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)

In order to investigate if a plasma profile of gastrointestinal peptides reflects changes in jejunal mucosa in celiac disease, we studied basal and postprandial plasma levels of gastrin, secretin, somatostatin, vasoactive intestinal polypeptide (VIP), and neurotensin in children with untreated and treated celiac disease and in a control group of children. Basal and 30-min postprandial secretin concentrations were statistically significantly lower in untreated celiac children compared to both treated celiac (p less than 0.01 and p less than 0.05, respectively) and control children (p less than 0.001). Plasma secretin levels 30 min after a breakfast meal were also statistically significantly lower (p less than 0.001) in treated celiac children with respect to the control group. In both untreated and treated celiac groups, basal and postprandial plasma levels of somatostatin and VIP were statistically significantly decreased (p less than 0.001) compared to control children. Moreover, there was a significant rise in postprandial levels of neurotensin after a breakfast meal in untreated celiac children. On the contrary, there was no rise of neurotensin in healthy children. These findings seem to indicate that determination of plasma profile of gastrointestinal peptides in children with celiac disease may be useful in monitoring the development of this disease and, thus, the number of jejunal biopsies could be decreased.
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PMID:Gastrointestinal peptide profile in children with celiac disease. 289 3

A case of malignant somatostatinoma is reported in a patient with long-standing dermatitis herpetiformis and coeliac disease. The patient had non-specific abdominal pain of several years duration and came to attention because of weight loss despite strict adherence to a gluten-free diet. Plasma somatostatin levels were raised, and laparotomy showed a pancreatic tumour with metastases, which on histology, electron microscopy and immunohistochemistry proved to be a somatostatinoma. After a promising initial response to streptozotocin, she died 30 months later. This is the first reported occurrence of a somatostatinoma in a patient with coeliac disease, adding to the growing list of neoplastic complications in this condition.
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PMID:Malignant pancreatic somatostatinoma in a patient with dermatitis herpetiformis and coeliac disease. 289 27

The role of calcium (Ca2+) in bombesin (BBS)-stimulated release of gastrin and somatostatin-like immunoreactivity (SLI) was examined in isolated perfused rat stomachs obtained from male rats fasted overnight. The stomachs were perfused via the celiac artery. BBS (1 nM) was perfused alone for 10 min or in combination with various Ca2+ antagonists, including 1) different doses of divalent cationic Ca2+ chelator (EGTA), 2) Ca2+ channel blockers (nifedipine, verapamil), and 3) calmodulin (Ca2+ binding protein) antagonist [trifluoperazine (TFP)]. The effluent was collected for measurement of gastrin and SLI. EGTA at doses of 2 or 5 mM blocked the BBS-mediated release of both gastrin and SLI. After removal of a low dose of EGTA from the perfusate, the release of both gastrin and SLI rebounded. On removal of a high dose of EGTA, however, SLI release remained depressed, but gastrin rebounded even more significantly. In the absence of BBS, the rebound of gastrin release was less dramatic, indicating that reexposure to Ca2+ partially contributed to the rebound phenomenon. Nifedipine (0.1-10 microM) markedly decreased BBS-stimulated release of gastrin and SLI in a dose-dependent fashion; the inhibitory effect of nifedipine on SLI release was significantly stronger than on gastrin release. Verapamil (10 microM) depressed BBS-induced SLI release but not gastrin release. TFP (50 or 100 microM) also resulted in inhibition of bombesin-elicited release of gastrin and SLI in a dose-related manner.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of Ca2+ in bombesin-stimulated release of gastrin and somatostatin from isolated perfused rat stomach. 290 76

Electric stimulation (ES) of the celiac vagus during tetragastrin infusion reduced significantly the portal plasma concentration of somatostatin (SS) from 113 +/- 11.3 pg/ml to 87.8 +/- 5.8 pg/ml (P less than 0.05) in anesthetized dogs, in parallel with marked decrease of gastric acid secretion (59.9 +/- 7.1% of the prestimulatory value; P less than 0.01). A similar change in the portal plasma SS concentration was observed by ES of the celiac vagus on infusion of saline, with a concomitant significant increase in the portal plasma level of gastrin from a basal value of 65.9 +/- 7.0 pg/ml to a peak value of 129 +/- 29.9 pg/ml (P less than 0.05). However, no fluctuation of the plasma SS or gastrin level in the gastroepiploic vein was detected during or after ES of the celiac vagus. These findings indicate that gastric SS and gastrin are not of primary importance in the mechanism of inhibition of gastric acid secretion induced by ES of the celiac vagus in the dog.
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PMID:Effect of electric stimulation of the celiac vagus on gastric acid secretion and plasma concentrations of somatostatin and gastrin in the portal and gastroepiploic veins of dogs. 290 24

