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

Secretory protein-I (SP-I) of parathyroid glands and chromogranin A ( CGA ) of adrenal medullary chromaffin cells are chemically similar if not identical proteins. Both proteins are contained within secretory granules and appear to be cosecreted with granule contents, for example, in the parathyroid with PTH and in the adrenal with epinephrine and dopamine beta-hydroxylase. Antisera to bovine SP-I and porcine CGA , together with antisera to a variety of peptide hormones, were used in an immunofluorescence study of rat tissues in order to determine the probable distribution and cellular localization of these proteins. In addition to their previously demonstrated presence in parathyroid and adrenal cells, the SP-I/ CGA protein family was detected in cells of the thyroid that contained calcitonin and often SRIF but not thyroglobulin; in cells of the anterior pituitary staining for the alpha-subunit of TSH/FSH/LH but not in cells staining for GH, PRL, ACTH, or beta-endorphin; in pancreatic islet cells staining for SRIF and pancreatic polypeptide-related peptides, but not for insulin or glucagon; in the celiac and mesenteric ganglia in cells some of which contained SRIF; and in the gastric antrum in cells containing SRIF, but not gastrin. SP-I/ CGA was not detected in cells of the liver, kidney, parotid gland, or acinar pancreas or in the intermediate or posterior lobes of the pituitary. These results suggest that this protein family enjoys a widespread but highly restricted distribution in many different endocrine-peptide cells of the rat, many that are believed to be of the APUD cell series. The possibility is raised that SP-I/ CGA plays some physiological role in the secretory process or exerts an effect of its own in the periphery after secretion.
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PMID:Selective localization of the parathyroid secretory protein-I/adrenal medulla chromogranin A protein family in a wide variety of endocrine cells of the rat. 623 31

Gastrin releasing peptide (GRP)-like immunoreactive fibers occurred among and around ganglion cells in the forms of punctate structures or varicose processes in the celiac ganglion of rats. The density of the fibers varied from region to region in single sections. The immunoreactive nerve fibers were characterized by abundant large granular vesicles mixed with small clear vesicles, and they formed axo-dendritic synapses with principal ganglion cells. The immunoreactive material was localized on the granular core and also in the axoplasm. No immunoreactive ganglion cells were found in any portion of the ganglion. The present findings suggest that the GRP fibers are of extraganglionic origin and that GRP is involved in the ganglionic transmission of the prevertebral ganglion.
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PMID:On the occurrence of gastrin releasing peptide (GRP)-like immunoreactive nerve fibers in the celiac ganglion of rats. 631 99

Effects of electrical stimulation to the posterior (P-S) and celiac (C-S) branches of the abdominal vagus on the secretion of pancreatic glucagon (GI), insulin (IRI), gastrin (IRG) and secretion (IRS) were studied in anesthetized mongrel dogs. Following P-S and C-S, plasma concentration of GI and IRI increased without any changes of blood flow in the cranial pancreaticoduodenal vein. The similar responses shown in their magnitudes and timing would indicate that the output of the hormones were accelerated by both branches to the same extent and subsequently the effect of the posterior branch was caused via the celiac one. Plasma concentration of GI and IRI in the portal vein increased was elevated following P-S, but remained unchanged following C-S. these data would account for that an increase in portal blood flow exceeded relatively that of the output of the hormones following C-S. Portal plasma concentration of IRG increased following P-S and this would be due to the accelerated production of antral gastrin via the posterior antral branches. No response shown following C-S would reveal that an increase of portal blood flow exceeded over the production of extragastric gastrin via the celiac branch. Portal plasma concentration of IRS remained unchanged following P-S, but decreased following C-S. However, as these results were strongly influenced by changes of portal blood flow, the effect of both branches on pancreatic secretion needed further investigation with blood flow measurement.
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PMID:[An experimental study of the effect of the posterior and celiac branches on the secretion of pancreatic glucagon, insulin, gastrin and secretin]. 638 87

Sympathetic involvement in the lateral hypothalamic (LH) lesion syndrome was examined. Male rats were surgically or chemically sympathectomized and then given LH lesions. At 24 hr postlesion, lesion-induced hyperglycemia but not hyperthermia was attenuated by splanchnicectomy and celiac ganglionectomy. Hyperthermia but not hyperglycemia was attenuated by adrenal demedullation, adrenalectomy, and neonatal guanethidine treatment. Guanethidine-sympathectomized rats also displayed lower basal temperatures, more perilesion chromatolysis, and severer external symptoms than their controls. No form of sympathectomy affected lesion-induced gastric pathology, plasma gastrin concentrations, or body weight loss. Nor did any sympathectomy influence the recovery of ingestive behavior, daily food intake, the feeding response to 2-deoxy-D-glucose, or body weight maintenance in recovered LH-lesion subjects. These results suggest that sympathetic hyperactivity contributes to some aspects of the acute LH syndrome: Hyperglycemia results from sympathetic outflow to the abdomen, whereas hyperthermia is determined by circulating catecholamines and extraabdominal sympathetic innervation. The results fail to support the hypothesis that chronic increases in sympathetic tone are responsible for the reduced food intake and body weight of the LH-lesion rat.
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PMID:Influence of sympathectomy on the lateral hypothalamic lesion syndrome. 639 14

