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 mucosal concentrations of seven regulatory peptides and the density properties and integrity of their storage granules have been studied in mucosal biopsies from the human jejunum in eight gastrointestinal disease states and compared with normal controls. In diseases with associated mucosal inflammation (coeliac disease, Crohn's disease with jejunal involvement, postinfective tropical malabsorption, and common variable immunodeficiency) there was a selective increase in fragility of the gastric inhibitory polypeptide (GIP) and somatostatin storage granules. The gastrin, motilin, enteroglucagon, secretin, and vasoactive intestinal polypeptide granules had normal properties in these conditions. In diseases in which diarrhoea occurred in the absence of changes in jejunal mucosal histology (irritable bowel syndrome, pancreatic insufficiency, jejuno-ileal bypass for morbid obesity, and purgative abuse) there were no abnormalities of the storage granules. Increased mucosal concentrations of all peptides except vasoactive intestinal polypeptide (VIP) were found in coeliac disease and selective increases of VIP found in Crohn's disease, motilin in the irritable bowel syndrome and gastrin and GIP in pancreatic insufficiency. It is suggested that the storage granule abnormalities in the diseases with abnormal mucosal histology are secondary to the inflammatory changes.
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PMID:Gastrointestinal regulatory peptide storage granule abnormalities in jejunal mucosal diseases. 614 62

A quantitative morphological investigation of eight endocrine cell types in mucosal biopsies from adults with untreated celiac sprue was undertaken. The quantitative data expressed as cells per millimeter of epithelium most accurately reflected the changes seen in celiac disease, as it takes into account changes in mucosal thickness due to the absence of villi in celiac biopsies. The results showed significant increases in the number of cholecystokinin and enterochromaffin cells, a significant decrease in somatostatin, gastric inhibitory polypeptide and secretin cells, and no change in the motilin, gastrin, and glicentin cells. Significant changes in cell size (cross-sectional area) were also demonstrated in the somatostatin and gastrin cells which were smaller in the celiac biopsies.
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PMID:A quantitative study of enteric endocrine cells in celiac sprue. 615 77

An 8-year-old boy with a convulsive disorder for 3 1/2 years remined seizure free for 20 months while being treated with phenytoin (diphenylhydantoin) sodium, and then he had a relapse. He first demonstrated hypoglycemia when he fasted prior to being placed on a ketogenic diet. An oral glucose tolerance test indicated fasting and postglucose hypoglycemia and substantial hyperinsulinemia. Somatostatin infusion resulted in a modest increase in plasma glucose levels and a decrease in serum insulin concentrations. A discrete pancreatic mass was demonstrated preoperatively by celiac angiography that on surgical extirpation, proved to be a benign intrapancreatic insulinoma. Evaluation for islet cell tumors is of importance in children with seizure disorders unresponsive to anticonvulsant medication. Furthermore, somatostatin may be useful preoperatively in maintaining normal blood glucose concentrations in patients with islet cell adenomas.
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PMID:Metabolic studies in a child with a pancreatic insulinoma. 624 3

Autoantibodies reacting with endocrine cells in the gastrointestinal mucosa were found by indirect immunofluorescence in 22 out of 268 sera (8.2%) obtained from patients with coeliac disease, Crohn's disease, ulcerative colitis, irritable bowel syndrome, and from subjects without bowel disease. A double immunofluorescence technique showed that the autoantibodies reacted with cells secreting gastric inhibitory polypeptide (glucose dependent insulinotropic polypeptide, GIP), secretin, somatostatin or enteroglucagon. Most sera contained antibodies against more than one cell type. Neither the presence of a particular antibody nor the pattern of antibody combinations appeared to be specific for any diagnostic category. The mean plasma GIP concentrations, however, both fasting and two hours after a test meal, were significantly lower in subjects with GIP cell autoantibodies. Thus gut hormone cell autoantibodies may be markers of impaired hormone secretion.
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PMID:Autoantibodies to gut hormone secreting cells as markers of peptide deficiency. 634 Nov 78

