Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been suggested that glucagon-like immunoreactivity (GLI) of gastrointestinal tissues might, like pancreatic glucagon, have calcium-lowering activity. Studies were designed, therefore, to determine if calcium absorption was associated with GLI release from the gut. The intraduodenal administration of 4.5 mmoles of calcium chloride per kg of body weight to conscious dogs was associated with a prompt rise in plasma GLI from a base line of 2.2 ng/ml (SEM +/-0.2) to a peak of 4.3 ng/ml (SEM +/-0.3) at 45 and 60 min, in association with a rise of plasma calcium from 8.6 to 10.4 mg/100 ml. Neither pancreatic glucagon, insulin, nor glucose changed. Smaller calcium loads had progressively diminishing effects on GLI release. Calcium lactate also appeared to stimulate effectively GLI release. Both magnesium chloride and sodium chloride given intraduodenally were associated with a significant though modest increase in GLI. To determine if stimulation of GLI release by substances other than calcium would lower serum calcium, glucose was administered intraduodenally. Despite a marked increase in GLI, plasma calcium fell only 9%, a decline which could be entirely accounted for by hemodilution. Although the physiologic significance of this demonstration that the absorption of calcium salts is associated with GLI release is open to serious question, the findings are not incompatible with the concept that glucagon-like polypeptides are released from the gut during the absorption of certain salts, possibly to alert appropriate homeostatic regulators so as to avoid major changes in electrolyte concentration after the ingestion of large salt loads.
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PMID:The effect of calcium and other salts upon the release of glucagon-like immunoreactivity from the gut. 501 13

Neuron-specific enolase (NSE) is a neuronal form of the glycolytic enzyme enolase, which was first found in extracts of brain tissue, and was later shown to be present in APUD (amine precursor uptake and decarboxylation) cells and neurons of the diffuse neuroendocrine system but not in other peripheral cells. 90 neuroendocrine neoplasias (APUDomas) (including islet-cell tumours, phaeochromocytomas, medullary thyroid carcinomas, oat-cell tumours, and APUDomas of the gut, pancreas, and lung) reacted strongly with antisera to NSE. In addition, large amounts of the enzyme were found by radioimmunoassay in the tumours (mean 1626 +/- 479 SEM ng of NSE/mg protein), whereas control non-endocrine neoplasias contained less than 15 ng NSE/mg protein. Thus NSE, a specific enzyme produced in the neural and endocrine systems, was found to be produced in considerable quantities by all types of APUDomas but not in any non-endocrine tumours. NSE seems to be a useful and easily detected marker which may be used to distinguish endocrine from nonendocrine neoplasias. Clinical detection of endocrine tumours is difficult and such tumours are often missed. Use of NSE as a marker may avoid this.
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PMID:Neuron-specific enolase is produced by neuroendocrine tumours. 611 74

We describe here a depletion of peptide containing nerves and cells in Hirschsprung's disease, in comparison with specimens of bowel taken from age-matched neonates with no evidence of chronic constipation. VIP content in the diseased specimens was reduced by almost 80%, from 110/+-10.6 (mean +/- SEM) pmol VIP/g wet weight of tissue in controls to 23.8 +/- 3.5 pmol/g in the mid-portion of the diseased specimens. In addition, the numbers of enteroglucagon and somatostatin cells in the mucosa were significantly reduced in the aganglionic portions. Enteroglucagon cells were reduced from 55 +/- 7 in controls to 27 +/- 2 in proximal portions rising to 44 +/- 3 and 49 +/- 4 cells/mm2 in middle and distal areas. Somatostatin cell numbers also fell, from 5.5 +/- 1.9 to 1.8 +/- 0.8, 2.5 +/- 0.7 and 3.8 +/- 0.9 cells/mm2 in similar areas. Further investigation of the abnormalities of the diffuse neuroendocrine system in Hirschsprung's disease may help in understanding the nature of this condition and provide additional information on the role of these peptides in the control of gut function.
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PMID:Abnormalities of the colonic regulatory peptides in Hirschsprung's disease. 617 58

