Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007570 (celiac disease)
 13,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical and pathological findings in patients with neurological disorders in association with disordered function of the small intestine, in particular coeliac disease, are outlined. The possible significance of the abnormalities of pyridoxine, tyrosine and tryptophan metabolism are considered in relation to biopterin derivatives and their relevance to neurological dysfunction.
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PMID:The neurological manifestations of malabsorption. 3 44

Patients with adult celiac disease excrete abnormal amounts of tryptophan metabolites after loading with this amino acid, suggesting vitamin B6 deficienty in these patients, In fact, the excretion of tryptophan metabolites returns to normal after administration of vitamin B6. The vitamin B6 nutriture was measured by means of determination of pyridoxal phosphate and activity of pyridoxalkinase in serum and in duodenal mucosa of 14 children with acute celiac disease and of six children with celiac disease in clinical and biochemical remission. Ten children with normal duodenal mucosa were studied as controls. Children with celiac disease had significantly decreased pyridoxal phosphate in serum and in duodenal mucosa when compared both with children in remission and controls. Activity of pyridoxalkinase, however, was significantly increased in serum and in duodenal mucosa when compared with controls but not when compared with children in remission. These children had the same increase in pyridoxalkinase activity as children with acute celiac disease. These data provide a strong evidence for the occurrence of vitamin B6 deficienty in children with acute celiac disease. The children with celiac disease in remission still had an increased activity of pyridoxalkinase which seems to be a compensating mechanism in consequence of vitamin B6 deficiency prior to the gluten-free diet.
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PMID:Vitamin B6 nutriture of children with acute celiac disease, celiac disease in remission, and of children with normal duodenal mucosa. 18 Jul 89

In four dogs with chronic pancreatic and gastric fistulas, dose-response studies of pancreatic bicarbonate and protein secretion were done with intravenous infusions of secretin, octapeptide of cholecystokinin (OP-CCK), and 2-deoxyglucose (2-DG). The pancreatic response to a meal and to duodenal perfusion of graded concentrations of HCl, sodium oleate, and tryptophan were also studied. These observations were repeated after division of both the hepatic and celiac vagal branches to produce extragastric vagotomy, and subsequently after transthoracic truncal vagotomy. The responses to secretin, OP-CCK, and to duodenal perfusion of HCl were either unaltered or only slightly decreased by either extragastric or truncal vagotomy. Basal pancreatic secretion and the responses to duodenal perfusion of oleate and tryptophan were markedly depressed by extragastric vagotomy. These findings indicate that tonic vagal activity contributes to basal pancreatic secretion but has little effect on the response of the pancreas to secretin or CCK or on the release of secretin from the intestine. The decreased pancreatic response to intestinally perfused oleate and tryptophan seen after extragastric vagotomy could be caused either by interruption of reflex paths between gut and pancreas or by interference with CCK release. Extragastric vagotomy reduced pancreatic responses to a meal and to 2-DG and subsequent truncal vagotomy caused still further reduction, possibly, at least in part, by depressing release of antral gastrin.
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PMID:Effect of extragastric and truncal vagotomy on pancreatic secretion in the dog. 113 May 17

Some children with coeliac disease show behavioural disorders such as depression and other signs which have been correlated with reduced central monoamine metabolism. We have therefore investigated the brain availability of the monoamine precursors tryptophan and tyrosine in 15 untreated children with coeliac disease and 12 treated children with coeliac disease as well as in 12 control children. Significantly decreased plasma concentrations of tryptophan were found in untreated children (mean (SD) 13 (4) mumols/l, p less than 0.001) compared with treated children (31 (13) mumols/l), and in both groups of coeliac children when compared with control children (81 (22) mumols/l). A significantly lower ratio of plasma tryptophan to large neutral amino acids (tyrosine, valine, isoleucine, leucine, and phenylalanine) was also observed, which could indicate impaired brain availability of tryptophan in coeliac children and was more pronounced in untreated children. The impaired availability of tryptophan could produce decreased central serotonin synthesis and in turn behaviour disorders in children with coeliac disease.
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PMID:Plasma precursor amino acids of central nervous system monoamines in children with coeliac disease. 177 52