A number of human diseases with intestinal adaptation have been investigated, including acute infective diarrhoea, intestinal resection, jejuno-ileal bypass, coeliac disease, tropical sprue, chronic pancreatitis and cystic fibrosis. In all, the newly isolated hormone enteroglucagon appeared to be elevated in proportion to the degree of adaptation. In rats after gut resection and cold adaptation, enteroglucagon was also elevated and the degree of elevation correlated closely with the crypt cell production rate (CCPR). Chronic administration of somatostatin suppressed both enteroglucagon and CCPR, while bombesin stimulated both. A crude preparation of enteroglucagon was found to directly stimulate DNA synthesis in enterocyte cultures. It is thus concluded that, at present, the most likely candidate for the humoral component of intestinal adaptation is the hormonal peptide enteroglucagon.
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PMID:The hormonal pattern of intestinal adaptation. A major role for enteroglucagon. 695 45

The presence of autoantibodies detected by immunofluorescence to single endocrine cells, of human duodenum is described in three groups of patients and two control groups. Of 173 coeliac cases, four had GIP cell antibodies, one had secretin cell antibodies and twenty-one reacted with both cell types. Of twelve tropical sprue sera, four reacted with the same two cells. Among fifty elderly diabetics treated with hypoglycaemic drugs, seven sera gave a positive cytoplasmic IFL on duodenal substrate. Four were identified as GIP cells by use of the appropriate hormone antiserum and three reactions were against cells distinct from those stained by anti-GIP, -secretin, -somatostatin, -glucagon and -gastrin. Additional gut hormone antisera will have to be tested to identify these APUD cells. Thirty blood donors and seventy-three sera from autoimmune endocrine patients gave entirely negative results on unfixed cryostat sections of duodenal mucosa. Although impaired GIP and secretin responses have been reported in coeliac disease, and abnormal GIP values were found in Type II diabetes, there is as yet no data to correlate these metabolic dificiencies with the presence of endocrine cell antibodies in the serum. These studies are in progress.
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PMID:Autoantibodies to duodenal gastric-inhibitory-peptide (GIP) cells and to secretin (S) cells in patients with coeliac disease, tropical sprue and maturity-onset diabetes. 700 90

To determine if dog galanin is a potent inhibitor of dog insulin secretion we determined its primary structure from its cloned cDNA, evaluated its expression in celiac ganglia and determined its effect on islet hormone secretion. The predicted amino acid sequence differs from the other known species of galanin by three to six amino acids in the C-terminal half of the molecule. In situ hybridization revealed the presence of dog progalanin mRNA in every neuronal cell body in the dog celiac ganglion. The predicted dog galanin peptide was synthesized and infused i.v. at 0.25, 2.5, 25 or 250 pmol/kg/min. It potently inhibited insulin secretion, less potently inhibited pancreatic somatostatin release and stimulated glucagon secretion, similar to the effects of porcine galanin in the dog. In summary, dog galanin is expressed in the neuronal cell bodies that innervate the pancreas and the sequence of the dog galanin preserves the potent insulin inhibitory part of the galanin molecule. These data support the hypothesis that galanin is a sympathetic neurotransmitter in dog pancreas.
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PMID:Canine galanin: sequence, expression and pancreatic effects. 751 38

