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:3.2.1.26 (invertase)
4,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After isolation of the hamster small intestine, the effects of a continuous infusion of cholecystokinin-pancreozymin (CCK-PZ) are studied. Several enzymic activities are measured in the intestinal lumen and compared with the level found in the intestinal homogenate. During CCK-PZ infusion we observed a direct stimulation of Paneth cells associated with an increase of lysozyme activity. Furthermore this work confirms the stimulating effect of CCK-PZ on alkaline phosphatase and amino-peptidase. Maltase and sucrase levels were unaffected. The liberation of the hydrolase of the brush border in the intestinal lumen is negligible and cannot be considered as a true secretion. Only granule content of Paneth cells is actually secreted. However, biochemical data, corroborated by morphological results, suggest that Paneth cell secretion could in part be absorbed on the outer surface of the brush border.
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PMID:Comparative effects of CCK-PZ on certain intestinal hydrolases in the mucosa and in the luminal content of the hamster jejuno-ileum. 39 57

Intravenous administration of 1 U cholecystokinin-pancreozymin (CCK-PZ) to rats caused the release of enteropeptidase, alkaline phosphatase (AP), and sucrase to the intestinal lumen in the absence of a concomitant increase in luminal DNA. Thus, the hormone elicited hydrolase secretion was not due to cell desquamation. Pentagastrin also stimulated hydrolase release. Following CCK-PZ administration enteropeptidase was released preferentially over sucrase and AP and showed a linear correlation with total protein output. The specific enteropeptidase activity was higher in the perfusate following secretion than in the mocosa. Enteropeptidase was found mainly in soluble form in both mucosa and perfusate; addition of bile following enteropeptidase release further increased its activity. In contrast, sucrase and AP were found mainly in insoluble form in both mucosa and perfusate and their specific activities were higher in the mucosa. The presence of bile rendered both sucrase and AP more soluble in the perfusate. The data indicate that enteropeptidase is released by a specific secretory process and that its subcellular site of origin is different from that of sucrase and AP. By eliciting the coordinated release of trypsinogen, enteropeptidase and bile, CCK-PZ plays a central role in the initiation of protein digestion.
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PMID:Studies on intestinal enzyme secretion; the action of cholecystokinin-pancreozymin, pentagastrin and bile. 68 84

Digestive enzymatic activities (disaccharidases, alkaline phosphatase, peptide hydrolases) have been determined in the mucosa of 14 patients with chronic pancreatitis. All had an abnormal secretin-pancreozymin test. Four patients had insulin-dependent diabetes mellitus, four a pathological glucose tolerance test. Nine patients had steatorrhoea. Maltase, sucrase, and alkaline phosphatase activity was significantly elevated in patients with exocrine pancreatic insufficiency, whereas those of lactase, trehalase, and peptide hydrolase were normal. Patients with steatorrhoea had higher maltase and sucrase activity than those without steatorrhoea, whereas decreased glucose tolerance had no effect on brush border enzymatic activity. It is suggested thatdecreased exocrine rather than decreased endocrine pancreatic function is responsible for the increase in intestinal disaccharidase and alkaline phosphatase activity, possible by the influence of pacreatic enzymes on the turnover of brush border enzymes from the luminal side of the mucosal membranes or by direct hormonal stimulation though cholecystokinin.
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PMID:Influence of exocrine and endocrine pancreatic function on intestinal brush border enaymatic activities. 109 2

Glucagon is structurally related to secretin but inhibits the effects of secretin and cholecystokinin (CCK) on pancreatic secretion in vivo. Because secretin is a weak stimulant of pancreatic growth and potentiates the trophic effects of CCK, we hypothesized that glucagon might inhibit CCK-induced pancreatic growth. Four groups of 10 rats were injected with saline, glucagon (30 micrograms/kg, equimolar to a known trophic dose of secretin), cerulein (0.67 microgram/kg), or glucagon plus cerulein every 8 h for 5 days. The pancreas was excised, weighed, and assayed for total content of DNA, protein, amylase, chymotrypsinogen, and lipase. In control and glucagon-alone groups, the small intestine was also removed, weighed, and assayed for DNA, protein, and disaccharidase content. Glucagon alone decreased pancreatic DNA and increased lipase content. Compared with cerulein-treated animals, animals treated with glucagon and cerulein showed significant decreases in pancreatic weight and content of protein, amylase, and chymotrypsinogen. Although glucagon had significant effects on intestinal protein, maltase, and sucrase contents in certain segments, there was no clear pattern of response. The data suggest that glucagon may be an inhibitory regulator of pancreatic growth, acting to block the effects of CCK on pancreatic hypertrophy.
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PMID:Glucagon inhibition of cerulein-induced hypertrophy of the exocrine pancreas. 336 38

The effect of pentagastrin, secretin and cholecystokinin on biochemical parameters of mucosal growth and differentiation was studied in organ cultured rabbit jejunum and ileum. Pentagastrin at 0.05-5.0 microgram/ml did not affect DNA content of the biopsy, but led to a significant decrease of sucrase and alkaline phosphatase activity in the ileum. Secretin prompted a significant decrease of DNA and protein in the ileum at a level of 10(-7) and 10(-5) M, but had no effect in the jejunum. Of the brush border enzymes, sucrase and alkaline phosphatase were suppressed in both parts of the intestine both with respect to specific activity and total biopsy content. Cholecystokinin, like pentagastrin, did not influence DNA or protein content, but reduced sucrase, maltase and alkaline phosphatase activity. HMG-CoA reductase, the key enzyme of cholesterol synthesis, was not significantly affected by any of the three hormones tested. When brush border enzymes or DNA from desquamated cells were measured in the post-culture medium, no consistent effect of any gastrointestinal hormone was apparent. The present study demonstrates a direct "antitrophic" effect of secretin in cultured mucosa. Pentagastrin and cholecystokinin did not influence mucosal DNA content in vitro but apparently inhibited villus cell differentiation.
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PMID:Effect of pentagastrin, secretin and cholecystokinin on growth and differentiation in organ cultured rabbit small intestine. 372 4

