bombesin-treated rats, decreased the sucrase and maltase SA in the whole intestine, and decreased the lactase SA in the proximal intestine. It has no effect on intestinal weight and length, and protein content. Oral administration of spermine had no effect on plasma concentration of bombesin, whereas it decreased the content of this peptide in the whole small intestine. It is possible that bombesin may control intestinal development in suckling rats and be a link between the ingestion of spermine and the liberation of corticosterone by the adrenal glands.
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PMID:Involvement of bombesin in spermine-induced corticosterone secretion and intestinal maturation in suckling rats. 920 97

Significant advances in intestinal stem cell biology have been made in murine models; however, anatomical and physiological differences between mice and humans limit mice as a translational model for stem cell based research. The pig has been an effective translational model, and represents a candidate species to study intestinal epithelial stem cell (IESC) driven regeneration. The lack of validated reagents and epithelial culture methods is an obstacle to investigating IESC driven regeneration in a pig model. In this study, antibodies against Epithelial Adhesion Molecule 1 (EpCAM) and Villin marked cells of epithelial origin. Antibodies against Proliferative Cell Nuclear Antigen (PCNA), Minichromosome Maintenance Complex 2 (MCM2), Bromodeoxyuridine (BrdU) and phosphorylated Histone H3 (pH3) distinguished proliferating cells at various stages of the cell cycle. SOX9, localized to the stem/progenitor cells zone, while HOPX was restricted to the +4/'reserve' stem cell zone. Immunostaining also identified major differentiated lineages. Goblet cells were identified by Mucin 2 (MUC2); enteroendocrine cells by Chromogranin A (CGA), Gastrin and Somatostatin; and absorptive enterocytes by carbonic anhydrase II (CAII) and sucrase isomaltase (SIM). Transmission electron microscopy demonstrated morphologic and sub-cellular characteristics of stem cell and differentiated intestinal epithelial cell types. Quantitative PCR gene expression analysis enabled identification of stem/progenitor cells, post mitotic cell lineages, and important growth and differentiation pathways. Additionally, a method for long-term culture of porcine crypts was developed. Biomarker characterization and development of IESC culture in the porcine model represents a foundation for translational studies of IESC-driven regeneration of the intestinal epithelium in physiology and disease.
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PMID:Cell lineage identification and stem cell culture in a porcine model for the study of intestinal epithelial regeneration. 2384 Apr 80