Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of antrectomy and proximal gastric vagotomy on the metabolism of histamine in the human gastric mucosa were studied in the basal state and during pentagastrin stimulation in patients with duodenal or gastric ulcer disease. Mucosal biopsy specimens were taken from the antral and oxyntic gland areas, whereafter histamine content, histidine decarboxylase activity, and histamine methyltransferase activity were simultaneously assayed. Vagotomy was followed by a decrease in the acid secretory capacity and an increase in basal serum gastrin levels. Histamine content of the oxyntic mucosa increased after vagotomy, but the ability of pentagastrin to form new amounts of the amine was impaired. Antrectomy caused a decrease in acid secretion and a fall in gastrin concentrations. Basal histamine content and rate of amine formation in the remaining oxyntic mucosa were unaffected by antrectomy. Antrectomy impaired the ability of pentagastrin to release histamine. Histamine methyltransferase was not affected by pentagastrin, vagotomy, or antrectomy. In conclusion, both antral gastrin and the vagus nerve seem to exert a regulatory influence on the metabolism of histamine in the human oxyntic mucosa. The withdrawal of these factors either causes impaired ability of pentagastrin to release histamine from its storage site or counteracts the ability of pentagastrin to accelerate histamine synthesis.
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PMID:The role of the antrum and the vagus nerve in the metabolism of histamine in the human gastric mucosa. 177 87

In order to elucidate the action of an H2 blocker (cimetidine) and gastric mucosal protection agents (sucralfate and sofalcone) on the relapse and recurrence of gastric ulcer, the effects of cimetidine, sucralfate and sofalcone on the contents of histamine and serotonin and histidine decarboxylase (HDC) activity in the gastric mucosa were examined in the ulcer region and the intact region at the 10th day after the operation to produce acetic acid-induced gastric ulcer in rats. The following results were obtained: 1) HDC activity in the gastric mucosa of rats treated with cimetidine (100 mg/kg twice daily) tended to increase in the intact region, and it was significantly increased in the ulcer region. 2) Increased HDC activity due to cimetidine treatment was observed at the 10th day after interruption of cimetidine administration. 3) The HDC activity in the gastric mucosa was not changed by the treatment with sucralfate (500 mg/kg/day) and sofalcone (200 mg/kg/day). The results suggest that the increased HDC activity in the gastric mucosa might participate in the relapse and recurrence of gastric ulcer after discontinuation of cimetidine administration.
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PMID:[Effects of the anti-ulcer agents on the amine contents and regulating enzyme activity of gastric mucosa during the healing process of acetic acid induced gastric ulcer in rats]. 196 27

Changes in the contents of various amines and histidine decarboxylase (HDC) activity in the gastric mucosa during the healing process of acetic acid induced gastric ulcer in rats were sequentially examined in the ulcer region and intact region at 2, 10, 40, 80, 180 and 365 days after the operation. The following results were obtained: 1) Histamine (HA) content in the ulcer region was decreased as compared with the intact region at 2 and 10 days and returned to the control level in 40 days. After 180 days, the contents in the ulcer region and intact region were also increased as compared with that of the normal control region. 2) Changes in serotonin (5-HT) content as well as HA content were observed. 3) Norepinephrine content in the ulcer region was decreased as compared with the intact region at 2, 10, 80 and 180 days. 4) HDC activity in the ulcer region was decreased as compared with the intact region at 2, 10 and 40 days, and a lower level was maintained still at 180 days. 5) In the relapse and recurrence of gastric ulcer at 365 days, HA and 5-HT contents in the intact region and ulcer region were not different from those in healing rats, but the contents of these amines were higher at 180 days. The results suggest that the change of HA, 5-HT contents and HDC activity in the gastric mucosa may be one of the factors involved in the relapse and recurrence of chronic ulcers.
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PMID:[Changes in amine contents and regulating enzyme activity of gastric mucosa during the healing process of acetic acid induced ulcer in rats]. 273 3