Three enzymes of intestinal origin-enterokinase, alkaline phosphatase, and sucrase-were released into the perfused small intestinal lumen of the rat upon intravenous injection of the gastrointestinal hormone cholecystokinin-pancreozymin (CCK-PZ). The presence of bile in the perfusion fluid greatly augmented this release. The results suggest that a combined mechanism of enzyme liberation due to direct hormonal stimulation of the gut wall and further solubilization of released intestinal enzymes by bile may be responsible for the appearance of these enzymes in the gut lumen.
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PMID:Hormone-elicited enzyme release by the small intestinal wall. 504 Aug 34

The results presented show striking differences in the response of the exocrine pancreas to fasting in suckling versus adult rats. In adult rats, fasting led to an increase in lipase to amylase ratio with a particularly sharp decrease in amylase concentrations, a generalized decrease in total protein, amylase, trypsinogen and lipase contents, and a decrease in responsiveness of the pancreatic acini to optimal and supraoptimal concentrations of secretagogues in vitro. In 15 day old pups, however, fasting led to an increase in total amylase, trypsin and lipase and a maintenance of the total protein content in their pancreases. Further, no decrease in responsiveness of their pancreatic acini to secretagogue stimulation is observed at the concentrations studied. The difference in the behavior of the exocrine pancreas during fasting can be partly explained by the changing pattern of their responses to hormonal stimulation, particularly that of corticosterone and cholecystokinin during various stages of development. Fasting led to an increase in corticosterone and presumable decrease in cholecystokinin. The pancreas of the suckling rat is very sensitive to the induction effect of corticosterone while that of the adult rats is relatively insensitive. Conversely, the pancreas of the adult rats is sensitive to the trophic effect of cholecystokinin while that of the suckling rat has the opposite reaction. The combination of these and other factors then resulted in an entirely different profile of the responses of the exocrine pancreas to fasting. Recent studies in our laboratory, and that of others, showed that an analogous situation also existed in the small intestine. Fasting of adult rats led to a general decrease in small intestinal enzymes including sucrase and maltase (29) but in suckling rats led to (30,31) increases of sucrase and maltase. Corticosterone again has been shown to be involved (30,31). Further, the small intestinal sucrase of the suckling rats responded to corticosterone by an increase in its level but the same hormone did not seem to control the sucrase concentrations in the small intestine of adult rats (32,33). Thus, both the small intestine and the pancreas responds very differently to fasting presumably mediated through a varying pattern of responses to selective hormonal stimulation, eg in this case, corticosterone. These results strongly suggest the importance of the interaction between environmental influences (fasting in this case) and the stage of development in determining the outcome of ontogenesis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Response of the pancreas to fasting: adult versus neonates. 620 75

The role of gastrin and cholecystokinin (CCK) in postnatal development of the small intestine was examined in infant rabbits. Experimental animals received daily intraperitoneal injections of pentagastrin, 500 micrograms/kg, or CCK-octapeptide, 40 micrograms/kg, starting on day 3 of life. The animals were sacrificed at age 17-18 days. Weight and histologic sections of pancreas, stomach, duodenum, proximal jejunum, and ileum were obtained and mucosal lactase and sucrase activities determined in the intestinal segments. No differences were seen in any of the parameters assessed in pentagastrin-treated animals compared to saline-injected littermate controls. Body weight, weight and morphology of pancreas, stomach and intestinal segments, and enzyme activities did not differ significantly. Na+ transport in proximal jejunum under short-circuited conditions was not altered by pentagastrin. CCK-octapeptide also had no effect on weight or morphology of pancreas, stomach, and duodenum, but did lead to a significant increase in weight of proximal jejunum and ileum. Mucosal enzyme activities and morphometric measurements of villus height and mucosal thickness, however, did not differ significantly between CCK-octapeptide-treated animals and saline-injected littermate controls. The increase in weight of jejunal and ileal segments was reflected by an increase in thickness of the muscle layer. The findings indicate that neither gastrin nor CCK plays a role in the ontogenic development of the small intestine.
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PMID:Role of gastrin and cholecystokinin in the ontogenic development of the gastrointestinal tract. 632 Sep 13

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

To evaluate whether the small bowel can be distracted by mechanical stress in analogy to limb lengthening by osteodistraction, a gut-lengthening apparatus was designed. This distractor was placed at the antimesenterical side of a defined jejunum segment in rabbits. Distraction was performed by 1 mm lengthening of the distractor once daily using extracorporal screws. An effective gut lengthening was achieved of 9.9 +/- 0.5 mm (approximately 100%) within 3 weeks. Treated animals gained weight and remained in good general condition. Fasting plasma levels of cholecystokinin, neurotensin, glucagon-like peptide-1, gastric inhibitory polypeptide, and insulin remained unaffected. Postoperative factor XIII levels were significantly diminished and gastrin was elevated during gut distraction. DNA and protein concentrations in the mucosa of the distracted gut segments corresponded to controls. Mucosal lactase and saccharase activities were reduced. In the distracted bowel segments total tunica muscularis thickness was more than doubled due to muscle cell hypertrophy. In distracted segments villous width was increased. Detection of proliferating mucosal crypt cells utilizing BrdUrd labeling revealed no effects. In conclusion, small gut lengthening by mechanical distraction is possible without major changes in gut morphology. This technique may hint a novel experimental approach for the treatment of short bowel syndrome.
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PMID:Small bowel lengthening by mechanical distraction. 924 19


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