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 neutralization of acid introduced into the duodenum has been found to be less intensive in patients with duodenal ulcer than in controls. The present work studied the possibility that chronic gastric hypersecretion injures the duodenal mucosa and thereby influences the neutralization system. Gastric hypersecretion was provoked for 3 weeks in 3 dogs by a daily injection of a gastrin preparation with prolonged effect. After a subcutaneous injection of this preparation given together with a test meal the acidity of both gastric and duodenal contents was found to increase significantly. After the 3 weeks of gastric hypersecretion the pancreatic bicarbonate response to exogenous secretin was unchanged, while the bicarbonate response to duodenal acidification was decreased from 2.03 mEq/30 min to 1.27 mEq/30 min (p less than 0.05), compatible with an impaired secretin release. Also the concentration of lactase, maltase, sucrase, and alkaline phosphatase in mucosal biopsies from the second part of the duodenum was significantly reduced (p less than 0.001). These results indicate that gastric hypersecretion causes mucosal damage in the duodenum and thereby reduces the release of secretin.
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PMID:Effect of gastric hypersecretion on the canine duodenum. 1 Jun 21

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

The diagnosis of pancreatic disease is difficult. The first step is clinical suspicion, based on the symptoms and signs. If pancreatic disease is suspected, investigation is necessary to prove this diagnosis. Investigation aims to answer two questions: a) is there pancreatic disease and b) if so, what type? The first question may be answered by demonstrating abnormal pancreatic function, using pancreatic function tests, whereas the second is answered by using techniques to demonstrate structural (anatomical) abnormalities of the pancreas. a) The methods to establish abnormal pancreatic function consist of 1. tests to demonstrate abnormal digestive capability, 2. tests to study pancreatic exocrine secretion, and 3. tests to study endocrine secretion. The tests of group 1 are: chemical fat balance study before and during enzyme replacement therapy, faecal nitrogen balance study, and the demonstration of either the malabsorption of vitamins A, D and K or the sequelae of their malabsorption (low serum calcium, high alkaline phosphatase, prolonged prothrombin time, etc.). Abnormal vitamin B12 absorption also may be present. 2. The tests designed to study pancreatic exocrine secretion are determination of the presence or absence of proteolytic enzymes in the stool, the secretion test, the pancreozymin stimulation test and the Lundh test. The serum amylase and lipase values are of little help in assessment of pancreatic function. 3. The tests to study endocrine function are the glucose tolerances test (which frequently gives abnormal results in pancreatic disease), and radioimmunoassays for insulin and gastrointestinal hormones (which may be increased in patients with functioning tumours of the islet cells). b) The techniques used to establish structural abnormalities of the pancreas are: duodenal cytology (during secretin tests), radiological techniques (abdominal survey films, barium meal, hypotonic duodenography, roentgenography of the biliary tract, barium enema, and angiography,) gastroscopy, duodensocopy, endoscopy and retrograde pancreatography, echography, scan and laparotomy. The relative value of these tests is discussed.
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PMID:Diagnosis of chronic pancreatic disease. 127 46

Duodenal aspirates were obtained before, during, and after stimulation with secretin-cholecystokinin in 26 patients whose pancreatic function was classified as normal, moderately reduced, or severely reduced. The activities of gamma-glutamyltransferase (GGT), alkaline phosphatase (ALP), and 5'-nucleotidase (5NT) in the aggregated duodenal aspirate collected 10-40 min after stimulation showed marked overlap between the functional groups and lacked diagnostic value. For all three enzymes, the peak response occurred later in the severely impaired group than in those with normal pancreatic function. The three enzymes showed significant positive correlations with each other, and were negatively correlated with the output of trypsin and chymotrypsin and, in contrast with these proteolytic enzymes which were reduced in pancreatic disease, GGT, ALP, and 5NT all tended to increase with pancreatic disease. Contrary to a previous report, GGT did not serve as a useful index of pancreatic cancer in this study.
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PMID:Activities of gamma-glutamyl transferase, 5'-nucleotidase and alkaline phosphatase in human duodenal aspirate. 287 69

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

The hormones secretin and cholecystokinin-pancreozymin (CCK) have been shown to release brush-border alkaline phosphatase into the small-intestinal lumen in the human subject. In contrast to the disaccharidases, large amounts of alkaline phosphatase are present in human duodenal juice. The range has been established in normal subjects. Following the intravenous administration of both secretin and CCK-pancreozymin there is a large rise in the output of alkaline phosphatase in human duodenal juice. These rises are also present in patients with complete obstruction of the common bile and pancreatic ducts, and since the pancreatic juice of man contains negligible amounts of alkaline phosphatase, it is clear that both hormones must cause small-intestinal alkaline phosphatase to be released into duodenal juice. The isoenzyme characteristics of bile, small-intestinal, and pancreatic alkaline phosphatase have been established, and isoenzyme studies used to confirm this new action of secretin and CCK-pancreozymin.
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PMID:The action of secretin and pancreozymin on small-intestinal alkaline phosphatase. 482 Jun 30