Using the indirect immunofluorescence method, the distribution of galanin (GAL)- and galanin message-associated peptide (GMAP)-like immunoreactivities (LI) were studied in sympathetic ganglia and the adrenal gland of the guinea pig. A rather dense network of GAL-immunoreactive nerve fibers was found in the inferior mesenteric ganglion (IMG) and in the superior mesenteric pole of the celiac-superior mesenteric ganglion complex (C-SMG). The celiac pole of the C-SMG, the stellate ganglion, and the superior cervical ganglion contained fewer, mostly scattered fibers. SIF-cells in prevertebral and paravertebral ganglia contained GAL-LI, as did the adrenal medullary cells. The GAL fibers in the IMG surrounded mainly principal ganglion cells containing somatostatin-immunoreactivity (SOM-IR), whereas fewer fibers were seen around neuropeptide Y (NPY) cells and cells in which SOM and NPY coexisted. Application of colchicine or vinblastine onto the IMG did not result in the appearance of GAL-IR in the principal ganglion cells. In denervation experiments it was revealed that most of the GAL fibers reach the IMG via the lumbar splanchnic nerves. GAL-IR appears to be colocalized with substance P (SP) in fibers of the IMG, indicating an origin of the GAL-containing fibers in dorsal root ganglia (DRG). This conclusion was supported by the finding in lumbar DRGs of GAL-positive cell bodies that contained SP. The role of GAL in prevertebral ganglia is unclear. It may be suggested that GAL modulates the slow, long-lasting membrane depolarization of the principal ganglion cells caused by SP in the primary afferents related to the IMG. GMAP-LI was detected in SIF cells and adrenal medullary cells in which GMAP-LI parallels the immunoreactivity of GAL. GMAP-LI was not observed in neuronal cell bodies or nerve fibers of the ganglia.
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PMID:Immunohistochemical demonstration of galanin-, and galanin message-associated peptide-like immunoreactivities in sympathetic ganglia and adrenal gland of the guinea pig. 752 69

Prolonged and severe diarrhoea after alcohol celiac plexus block is a rare, but life-threatening, complication if not recognized. This type of diarrhoea may be considered an autonomic neuropathy due to sympathetic denervation. A 65-year-old pancreatic cancer patient developed serious diarrhoea after celiac plexus block which was unresponsive to traditional treatment such as loperamide, dyphenoxylate and opioids. Subcutaneous octreotide, 0.1 mg twice a day, achieved a complete resolution of the symptom. This drug was maintained at the same dosage and was well tolerated for 4 months until death. Octreotide, an analogue of somatostatin, reduces diarrhoea by suppression of intestinal motility and secretion and offers a useful option in the treatment of this complication of celiac plexus block.
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PMID:Octreotide in the treatment of diarrhoea induced by coeliac plexus block. 765 45

The aim of the present study was to evaluate the effect of the opiate receptor antagonist naloxone on vagally stimulated secretion of bombesin-like immunoreactivity (BLI), somatostatin and gastrin from the isolated rat stomach, which was perfused via the celiac artery with Krebs-Ringer buffer. Vagal stimulation was performed for 10 min with 1 ms, 10 V and 2, 5, 10 or 20 Hz, respectively. In control experiments BLI release increased significantly above basal secretion during a stimulation frequency of 10 Hz (1367 +/- 357 pg/10 min; P < 0.001) and 20 Hz (996 +/- 202 pg/10 min; P < 0.01), but not at 2 and 5 Hz. In comparison to the controls naloxone (10(-6) M) significantly increased BLI secretion at 5 Hz by 573 +/- 150 pg/10 min (P < 0.05), but attenuated the BLI response to higher stimulation frequencies of 10 and 20 Hz to 284 +/- 143 pg/10 min (P < 0.001) and 490 +/- 114 pg/10 min (P < 0.01), respectively. At 2 Hz naloxone had no effect on BLI release. As shown previously the cholinergic blocker atropine (10(-7) M) induced a significant BLI release during vagal stimulation at 2 Hz (680 +/- 233 pg/10 min; P < 0.01) and 5 Hz (935 +/- 324 pg/10 min; P < 0.05), but was without effect at 10 and 20 Hz compared to the controls. The effects of the combination of naloxone and atropine were similar to naloxone and atropine alone. Naloxone had no effect on vagal or GRP-induced regulation of gastrin and somatostatin release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of endogenous opioids on vagally induced release of gastrin, somatostatin and bombesin-like immunoreactivity from the perfused rat stomach. 775 6


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