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)

Glucagon-like peptide-2 (GLP-2) stimulates small intestinal growth through induction of intestinal epithelial proliferation. To examine the physiology of GLP-2-induced bowel, mice were treated with GLP-2 (2.5 micrograms) or vehicle for 10 days. Small intestinal weight increased to 136 +/- 2% of controls in GLP-2-treated mice, in parallel with 1.4 +/- 0.1- and 1.9 +/- 0.5-fold increments in duodenal RNA and protein content, respectively (P < 0.05-0.001). Similarly, the activities of duodenal maltase, sucrase, lactase, glutamyl transpeptidase, and dipeptidyl-peptidase IV (215 +/- 28% of controls; P < 0.001) were increased by GLP-2. Oral or duodenal administration of glucose or maltose did not reveal any differences in the ability of GLP-2-treated mice to absorb these nutrients, possibly because of decreases in expression of the glucose transporters sodium-dependent glucose transporter-1 (SGLT-1) and GLUT-2. In contrast, absorption of leucine plus triolein was increased after duodenal administration in GLP-2-treated mice (P < 0.01-0.001). Finally, GLP-2 did not alter other markers of intestinal or pancreatic gene expression, including levels of mRNA transcripts for ornithine decarboxylase, multidrug resistance gene, amylase, proglucagon, proinsulin, and prosomatostatin. Thus induction of intestinal growth by GLP-2 in wild-type mice results in a normal-to-increased capacity for nutrient digestion and absorption in vivo.
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PMID:Intestinal function in mice with small bowel growth induced by glucagon-like peptide-2. 922 51

Distribution of ornithine decarboxylase activity in rat intestinal villi and crypts was determined by serially sectioning frozen mucosa and measuring enzyme activity in pools of sections composed of villi or crypts. Contents of the pools was determined by histological examination of representative sections, and simultaneous measurement of sucrase as a marker of villus samples demonstrated excellent separation of villi and crypts. In fasted and ad lib fed rats, enzyme activity was highest in the villus-crypt junctional area and in crypts (P < 0.05). Refeeding after a fast increased enzyme activity 15-fold, with greatest activity in villus tips and the villus-crypt junctional area. Luminal 0.4 M glycine stimulated enzyme activity only in villus and villus-crypt junctional samples, while luminal 10 mM putrescine stimulated activity only in crypts. Parenteral epidermal growth factor caused increased enzyme activity in all mucosal areas, but the 18-28-fold increase in the three villus samples (top, middle and bottom) was significantly greater (P < 0.05) than the 7-9-fold increase in crypt and junctional samples. In rats refed after a fast, parenteral putrescine (2 mmol/kg) depressed enzyme activity in all mucosal areas. Ornithine decarboxylase activity is usually greatest in junctional and crypt cells, and villus and crypt cells respond differently to luminal and systemic stimuli.
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PMID:Distribution and regulation of ornithine decarboxylase activity along the villus-crypt axis in the small intestine. 930 91

The effects of CGP 48664 and DFMO, selective inhibitors of the key enzymes of polyamine biosynthesis, namely, of S-adenosylmethionine decarboxylase (AdoMetDC) and ornithine decarboxylase (ODC), were investigated on growth, polyamine metabolism, and DNA methylation in the Caco-2 cell line. Both inhibitors caused growth inhibition and affected similarly the initial expression of the differentiation marker sucrase. In the presence of the AdoMetDC inhibitor, ODC activity and the intracellular pool of putrescine were enhanced, whereas the spermidine and spermine pools were decreased. In the presence of the ODC inhibitor, the AdoMetDC activity was enhanced and the intracellular pools of putrescine and spermidine were decreased. With both compounds, the degree of global DNA methylation was increased. Spermine and spermidine (but not putrescine) selectively inhibited cytosine-DNA methyltransferase activity. Our observations suggest that spermidine (and to a lesser extent spermine) controls DNA methylation and may represent a crucial step in the regulation of Caco-2 cell growth and differentiation.
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PMID:Concomitant changes in polyamine pools and DNA methylation during growth inhibition of human colonic cancer cells. 974 91

Increased ornithine decarboxylase (ODC) activity is associated with rapid cell proliferation in many cell types. The cellular effects of early weaning on intestinal development are not well established. To investigate whether ODC is involved in intestinal growth after early weaning, we precociously weaned suckling rats on postnatal d 15 and followed through d 21 (6 d after early weaning). Age-matched suckling pups served as controls. Rat pups were killed 1, 2, 3 and 6 d after early weaning and jejunal mucosa was assayed for ODC and sucrase activities, and protein and DNA contents. Jejunal cell proliferation was monitored by bromodeoxyuridine immunohistochemistry. Elevated jejunal ODC activity 1 d after early weaning was the earliest cellular event that was detected in the current study. ODC activity peaked at d 3 (about 15-fold greater than age-matched unweaned suckling controls). Sucrase activity was elevated at d 2 after weaning and peaked at d 3 (about 10-fold greater than controls). Greater bromodeoxyuridine immunostaining in early weaned rats occurred on d 3. Protein and DNA contents were greater in jejunal mucosa of early weaned rats at d 6. Serum corticosterone levels were elevated on d 1 and d 2 after early weaning compared to controls. To explore whether the intake of nonpurified diet played a role, we also compared the induction of jejunal ODC activity in early weaned pups and pups that were food-deprived for 1 d. ODC activity was not greater in the food-deprived group compared to suckling controls while the early weaned group had 6-fold greater activity 1 d after early weaning. Early weaning stimulates jejunal cell proliferation and differentiation. The temporal sequence of increased ODC activity followed by increases in other growth variables suggests that the induction of ODC activity may act as an early marker of intestinal growth during early weaning.
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PMID:Early weaning induces jejunal ornithine decarboxylase and cell proliferation in neonatal rats. 977 29

Ornithine decarboxylase (ODC) has been shown to play an essential role in intestinal growth and maturation in rats. However, the regulatory mechanisms have not been fully elucidated. We studied the mechanisms of expression of intestinal ODC during postnatal development. Rat small intestinal mucosa was obtained from postnatal days 10, 15, 17, 19, 21, 24 and 30. Intestinal mucosa was assayed for ODC and sucrase activities. In addition, intestinal ODC mRNA, and ODC protein levels were also measured. The results showed that the intestinal sucrase activity was low before postnatal day 19. The sucrase activity then increased steadily from day 19 up to day 30. Intestinal ODC activities remained low from postnatal day 10 to day 17. A sharp increase in ODC activity was noted on day 19, which peaked on day 24 (a 20-fold increase from its low basal level) and declined on day 30. Intestinal ODC proteins followed the same pattern of postnatal expression as that of ODC activity. In contrast, ODC mRNA did not show significant change throughout the study period. The possible mechanisms by which intestinal ODC mRNA levels remain practically unchanged during postnatal development are discussed. We conclude that the ontogenic increase in sucrase activity, a marker for intestinal maturation, occurs at the same time to that of the induction of ODC activity. We also suggest that the induction of intestinal ODC activity during postnatal development is the result of post-transcriptional events or other cellular mechanisms. A better understanding of the regulation of polyamine biosynthesis during postnatal development of the small intestine will provide insights contributing to the maturation of the small intestine.
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PMID:Expression of intestinal ornithine decarboxylase during postnatal development in neonatal rats. 1203 96


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