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)

After prolonged fasting the activity of histidine decarboxylase in the oxyntic mucosa of the rat stomach is low. Feeding or injection of gastrin or insulin rapidly raises the enzyme activity. It was earlier suggested that all enzyme-activating agents act through release of gastrin. This view has found experimental support in studies which show that in antrectomized rats the enzyme is activated by gastrin but not by gastrin-releasing stimuli like feeding or vagal excitation (insulin hypoglycemia). In the present investigation rats were subjected to a variety of treatments and serum gastrin concentrations and gastric histidine decarboxylase activities were measured. The main findings were as follows.1. Feeding raised the serum gastrin level and the enzyme activity in unoperated rats. In fasted antrectomized rats the serum gastrin concentration was low; in freely fed antrectomized rats it was at the same level as in fasted unoperated rats. In antrectomized rats the enzyme activity was low and not raised by feeding.2. Acid in the antrum inhibits the release of gastrin whereas an alkaline pH may facilitate such release. All treatments that blocked acid secretion, thereby raising the antral pH, also raised the serum gastrin concentration and concomitantly the histidine decarboxylase activity. Thus, vagotomy increased the serum gastrin level and the histidine decarboxylase activity in fasted rats. Treatment of fasted unoperated rats with atropine or hexamethonium had similar effects. Antral exclusion, which prevents HCl from reaching the pyloric glands, resulted in marked increase in the serum gastrin concentration and in the enzyme activity of fasted rats.3. Injection of insulin resulted in a rather slow, progressive increase in the serum gastrin concentration. The peak was reached after about 4 hr. The enzyme activity was also raised markedly and the peak response occurred about 1 hr later.4. An increase in the histidine decarboxylase activity was invariably preceded or accompanied by a raised serum gastrin level. With fasted or fed unoperated, vagotomized, antrectomized or antrally excluded rats, the correlation coefficient for the relation between enzyme activity and serum gastrin concentration was 0.69 (P < 0.05).5. Porta-caval-shunted fasted rats responded to feeding or injection of insulin with marked activation of gastric histidine decarboxylase. The response after feeding was at least 5 times higher in shunted than in nonshunted rats but serum gastrin was only slightly higher. Following antrectomy of porta-caval-shunted rats feeding no longer raised the enzyme activity. Thus, the enzyme-activating agent was of antral origin. In the shunted rats injection of pentagastrin induced an enzyme activation about 5 times that seen in intact rats. This response was not significantly reduced by antrectomy. In conclusion, we have observed a correlation between serum gastrin concentration and histidine decarboxylase activity. We have failed to obtain evidence for the existence of any physiological intermediate other than gastrin in the activation of histidine decarboxylase induced by feeding, vagal stimulation or inhibition of acid secretion.
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PMID:Correlation between serum gastrin concentration and rat stomach histidine decarboxylase activity. 444 71

1. In conscious rats provided with Pavlov or Heidenhain pouches the acid and pepsin responses to vagal stimulation, or infusions of gastrin, histamine, methacholine, and to various combinations of these stimulants have been established. The concomitant mobilization and increased formation of gastric mucosal histamine have also been examined.2. Histamine evoked graded acid responses in the Pavlov and Heidenhain pouches. The innervated pouch was more sensitive to histamine than the denervated. Stimulation of pepsin secretion was apparent only in the Heidenhain pouch.3. The acid response to vagal stimulation evoked by 2-deoxy-D-glucose was facilitated by infusion of histamine, but not that of pepsin, the secretion of which was depressed.4. Acid secretion in response to graded infusion of methacholine was enhanced by background infusions of histamine in subthreshold, sub-maximal and maximal dosages.5. The acid response to vagal stimulation was enhanced by a background infusion of gastrin, but not that of pepsin, the secretion of which was depressed.6. A background infusion of a large dose of histamine depressed the maximal acid response to gastrin in both types of pouches.7. Administration of histamine restrained the accelerating effect of gastrin on histidine decarboxylase activity, probably by a feed-back coupling.8. The increase in gastric mucosal histamine, as reflected in its urinary excretion, in response to gastrin infusion was enhanced by vagal stimulation.9. The amounts of histamine that can be mobilized and newly formed in the gastric mucosa have been evaluated and found to be fully adequate for efficient stimulation of the parietal cell.
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PMID:Gastric secretion and its facilitation as related to gastric mucosal histamine. 456 31

1. Prostaglandin E(1) inhibits basal and pentagastrin-stimulated gastric acid secretion. The mechanism of this action is not clear. One possible explanation might be that prostaglandin E(1) interferes with the local release or synthesis of histamine which has been proposed as the mediator of the effects of gastrin on the parietal cell.2. A single injection of prostaglandin E(1) did not affect mucosal histamine content or histidine decarboxylase activity in the rat stomach. Pentagastrin lowered the histamine content and activated the histidine decarboxylase to the same extent in prostaglandin E(1)-pretreated and in control rats. We conclude therefore that the inhibitory effect of prostaglandin E(1) on basal and pentagastrin-stimulated acid secretion is not caused by inhibition of histamine release or histamine synthesis.3. Repeated injections of prostaglandin E(1) resulted in a significant elevation of the gastric histidine decarboxylase activity in normal but not in antrectomized rats. Conceivably, this increase in enzyme activity is secondary to prostaglandin E(1)-induced inhibition of acid secretion, which will stimulate release of gastrin due to the rise in intragastric pH.
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PMID:Effects of prostaglandin E1 on acid secretion, mucosal histamine content and histidine decarboxylase activity in rat stomach. 473 Aug 28

