Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interleukin-1 beta (IL-1 beta) is the most potent inhibitor of gastric acid secretion known at present. Although histamine has been shown to be an important mediator of gastric acid secretion, the effect of IL-1 beta on gastric histamine mobilization has not been studied. In the present study, the effects of IL-1 beta on gastric acid secretion and gastric histamine mobilization were investigated in conscious rats with both gastric and vesical fistulas. IL-1 beta (5 micrograms/kg iv) significantly inhibited basal acid secretion but did not affect basal urinary histamine excretion and fundic histidine decarboxylase (HDC) activity. Gastrin-17-I (1 nmol.kg-1.h-1) caused a marked increase in acid secretion, urinary histamine secretion, and fundic HDC activity. IL-1 beta (5 micrograms/kg iv) completely inhibited gastrin-induced acid secretion and partially inhibited urinary histamine excretion and fundic HDC activity. Pretreatment with indomethacin (10 mg/kg ip) partially reversed the inhibitory effects of IL-1 beta on gastrin-stimulated fundic HDC activity and acid secretion. These findings indicate that IL-1 beta inhibits gastric histamine mobilization through both prostaglandin-dependent and prostaglandin-independent pathways. Furthermore, it is suggested that the inhibitory action of IL-1 beta on gastric acid secretion is mediated by the inhibition of gastric histamine mobilization.
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PMID:Interleukin-1 beta inhibits gastric histamine secretion and synthesis in the rat. 781 Jun 64

To evaluate whether the general trophic effect of gastrin on the oxyntic mucosa is an indirect effect mediated by histamine H2 receptors, sustained 24 hour hypergastrinaemia was induced in Sprague-Dawley rats by treatment with the long acting and potent histamine H2 antagonist loxtidine for five months. The trophic effect was assessed by weight, enumeration of total mucosal cells, parietal cells, and enterochromaffin like cells in smears stained for the actual cells after enzymatic dispersion of the mucosa, and by biochemical analysis of oxyntic mucosal homogenates. The weight of the whole stomach and the oxyntic mucosa increased by 12.7% (p = 0.016) and 27.5% (p = 0.006), respectively. Total oxyntic mucosal protein content increased by 28.7% (p = 0.058). Total numbers of mucosal cells and parietal cells increased by 11.9% (NS) and 24.1% (NS), respectively. The amount of the parietal cell specific enzyme H+,K(+)-ATPase was unchanged. On the other hand, the number of enterochromaffin like cells and related parameters, histidine decarboxylase activity and histamine content of the oxyntic mucosa, showed a pronounced and significant increase. It is concluded that the general trophic effect of gastrin on the oxyntic mucosa is not mediated by the histamine H2 receptor. The tropic effect of gastrin on the parietal cell seems, in contrast with that on the enterochromaffin like cell, not to be specific but only reflecting the general trophic effect on the oxyntic mucosa.
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PMID:Evaluation of the trophic effect of longterm treatment with the histamine H2 receptor antagonist loxtidine on rat oxyntic mucosa by differential counting of dispersed cells. 782 70

Although gastric enterochromaffin-like (ECL) carcinoid tumors are known to develop in patients with long-standing hypergastrinemia, the expression of the gastrin receptor gene in ECL cells has not yet been demonstrated. Therefore, this study was designed to examine gastrin receptor gene expression in ECL cells. Mastomys gastric mucosal cells isolated by enzyme dispersion were separated into 10 fractions (F1-10) by centrifugal elutriation. Each fraction was examined histologically to determine whether they contained ECL and/or parietal cells and Northern blot analysis was used to confirm the presence of histidine decarboxylase and H+, K(+)-ATPase gene expression. ECL cells were found only in fractions 1 and 2, whereas parietal cells were detected in fractions 6-10. Gastrin receptor gene expression was demonstrated in both parietal cell-rich and ECL cell-rich fractions. In addition, the gastrin receptor cDNA sequences obtained from the two of the fractions (F1 and 8) were identical. These results suggest that gastrin receptor genes are expressed in ECL cells as well as in parietal cells and that these receptors are identical.
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PMID:Gastrin receptor genes are expressed in gastric parietal and enterochromaffin-like cells of Mastomys natalensis. 792 34