1. The gastrin concentrations in serum were elevated after nephrectomy in rats and mice indicating the importance of the kidney for elimination of gastrin in these species. In guinea-pigs and rabbits nephrectomy did not cause increased serum gastrin concentrations. In rats there was a gradual rise in the serum gastrin level up to 48 hr after bilateral nephrectomy and also after ureteral ligation. After the latter operation the concentrations of gastrin in serum were lower than after nephrectomy. Significant elevation of the gastrin level 48 hr after ureteral ligation indicates that gastrin is eliminated at least partly through glomerular filtration. The gastric histidine decarboxylase activity after nephrectomy or ureteral ligation generally reflected the concentration of circulating gastrin.2. After bilateral ureteral ligation gastric acid secretion in conscious fistula rats was uniformly inhibited with no response to pentagastrin or histamine 24 or 48 hr after the operation. After nephrectomy basal acid secretion was reduced and there was no response to pentagastrin. The response to histamine was still present, although reduced at all dose levels. Linear transformation of the dose-response curve indicated mixed inhibition. The incidence of gastric ulcer was 75% 48 hr after nephrectomy and 30% after ureteral ligation. Since basal and pentagastrin-stimulated acid secretion were unaffected by nephrectomy in rats with the upper two-thirds of the intestine removed, the intestine appears to produce factors which are responsible for the inhibition of gastric secretion.2. On the whole, the gastrin concentration in serum and gastric histidine decarboxylase activity were not increased after five-sixths nephrectomy. Gastric ulcers were seen in the rats with the highest serum urea levels; one in addition had high serum gastrin concentration and gastric histidine decarboxylase activity. Basal, pentagastrin- and histamine-stimulated acid secretion were not affected by subtotal nephrectomy. It appears that in the rat about one sixth of the renal mass is the minimum required for handling gastrin degradation and excretion.
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PMID:Importance of the kidneys for gastrin elimination and gastric function. 738 64

We encountered a patient with chronic myelogenous leukemia in basophilic crisis accompanied with histamine excess symptoms including bronchial asthma and gastric ulcer. The concentrations of histamine and histidine decarboxylase in leukemic cells containing granules typical for basophils were similar to those in mature basophils. His histamine excess symptoms rapidly disappeared concomitant with the reduction of blast cells after chemotherapy. We speculate that his histamine excess symptoms were induced by the leukemic cells.
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PMID:Histamine excess symptoms in basophilic crisis of chronic myelogenous leukemia. 872

For the production and vesicle storage of histamine, Enterochromaffin-like (ECL) cells express histidine decarboxylase (HDC) and vesicular monoamine transporter 2 (VMAT2). Although HDC and VMAT2 show dynamic changes during gastric ulcer healing, the control system of their expression has not been fully investigated. In the present study, we investigated the effect of transforming growth factor-alpha (TGF-alpha) and proinflammatory cytokines on HDC and VMAT2 expression in rat ECL cells. Time course changes in the expression of TGF-alpha during the healing of acetic acid-induced ulcers were studied. EGF receptor (EGFR) expression was also examined in ECL cells, whereas the direct effects of TGF-alpha and proinflammatory cytokines on HDC and VMAT2 expression in ECL cells were investigated using in vivo and in vitro models. During the process of ulcer healing, expression of TGF-alpha mRNA was markedly augmented. Furthermore, EGFR was identified in isolated ECL cells. TGF-alpha stimulated HDC and VMAT2 mRNA expression and protein production and also increased histamine release from ECL cells. Selective EGFR tyrosine kinase inhibitor tyrphostin AG1478 almost completely inhibited HDC and VMAT2 gene expression induced by TGF-alpha in vivo and in vitro. During gastric mucosal injury, TGF-alpha was found to stimulate ECL cell functions by increasing HDC and VMAT2 expression.
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PMID:Transforming growth factor-alpha directly augments histidine decarboxylase and vesicular monoamine transporter 2 production in rat enterochromaffin-like cells. 1456 68

The human body is made of some 250 different cell types. From them, only a small subset of cell types is able to produce histamine. They include some neurons, enterochromaffin-like cells, gastrin-containing cells, mast cells, basophils, and monocytes/macrophages, among others. In spite of the reduced number of these histamine-producing cell types, they are involved in very different physiological processes. Their deregulation is related with many highly prevalent, as well as emergent and rare diseases, mainly those described as inflammation-dependent pathologies, including mastocytosis, basophilic leukemia, gastric ulcer, Crohn disease, and other inflammatory bowel diseases. Furthermore, oncogenic transformation switches some non-histamine-producing cells to a histamine producing phenotype. This is the case of melanoma, small cell lung carcinoma, and several types of neuroendocrine tumors. The bioactive compound epigallocatechin-3-gallate (EGCG), a major component of green tea, has been shown to target histamine-producing cells producing great alterations in their behavior, with relevant effects on their proliferative potential, as well as their adhesion, migration, and invasion potentials. In fact, EGCG has been shown to have potent anti-inflammatory, anti-tumoral, and anti-angiogenic effects and to be a potent inhibitor of the histamine-producing enzyme, histidine decarboxylase. Herein, we review the many specific effects of EGCG on concrete molecular targets of histamine-producing cells and discuss the relevance of these data to support the potential therapeutic interest of this compound to treat inflammation-dependent diseases.
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PMID:Targeting of histamine producing cells by EGCG: a green dart against inflammation? 2065 70