Using the methods of immunocytochemistry and radioimmunoassay, five peptides (vasoactive intestinal polypeptide (VIP), substance P, somatostatin, met-enkephalin, and bombesin) have been found in the gall bladder and the biliary tracts of guinea pig and each of them possesses a characteristic distribution pattern. Networks of nerves containing each peptide were found in the smooth muscle, around blood vessels and, occasionally, in the lamina propria. The distribution of the peptide immunoreactive nerves in the gall bladder and biliary tract is similar to those found in the gut. Vasoactive intestinal polypeptide (11 +/- 1.5 pmol/g in the sphincters, mean +/- SEM) and substance P (21.5 +/- 1.8 pmol/g in the common bile duct) were found to be the most abundant peptides and a few VIP and substance P immunoreactive neurones were localised in the ganglionated plexus. Bombesin immunoreactive nerves were mainly seen in the sphincter of Oddi, where the mean concentration of extractable bombesin was 14.6 +/- 2 pmol/g. Somatostatin immunoreactive mucosal endocrine cells were identified in the epithelium of the common bile duct and the sphincter. The extractable somatostatin in these regions were 76 +/- 19 pmol/g and 162 +/- 30 pmol/g respectively.
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PMID:Peptide immunoreactive nerves and cells of the guinea pig gall bladder and biliary pathways. 619 57

In recent years, distinct changes in regulatory peptides have been found in a number of gastrointestinal diseases. Grass sickness is a fatal disease of horses for which the etiology has yet to be fully ascertained. In this study, the peptide-containing nerves and ganglionic and mucosal endocrine cells of the ileum, colon and rectum were investigated in horses with sub-acute or chronic grass sickness and compared with normal controls using immunocytochemistry, at both the light and electron microscopical levels, and radioimmunoassay. A substantial loss of both peptide-containing cells and nerves was found in all of the sick horses, particularly in the ileum. Electron microscopy revealed marked degeneration of nerves in the gut wall. Fibers containing granules immunostained for substance P or VIP, using the immunogold staining technique, underwent extensive degranulation in grass sickness, with the formation of multiple vacuoles. Radioimmunoassay of peptide content also showed that the most drastic changes occurred in the ileum. For example, VIP content was significantly reduced from 109 +/- 19.8 (mean +/- SEM) pmoles/g in controls to 6.8 +/- 1.4 pmoles/g in grass sickness (p less than 0.001) and substance P from 65.9 +/- 8.1 to 31.3 +/- 9.5 (p less than 0.02). These results may have applications in the diagnosis and treatment of grass sickness.
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PMID:The regulatory peptide system of the large bowel in equine grass sickness. 620 92

The action of watery rat gut extracts on glucose-induced insulin release in anaesthetized rats was examined before and after removal of GIP by immunoadsorption. Infusions of GIP-containing rat gut extracts nearly doubled the insulin release induced by intravenous glucose (1 g X kg -1 X h -1). Peak insulin secretion was 98 +/- 11 mU/l (mean +/- SEM) after intravenous glucose and increased to 178 +/- 16 mU/l following infusion of glucose plus gut extract (p less than 0.005). After injection of GIP antiserum in sufficient amounts to neutralize the GIP activity in the gut extract preparation, the additional insulin release due to the gut extract was reduced by only 30%. After complete removal of GIP from gut extracts by immuno-absorption, more than 50% of the incretin effect remained. These data suggest that the insulinotropic activity of rat gut extracts can only be partially related to GIP. The existence of additional insulinotropic gut factors which may also be released following oral glucose is postulated.
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PMID:Preservation of incretin activity after removal of gastric inhibitory polypeptide (GIP) from rat gut extracts by immunoadsorption. 635 81

Previous reports suggest that prolactin could be one of the factors controlling intestinal mucosal growth. Therefore plasma levels of prolactin have been measured at the time of jejunal biopsy performed for suspicion of celiac disease. One hundred eighty-seven biopsies from 166 children have been reviewed according to histology, age, diagnosis, and plasma prolactin. No difference in the plasma prolactin could be detected among a group of 117 normal biopsies (9.4 +/- 0.4 ng/ml, mean +/- SEM), 31 biopsies with partial atrophy of various degree (9.0 +/- 0.9 ng/ml), and 39 biopsies with flat mucosa (9.1 +/- 0.7 ng/ml), nor could we demonstrate an increase in prolactin according to age and diagnosis (celiac disease before and after treatment, cow's milk protein intolerance, isolated postenteritic syndrome, selective sugar intolerance, and functional gut problems). Prolactinlike material has been detected by immunoperoxidase in the jejunal mucosa. The intracellular granules are located in the infranuclear portion of isolated epithelial cells mainly in the crypts. This material could not be correlated with the corresponding prolactinemias, whatever the histological appearance of the mucosa. These results would suggest that plasma prolactin is not a marker of jejunal regeneration in children. The nature and function(s) of this prolactinlike material remain to be established.
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PMID:Prolactin and the gut: a controversy. 638 57