Aminopeptidase W is a newly discovered enzyme of the renal and intestinal brush borders, having been first isolated as a 130 kDa glycoprotein recognized by a monoclonal antibody [Gee & Kenny (1985) Biochem. J. 230, 753-764]. It is particularly effective in the hydrolysis of dipeptides, Glu-Trp (Km 0.57 mM; kcat. 6770 min-1) being a favoured substrate. Dipeptides with tryptophan, phenylalanine or tyrosine in the P1 position were rapidly hydrolysed, but the requirements in respect of the P1 residue were not stringent. The activity of aminopeptidase W is markedly influenced by ionic conditions. The highest activity was observed in 100 mM-Tris/HCl, pH 8; phosphate ions were strongly inhibitory. Activity was also greatly affected by bivalent metal ions, and the magnitude and direction of the effects depended on the nature of the buffer anions and on pH. The most effective inhibitors were amastatin and bestatin. Some thiols also inhibited, but other chelating agents, EDTA and 1,10-phenanthroline, had no effect over the concentration range 1-10 mM. Other group-specific inhibitors, for cysteine, serine or aspartic peptidases, were also ineffective. Some molecular properties were studied. Deglycosylation by treatment with N-glycanase diminished the apparent subunit Mr from 130,000 to 90,000. The enzyme contained zinc, 1.2 atoms/subunit, and in spite of the atypical properties of this enzyme in respect of chelating agents, a zinc-catalysed mechanism is the most probable. Its roles in digestion and in renal function are not yet clear.
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PMID:Proteins of the kidney microvillar membrane. Enzymic and molecular properties of aminopeptidase W. 289 Mar 46

In two sets of 6 dogs with gastric and pancreatic fistulas, we studied the effect of atropine (14 nmol/kg.h i.v.) on the pancreatic secretory response to intravenous caerulein and to intraduodenal perfusion with tryptophan (both given with a secretin background) before and after stepwise removal of the extrinsic nerves of the pancreas, i.e., celiac and superior mesenteric ganglionectomy alone or truncal vagotomy alone and truncal vagotomy plus celiac and superior mesenteric ganglionectomy. Atropine significantly (p less than 0.05) depressed the protein output in the basal state and in response to secretin at each stage of innervation. The incremental protein response to caerulein was not altered by the various denervation operations nor by atropine. Truncal vagotomy alone significantly decreased the incremental protein response to low (0.12, 0.37, and 1.1 mmol/h) but not high loads of tryptophan. Ganglionectomy in combination with vagotomy did not further depress the incremental protein response to low loads of tryptophan. Atropine significantly reduced the incremental protein response to low loads of tryptophan only in intact innervated animals. Ganglionectomy alone did not alter the incremental protein response to any load of tryptophan. Ganglionectomy, truncal vagotomy, and atropine did not alter basal or tryptophan-stimulated levels of plasma cholecystokininlike immunoreactivity. We conclude that (a) neither the extrinsic nor the intrinsic cholinergic pancreatic nerves modulate the protein response to caerulein; (b) the sympathetic pancreatic nerves do not mediate the response to tryptophan; (c) the protein response to intraduodenal tryptophan is at least in part mediated by long, cholinergic, enteropancreatic reflexes with both afferent and efferent fibers running within the vagus nerves; and (d) release of cholecystokinin by intestinal tryptophan is not under cholinergic or splanchnic control.
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PMID:Pancreatic secretory response to intravenous caerulein and intraduodenal tryptophan studies: before and after stepwise removal of the extrinsic nerves of the pancreas in dogs. 291 53