The action of somatostatin on intestinal alkaline phosphatase activity (IAP) in the duodenal juice was examined in 22 subjects undergoing diagnostic secretin-CCK-PZ-tests. Under continuous secretin-CCK-PZ-stimulation there is an increase of IAP which is followed by a period of exhaustion after 1 h of stimulation. The intravenous administration of somatostatin induces a distinct inhibition of IAP which cannot be due to the exhaustion of the enzyme synthesis. As there is a functional relationship between fat absorption and alkaline phosphatase, it is suggested that this inhibition of IAP is one of the mechanisms of the somatostatin-induced inhibition of intestinal fat absorption.
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PMID:The action of somatostatin on intestinal alkaline phosphatase stimulated by secretin and cholecystokinin-pancreozymin. 610 6

Thrombosis of the left subclavian vein occurred in a 44-year-old man. It was found to be caused by an atypical thymus carcinoid of the anterior mediastinum without carcinoid syndrome. Primary resection was not possible, but it was removed after three cycles of neoadjuvant chemotherapy with doxorubicin, cisplatin, vincristine and cyclophosphamide. Increased concentrations of alkaline phosphatase and parathormone were then noted. Subtotal parathyroidectomy revealed hyperplastic parathyroids. A gastrinoma was suspected from a history of peptic ulcer for many years which had persisted despite a Billroth II gastric resection 10 years ago. Serum gastrin, analysis of gastric secretion and a secretin-stimulating test confirmed the diagnosis. Recurrent episodes of weakness and syncope, in the presence of low blood sugar levels and a positive C-peptide suppression test, were interpreted as due to an insulinoma. There was no evidence of increased hypophyseal or adrenal function. Finally, in the absence of a family history, multiple endocrine neoplasia type 1 (MEN 1) was diagnosed with co-existing primary hyperparathyroidism, gastrinoma, insulinoma and thymus carcinoid. Somatostatin-receptor scintigraphy provided localization of the MEN 1 with enrichment in the thorax and abdomen.
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PMID:[Thymus carcinoid in multiple endocrine neoplasms type I]. 790 23

The influence of gastric pH on intestinal metaplasia was examined in male Crj:CD(SD) rats. At the age of 5 weeks, animals were irradiated with two 10 Gy doses of X-rays to the gastric region at a 3-day interval (total 20 Gy), and 6 months after irradiation, received either secretin or histamine in silicon tubes for 2 months or had their bilateral submandibular salivary glands removed. The incidence of intestinal metaplasia in the fundus of animals after administration of secretin or histamine, or removal of the salivary glands were reduced, along with the pH values, as compared with values for rats given X-rays alone. In both the pyloric and the fundic gland mucosae, the numbers of alkaline phosphatase (ALP)-positive foci and type B metaplasias (intestinal crypts without Paneth cells) were also significantly decreased (P < 0.01). In a second experiment, started six months after irradiation, rats were kept on 1% sodium chloride (NaCl) diet for 6 months. Subsequent removal of salivary glands along with histamine treatment brought about a marked drop in pH and in numbers of ALP-positive foci after three and five days. The present results thus indicated that development and maintenance of intestinal metaplasia can be influenced by a decrease of pH value.
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PMID:Influence of gastric pH modifiers on development of intestinal metaplasia induced by X-irradiation in rats. 822 78

The histological change of the biliary mucosa in clonorchiasis is characterized as adenomatous hyperplasia, and cross-sectioned mucosa looks like intestinal mucosa. In addition to the glandular hyperplasia, the metaplasia of mucin secreting cells is also known. The present study investigated the presence of intestinal secretion from the biliary mucosal cells of rabbits and rats with Clonorchis sinensis infection. The rabbit was infected with 300 and the rat was infected with 100 metacercariae of C. sinensis. A part of the animals were followed up after praziquantel treatment. The rabbit livers were prepared for histochemistry to observe any endocrine secretion and the bile duct mucosa of the mice was processed for the activity of brush border membrane (BBM)-bound enzymes of the small intestine. Immunohistochemistry with the polyclonal antibodies and biotin-streptavidin-peroxidase staining kit showed no positive cells for gastrin and secretin, but a few cells were positive for serotonin. The proliferated biliary mucosa of the mice revealed no activity of disaccharidases and aminopeptidase. Only alkaline phosphatase activity was found both in the control and the infected. The hyperplastic biliary mucosal cells showed no gastrointestinal secretory functions. The serotonin secreting cells may be one of the inflammatory cells.
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PMID:Secretions of the biliary mucosa in experimental clonorchiasis. 851 95


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