Sympathetic hyperactivity is considered to be the most important factor in the development of postoperative bowel atonia. In a double-blind study we evaluated the gut motor effects of dihydroergotamine, which predominantly acts as a sympatholytic agent in the gastrointestinal tract. Forty-six patients undergoing cholecystectomy received either 0.5 mg dihydroergotamine + 5000 U heparin or 5000 U heparin alone (controls) twice daily in a randomized order starting on the morning of the operation. The first postoperative bowel movement occurred 57 +/- 4 h (means +/- SEM) after operation in the patients receiving dihydroergotamine, compared with 102 +/- 4 h in the control patients (p less than 0.001). Electromyography performed in the stomach and upper small bowel on the 3rd postoperative day showed an increase in the number of activity fronts of the interdigestive migrating motor complex and in the duration of spike activity under the influence of dihydroergotamine compared with the controls (p less than 0.001). It is concluded that dihydroergotamine stimulates depressed gut motility after abdominal surgery and that sympatholysis is the likely mechanism of action.
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PMID:Modulation of the adrenergic system in the treatment of postoperative bowel atonia. 639 10

There is evidence for both humans and rats that malnutrition frequently occurs when ethanol is chronically ingested. Small bowel 14C-labelled glucose absorption was measured with an ex vivo system in which the small bowel of the rat was surgically removed and then arterially perfused with an artificial medium. Glucose absorption for a control group of seven rats was 248 +/- 8 microM/min/gm dry weight of small bowel (mean +/- SEM). This was significantly greater than the value 112 +/- 12 microM/min/gm dry weight (P less than 0.005) for a group of five rats in which a competitive inhibitor of glucose absorption, phlorizin (0.2 mM), was added to the bowel lumen. In the presence of 3% ethanol within the gut lumen of five rats, glucose absorption was also reduced (to 131 +/- 12 microM/min/gm dry weight) compared to absorption in the control group (P less than 0.005). The calculated amount of glucose absorbed was corrected for metabolism to lactate and carbon dioxide. We conclude that both phlorizin and ethanol inhibit glucose absorption in the isolated and perfused small bowel of rats and that probably at least part of the malnutrition in ethanol-fed rats is due to glucose malabsorption.
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PMID:Ethanol inhibition of glucose absorption in isolated, perfused small bowel of rats. 641 May 24

Endogenous steatorrhea has only been evaluated in patients with non-pathological digestive tract. We decided, therefore, to study this parameter in 22 consecutive patients submitted to total parenteral nutrition for severe gastrointestinal diseases. The determination of steatorrhea, creatorrhea, and fecal clearance of alpha 1-antitrypsin was performed by three days stool collections. After 10 days of parenteral nutrition, 13 of the 22 patients still had measurable stool losses and 106 fecal collections were done. In these 13 patients, fecal weight was 610 +/- 130 g.d-1, (mean +/- SEM), steatorrhea was: 3.1 +/- 0.4 g.d-1, creatorrhea was: 1.7 +/- 0.6 g.d-1, alpha 1-antitrypsin clearance was: 58 +/- 13 ml.d-1 (N less than 10 ml.d-1). The mean endogenous steatorrhea was therefore 5 fold larger than normal and creatorrhea 1.8 fold larger than normal. This discrepancy could be due to metabolism of nutrients by colonic bacterial flora. The comparison of patients with and without increased endogenous losses showed significant differences in the mean number of intestinal lesions (1.4 +/- 0.3 versus 0.5 +/- 0.2) and in the presence or absence of ileal involvement (p less than 0.05). A positive correlation was found between steatorrhea and stool weight but not between steatorrhea and creatorrhea or fecal clearance of alpha 1-antitrypsin. This first study of pathological endogenous steatorrhea does not suggest a relationship of this parameter with protein losing enteropathy. The main contribution to increased endogenous losses may be related to increased epithelial cell renewal of the intestine associated with malabsorption. The role of bacterial overgrowth in the gut cannot be ruled out by the present data.
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PMID:[Endogenous steatorrhea during total parenteral nutrition. Study of 22 patients with gastrointestinal diseases]. 642 Feb 23


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