The aim of this work was to show that the dynamic study of the amino acid pattern in plasma and urine following an oral load of tryptophan might confirm anomalies suggested by inconsistent clinical data and below-normal biological values. Such oral loads were administered to five control subjects and one patient who had recovered from a celiac condition but was suffering from a complex deficiency syndrome associating a polyneuritis due to a lack of folic acid and the excretion of blue-colored transpiration. Thirty minutes following the load a slowing in the rate of tryptophan absorption was observed (p less than 0.05) and, during the first 6 hours, increased urinary excretion of tryptophan (p less than 0.01) and indican (p less than 0.05). Similarly, changes in the metabolism of other amino acids were either revealed or accentuated by this oral load test (ornithine, glycine, lysine, phenylalanine). It is probable that in this patient a problem of tubular re-absorption led to tryptophan being less available for metabolization along the kynurenine pathway, accounting for the increase in urinary excretion of the amino acids concerned. The diagnosis put forward is that of an unexpressed form of Hartnup's disease in association with a folic acid deficiency.
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PMID:[Dynamic study of plasma and urine amino acid patterns after an oral load of tryptophan. Application to a patient with a complex deficiency syndrome]. 355 Jun 24

Serotonin (5-HT) in the guinea pig celiac-superior mesenteric plexus was quantitatively measured by HPLC and visualized by an immunohistochemical method. Preincubation of the ganglia in a Krebs solution containing L-tryptophan and pargyline markedly elevated the content of 5-HT and K+ solution caused a release of 5-HT into the incubation medium. 5-HT immunoreactivity was localized to dense but unevenly distributed nerve fibers throughout the plexus and to small diameter cells commonly referred to as small intensely fluorescent cells. These findings provide evidence of an extensive network of 5-HT-containing neural elements in the guinea pig prevertebral ganglia.
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PMID:Immunohistochemical and biochemical detection of serotonin in the guinea pig celiac-superior mesenteric plexus. 389 74

Adults with intestinal malabsorption due to celiac disease show reduced central serotonin metabolism, probably induced by a lack of essential dietary factors. Investigating a role proposed for vitamin B6 deficiency, a regular finding in untreated celiacs, the present study yields no support for the hypothesis that direct inhibition at the decarboxylation step by vitamin B6 deficiency accounts for low central serotonin turnover in adult celiacs: 11 untreated patients showing reduced 5-HIAA in the cerebrospinal fluid (71+/- 26.8 pmol/ml) had a significantly higher concentration of the metabolically active B6 vitamer pyridoxal 5'-phosphate in lumbar cerebrospinal fluid (0.06 +/- 0.34 ng/ml) than controls (0.24 +/- 0.07 ng/ml) (p less than 0.01). Cerebrospinal fluid tryptophan, precursor of serotonin, was normal (2035 %/- 649 pmol/ml). Raised pyridoxal 5'-phosphate in the cerebrospinal fluid in untreated celiac disease is an unexpected finding. Possibly it is secondary to the diminished central monamine metabolism in these patients, but further studies are needed bearing in mind that mental depression is a major cause for disability in adult celiac disease.
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PMID:High level of pyridoxal 5'-phosphate in the cerebrospinal fluid of adult celiac patients. 618 88

Neuropharmacological and histochemical evidence presented here indicates that serotonin (5-HT) is the transmitter mediating one of the postsynaptic potentials in the guinea pig celiac ganglion. Repetitive nerve stimulation elicited in celiac neurons, in addition to the nicotinic fast excitatory postsynaptic potential (EPSP), a slow EPSP that was resistant to cholinergic antagonists. Application of 5-HT caused a depolarization with membrane characteristics similar to those of the slow EPSP; furthermore, the latter was reversibly suppressed by 5-HT. The slow depolarization evoked by either nerve stimulation or 5-HT was augmented by fluoxetine, a 5-HT reuptake blocker, and depressed by cyproheptadine, a 5-HT receptor blocker; in addition, tryptophan, a precursor of 5-HT, enhanced differentially the slow EPSP. Lastly, histochemical study revealed dense networks of 5-HT immunoreactive nerve fibers encircling many ganglionic neurons.
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PMID:Serotonin mediates a slow excitatory potential in mammalian celiac ganglia. 660 77


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