Gastrin release histamine from the oxyntic mucosa, stimulates the enzymatic activity of histidine decarboxylase (HDC), increases HDC mRNA abundance, and has a trophic effect on the enterochromaffin-like (ECL) cell. In the present study, we examined the effect of exogenous gastrin on HDC activity and mRNA and the time scale of increase and decline of HDC activity and mRNA. Rats received intravenous infusion of gastrin-(1-17) in different doses or periods of time. Oxyntic mucosal HDC activity and mRNA abundance increased significantly with serum gastrin concentrations in the physiological range. The onset of response was rapid and maximal for both parameters after 2 h. Poststimulatory decrease was maximal 2 h after cessation of gastrin infusion. Those observations suggest that HDC enzymatic activity and mRNA abundance are important in meal-to-meal regulation of gastric secretion. Furthermore, HDC enzymatic activity and mRNA abundance varied in parallel, indicating that HDC mRNA abundance is important in the overall regulation of gastric mucosal HDC activity.
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PMID:Gastrin regulates histidine decarboxylase activity and mRNA abundance in rat oxyntic mucosa. 807 25

The effect of acid inhibition on gastric endocrine cells was investigated in Praomys (Mastomys) natalensis. Long-term treatment (1 to 32 weeks) with an irreversible histamine 2-receptor blocker (loxtidine) caused a sustained increase in plasma gastrin levels, which was accompanied by a gradual increase in histamine and histidine decarboxylase activity of the gastric oxyntic mucosa. The density of endocrine cells in the oxyntic mucosa increased gradually, doubled by 8 weeks, and was three times that of controls after 24 weeks of treatment. Hyperplastic changes in the endocrine cell population were evident after 2 to 8 weeks in all animals, whereas dysplastic or neoplastic lesions were observed in half the animals after 16, 24, and 32 weeks of treatment. Gross tumors in the oxyntic mucosa were observed in 1/4 of the animals treated for 24 or 32 weeks. Proliferating cells were identified as enterochromaffinlike cells because they were argyrophilic and immunopositive for chromogranin A and histamine. The results demonstrate that histamine 2-receptor blockade initiated by loxtidine promotes a rapid development of enterochromaffinlike cell tumors in Mastomys and suggest a critical role for gastrin in the formation of these tumors. However, the rate and frequency by which carcinoid tumors appeared in Mastomys after acid inhibition was much greater than that reported in other species, indicating that several factors, including hormonal and genetic factors, are important in the development of gastric endocrine tumors.
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PMID:Rapid induction of enterochromaffinlike cell tumors by histamine2-receptor blockade. 809 70

The gastric proton pump H+/K(+)-ATPase in the parietal cell is central to acid secretion into the stomach. We performed the following experiment to examine the pattern of expression of the alpha- and beta-subunits of the H+/K(+)-ATPase at the transcriptional level during 7 days' application of the proton pump inhibitor omeprazole, in relation to the expression of gastrin and histamine, two stimuli of gastric acid secretion. Serum gastrin concentrations and mRNA levels of antral gastrin, fundic histidine decarboxylase (HDC) and H+/K(+)-ATPase alpha- and beta-subunits were determined after 8 h, 1, 3 and 7 days. Omeprazole treatment rapidly caused an increase in the serum gastrin concentration and the antral gastrin mRNA level after 3 days. HDC mRNA expression showed a steady increase with a 5-fold induction after 1 week. However, mRNA levels of the alpha- and beta-subunits of the H+/K(+)-ATPase were unchanged during the course of omeprazole treatment. These results suggest that omeprazole inhibition of the gastric proton pump does not result in feedback activation of H+/K(+)-ATPase gene expression despite adaptive changes of the endocrine stomach.
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PMID:Expression of the gastric H+/K(+)-ATPase and histidine decarboxylase during omeprazole treatment. 818 77