Nerve terminals in pancreatic islets and ganglia containing cholecystokinin (CCK)/gastrin-like peptides are particularly abundant in the cat. In order to elucidate the possible origin and molecular nature of the peptides in these nerves, extracts of the feline pancreas, vagus, sympathetic trunk, and celiac-superior mesenteric ganglion were examined by gel chromatography monitored by sequence-specific radioimmunoassays. Small amounts of CCK-33 and CCK-8 were present in the pancreatic terminals. In the vagus and the sympathetic trunk, CCK, mainly as CCK-8, occurred in concentrations of 3.5 and 3.7 pmol/g. The celiac-superior mesenteric ganglion contained 40 pmol CCK/g distributed in five forms, including a predominant CCK-8-like component and a component eluting like CCK-4. Gastrins were not detected in the nervous structures. The results suggest that the celiac-superior mesenteric ganglia, the vagal nerves and the sympathetic trunks all may contribute to the CCK nerve terminals in the feline pancreas.
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PMID:The molecular nature of cholecystokinin in the feline pancreas and related nervous structures. 646 84

We have investigated the effect of cystic fibrosis on alimentary hormones in 10 children by measuring the pancreatic and gut hormone rsponse to a milk drink. Plasma insulin and gastric inhibitory peptide were both significantly reduced (P < 0.05 and P < 0.005, respectively, at 15 min) in the patients with cystic fibrosis, compared with controls, even though the early glucose rise was greater in the former group (P < 0.05 at 15 min). Fasting levels of pancreatic polypeptide were significantly lower in the fibrocystic children (P < 0.01), and the normal response to milk was completely abolished in these patients (P < 0.001). Fasting plasma enteroglucagon concentrations were grossly abolished in the cystic fibrosis patients (P < 0.001) and these remained elevated throughout the test. No significant differences were seen in basal or postmilk responses of plasma glucagon, gastrin, secretin, vasoactive intestinal peptide, or motilin in cystic fibrosis. It would thus appear that the pancreatic polypeptide cell is more susceptible to the effects of the disease process than the beta or alpha cell in cystic fibrosis. Some aspects of the abnormalities in the gastrointestinal endocrine system were similar to those seen in celiac disease and tropical sprue and may, therefore, effect a similar hormonal response in these patients with cystic fibrosis to those with mucosal damage.
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PMID:Hormonal abnormalities of the pancreas and gut in cystic fibrosis. 700 Jun 12

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

This study examines the effect of graded antral distension with acid (0.1 M HCl) or alkali (0.1 M NaHCO3) on pentagastrin-stimulated acid secretion in two groups of dogs. Group A consisted of six dogs provided with innervated antral pouch. In these dogs, the vagal branches to the fundus, as well as the extragastric vagal divisions (hepatic and celiac), were preserved. All of these animals had a gastric fistula in the main stomach, and in two a denervated fundic pouch or Heidenhain pouch was constructed in addition. Group B consisted of four dogs with an innervated antral pouch and gastric fistula. In this latter group, however, parietal cell vagotomy as well as extragastric vagotomy (division of the hepatic and celiac branches) was performed so that the only vagal communication was between the antrum and the CNS. Antral distension with acid caused significant inhibition of pentagastrin-stimulated acid secretion from both the gastric fistula and the Heidenhain pouch in Group A dogs. Antral acidification without distension did not inhibit. Alkaline antral distension in this group caused much less inhibition of acid secretion, but did cause significant increase in circulating immunoreactive gastrin. In Group B dogs, antral distension with neither acid nor alkali caused inhibition of pentagastrin-stimulated acid secretion, indicating that intact vagal supply to the oxyntic mucosa and/or to the extragastric abdominal organs is necessary for the inhibitory mechanism to operate. The results of this study suggest that: a) antral acidification per se does not inhibit pentagastrin-stimulated acid secretion; and b) antral distension with acid, and to a lesser extent with alkali, is inhibitory only if vagal innervation to the fundus and other abdominal viscera is preserved. The observations are compatible with the hypothesis that antral distension activates a neurohumoral inhibitory mechanism releasing the inhibitor reflexly from sites other than the antrum or CNS.
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PMID:Neurohumoral inhibitory mechanism initiated by antral distension. 721 91


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