Celiac disease is characterized by reversible, gluten-induced, architectural abnormalities of the intestinal mucosa. Villus atrophy is compensated for by an increase in the number of proliferating cells and an increase in crypt cell production rate, resulting in increased crypt length and girth. Several authors, employing various methods of quantitation, have reported enteric endocrine cell hyperplasia in celiac disease. The present study has re-evaluated enteric endocrine cell status in this disorder by employing methods of quantitation which more accurately take account of alterations of crypt morphology than those previously used. Numbers of endocrine cells expressed as cells per unit of crypt length are not increased in the celiac biopsies when contrasted with those from controls. Indeed, numbers of cells immunoreactive for gastrin, GIP, motilin and somatostatin were reduced in the celiac mucosa. Endocrine cell hyperplasia in the celiac small bowel is not as marked as was previously thought, and may lag behind that of the enterocyte population.
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PMID:Reassessment of enteric endocrine cell hyperplasia in celiac disease. 321 24

The isolated perfused human pancreas was used as a model to assess factors mediating the pancreatic polypeptide cell response to glucose, insulin, gastric inhibitory polypeptide, and splanchnic nerve stimulation. Pancreases obtained from 18 cadaveric organ donors were isolated and perfused by way of the splenic artery utilizing a Krebs bicarbonate buffer in a single-pass perfusion system. Hormonal stimulation and inhibition of pancreatic polypeptide secretion were assessed, as was the influence of direct electrical stimulation of celiac neural fibers innervating the pancreas. In this in vitro human model, pancreatic polypeptide cell secretion was inhibited by hyperglycemia, although the presence of gastric inhibitory polypeptide augmented the pancreatic polypeptide cell response. Perfusion with low levels of insulin and splanchnic nerve stimulation augmented the response of the pancreatic polypeptide cell to hyperglycemia and gastric inhibitory polypeptide. Since the immunoreactive pancreatic polypeptide response was augmented when insulin and somatostatin release was inhibited by perfusion insulin or nerve stimulation, we conclude that the pancreatic polypeptide cell is regulated by the ambient degree of somatostatin release, insulin release, or both. These findings support a centrifugal pattern of intraislet blood flow.
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PMID:Regulation of pancreatic polypeptide secretion in the isolated perfused human pancreas. 327 67

The superior cervical ganglia (SCG), celiac superior mesenteric ganglia (CMG), and splanchnic nerve of unoperated guinea pigs, as well as both proximal and distal stumps of a previously transected branch of the postganglionic plexus of the CMG, were immunostained for somatostatin (SS). In addition, the PAP technique was adapted for fine-structural visualization of SS. A greater proportion of cells were labeled for SS in the CMG than in the SCG. PAP molecules were present in one type of intraganglionic axons. Only two labeled axons were found in the splanchnic nerve. Neither proximal nor the distal stump of the transected CMG postganglionic nerve contained labeled axons. The present results support the hypothesis that the intraganglionic axons labeled for SS arise from SS-containing intraganglionic neurons.
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PMID:Immuno-electron microscopic identification of somatostatin in cells and axons of sympathetic ganglia in the guinea pig. 610 63

The frequency of duodenal somatostatin cells was assessed and correlated to the number of enterocytes in patients with coeliac disease and in patients with a normal duodenal mucosa. The concentration of somatostatin in the duodenal mucosa was also determined. The number of duodenal somatostatin cells was increased in coeliac disease, whereas the somatostatin concentration did not differ significantly from that of the control patients.
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PMID:Duodenal somatostatin in coeliac disease. 613 42

Regulation of pancreatic exocrine secretion is comprised of a complex interplay between hormonal and nervous mechanisms. Stimulatory gut hormones which act via the circulation include secretin, CCK, gastrin and bombesin, while VIP operates through peptidergic nervous release. Pancreatic polypeptide and glucagon are two examples of circulating inhibitory hormones while inhibition by somatostatin is through a paracrine release mechanism. Although the effects of vagal cholinergic nerves have been previously thought to be indirect through hormone release evidence is now accumulating for a direct role. Altered hormone release has been noted in chronic pancreatic insufficiency, cystic fibrosis and coeliac disease and may contribute in an important way to the pathophysiology of these malabsorptive disorders.
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PMID:Neuro-hormonal control of pancreatic function in man and its failure. 613 50

Jejunal biopsies and the postprandial response of pancreatic polypeptide (PP), gastrin, gastric inhibitory polypeptide (GIP), and somatostatin have been examined in nine patients with celiac disease before and 1 year after gluten withdrawal. All presented initially with total villous atrophy of the jejunal mucosa. After gluten withdrawal five showed marked mucosal regeneration on light microscopy examination (responders) and four only moderate or no regeneration (nonresponders). Before treatment the celiac patients had enhanced gastrin response and normal PP response compared with normal controls. After gluten withdrawal the integrated gastrin release was reduced to normal in the responders (275 versus 114; p less than 0.05) but remained elevated in the nonresponders (231 versus 204). Postprandial PP release was similar before and after treatment regardless of the degree of mucosal regeneration. In the responders the integrated release of GIP was increased (180 versus 241; p less than 0.05), and the somatostatin release was enhanced (-2.6 versus 8.4; p less than 0.05) after gluten withdrawal. We conclude that the postprandial release of GIP and somatostatin increases and that the release of gastrin decreases when the intestinal mucosa is regenerated in celiacs on a gluten-free diet. The release of PP after food is not influenced by mucosal regeneration.
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PMID:The release of human pancreatic polypeptide, gastrin, gastric inhibitory polypeptide, and somatostatin in celiac disease related to the histological appearance of jejunal mucosa before and 1 year after gluten withdrawal. 614 93


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