1. Histidine decarboxylase in the enterochromaffin-like cells of the gastric corpus mucosa converts histidine to histamine which in turn stimulates gastric acid secretion. The control of histidine decarboxylase activity is poorly understood. We have examined how fasting and refeeding influence the abundance of the messenger RNA encoding histidine decarboxylase in the gastric corpus of the rat. 2. The polymerase chain reaction was used to generate a probe for detection of histidine decarboxylase messenger RNA in Northern and slot blots of total RNA from the gastric corpus of rats fasted for up to 48 h, or fasted and then refed. A gastrin monoclonal antibody was used to neutralize the action of endogenous gastrin. 3. Fasting progressively reduced histidine decarboxylase messenger RNA abundance by 3- to 4-fold after 48 h. Refeeding induced a rapid increase in histidine decarboxylase messenger RNA abundance which was detectable after 30 min. 4. There was a significant correlation between histidine decarboxylase messenger RNA abundance and plasma gastrin. Administration of gastrin antibody inhibited the increase in histidine decarboxylase activity after 6 h refeeding, but not after refeeding for 30 min. 5. The results suggest that histamine-mediated changes in postprandial acid secretion depend on control of histidine decarboxylase mRNA levels, and that gastrin regulates production of this enzyme in the rat over periods of a few hours.
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PMID:Food stimulation of histidine decarboxylase messenger RNA abundance in rat gastric fundus. 822 45

Gastrin and possibly cholecystokinin (CCK) control the activity and growth of the histamine-containing endocrine cells, the enterochromaffin-like (ECL) cells, in the oxyntic mucosa of the rat. Portacaval shunting (PCS) is known to activate the ECL cells through as yet unknown mechanisms. PCS also exaggerates the ECL cells' response to gastrin, whereas antrectomy causes hypotrophy and hypoplasia of the ECL cells. A recent study showed that the ECL cells failed to respond to sustained hyperCCKemia caused by pancreaticobiliary diversion (PBD). In the present study we investigated whether PBD-produced hyperCCKemia influenced the effects of PCS or antrectomy on the ECL cells. The results show 1) that hyperCCKemia raised the histidine decarboxylase (HDC) activity of the ECL cells in PCS rats but not in control rats, and the CCK-A receptor blockade failed to prevent the enzyme activation; and 2) that PBD prevented the ECL cell hypoplasia and the decrease in HDC activity induced by antrectomy. The findings suggest that under special circumstances endogenous CCK may stimulate the ECL cells.
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PMID:Hypercholecystokininemia produced by pancreaticobiliary diversion causes gastrin-like effects on enterochromaffin-like cells in the stomach of rats subjected to portacaval shunting or antrectomy. 828 36

A 63-year-old woman was diagnosed as autoimmune gastritis by the presence of serum antibody against alpha-subunit of gastric H+,K(+)-ATPase. The patient did not have pernicious anemia, but showed achlorhydria, marked hypergastrinemia, enterochromaffin-like cell hyperplasia and an extremely high histidine decarboxylase activity in the gastric fundic mucosa. Intragastric acidification by infusion of hydrochloric acid via a nasogastric tube induced a transient reduction of serum gastrin level and fundic mucosal histidine decarboxylase activity. A marked increase in fundic mucosal histidine decarboxylase activity as well as hypergastrinemia appears to be the pathophysiologic response to achlorhydria caused by autoimmunity against gastric H+,K(+)-ATPase.
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PMID:Marked increase in fundic mucosal histidine decarboxylase activity in a patient with H+,K(+)-ATPase antibody-positive autoimmune gastritis. 828 44

Young male rats (100 g body weight) were fed diets containing varying amounts of calcium. Body weight and bone development were studied together with various endocrine parameters, including blood levels of Ca2+, calcitonin, parathyroid hormone, vitamin D, and gastrin, and the enterochromaffin-like (ECL) cell-related parameters gastric mucosal histidine decarboxylase activity and histamine concentration. A diet containing 0.5% calcium resulted in optimum body weight gain and bone development. A lower calcium intake impaired body weight gain and bone development. The impairment was manifested in reduced bone calcium content whereas the size of the bones was unaffected. The net absorption of calcium seemed to be proportional to the calcium intake. A low calcium diet (0.03%) raised the circulating levels of 1,25(OH)2D and parathyroid hormone and lowered 25(OH)D3 and Ca2+, whereas a high calcium diet (5.46%) raised calcitonin, Ca2+, 25(OH)D3, and 1,25(OH)2D. In addition, the low calcium diet lowered the circulating gastrin concentration and the histidine decarboxylase activity and histamine content of the ECL cells in the gastric mucosa. A high calcium diet raised the circulating gastrin concentration, but the rise was not associated with an increase in the histidine decarboxylase activity and histamine content.
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PMID:The effect of high or low dietary calcium on bone and calcium homeostasis in young male rats. 836 95


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