1. The effects of the vagus nerve and of antral gastrin on the rate of histamine formation (histamine forming capacity, HFC, i.e. histidine decarboxylase activity) in the parietal cell region of the gastric mucosa has been investigated in the following stomach preparations: gastric fistula, denervated Heidenhain pouch, antral resection with gastrojejunostomy, gastrojejunostomy with exclusion of the duodenum and in the intact stomach. The determinations of mucosal HFC were made on fasting rats and on re-fed animals when the effect of feeding was studied.2. In fasting rats with a gastrojejunostomy and the antrum intact the mucosal HFC of the innervated stomach was about 4 times higher than in the corresponding preparation with the antrum resected. In the innervated main stomach the mucosal HFC was about twice as high as in the denervated pouch, indicating that the vagus and endogenous antral gastrin each contribute to maintaining mucosal HFC in the fasting state.3. Acidifying the stomach caused a substantial lowering of the mucosal HFC presumably by inhibiting antral gastrin release, whereas acid in the stomach did not interfere with the elevation of mucosal HFC evoked by injection of gastrin.4. Injection of gastrin elevated mucosal HFC in the innervated main stomach and in the denervated pouch to approximately equal levels. With the dose of gastrin employed there was about a fourfold increase in the HFC of the pouch mucosa.5. In antrectomized rats enhanced vagal influence, evoked by insulin injection or by feeding, raised the mucosal HFC. In rats with the antrum intact and the stomach acidified, insulin injection produced an increased HFC. Thus, a vagal effect on mucosal HFC exists independent of participation of antral gastrin.6. The stable choline esters carbachol and methacholine act directly on the parietal cell without involving mucosal HFC. The vagus nerve and gastrin, however, are assumed to provide secretory stimulation by means of accelerated histamine formation.7. The interrelation between increased histamine formation and hydrochloric acid secretion is discussed.
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PMID:The role of the antrum and the vagus nerve in the formation of gastric mucosal histamine. 535 33

1. In conscious rats provided with a Heidenhain pouch, the changes in the secretion of acid and pepsin following antrectomy were investigated in the interdigestive state and in response to graded doses of intravenous hog gastrin II and methacholine. The change in mucosal histamine formation (histamine-forming capacity, HFC, i.e. histidine decarboxylase activity) was determined in the fasting state in the Heidenhain pouch following antrectomy.2. Antrectomy was followed by a substantial reduction in the interdigestive secretion of acid.3. Methacholine infusion when the antrum was intact evoked a maximal acid secretory response that exceeded twice the response obtained with gastrin.4. After resection of the antrum the acid response to graded doses of methacholine and to gastrin at maximal but not at submaximal dose levels was significantly reduced.5. After antrectomy, threshold or submaximal infusion of gastrin accentuated the acid secretory responses to methacholine, but did not restore the maximal secretory response to methacholine obtained before antrectomy.6. The changes in pepsin secretion following antrectomy were similar to those in acid secretion but smaller.7. Mucosal HFC of the pouch was significantly lowered following antrectomy.8. After antrectomy gastrin failed to accelerate histamine formation in the mucosa in the usual way.
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PMID:Secretory behaviour and histamine formation in the rat Heidenhain pouch following antrectomy. 549 42

Histamine is not uniformly distributed in the human and animal organisms, but occurs in high concentrations in the gastric mucosa. The enzymes responsible for its metabolism--histidine decarboxylase, histamine N-methyltransferase and diamine oxidase--seem to be less predominantly localized in the stomach. Considerable effort was necessary to detect and measure histamine formation in the gastric mucosa. This was a controversial subject that only was solved recently. Histamine inactivation by histamine methyltransferase occurs in man in the fundic gastric mucosa that has reasonable enzymic activity. However, liver, spleen and intestine show much higher activities indicating less specificity of histamine catabolism in the gastric mucosa. Finally, diamine oxidase activity was once thought to be absent in the corpus mucosa, but more recently, moderate activities of this enzyme were found in several species, including man. Thus, histamine metabolism in the gastric mucosa is by no means unique in mammalian tissues, but the presence of these enzymes may be regarded as an indicator of its physiological function. To some extent enzymic activities involved in histamine formation and inactivation are regulated in the process of acid secretion. Histidine decarboxylase and histamine N-methyltransferase activities are enhanced by gastrin, but are not influenced by vagal stimulation. Hitherto, only histamine methylation was found to be diminished in duodenal ulcer disease. Vagotomy and histamine H2-receptor antagonists modulate histamine catabolism by histamine methyltransferase. The implication of these findings for treatment of duodenal ulcer are discussed.
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PMID:Metabolism and function of gastric histamine in health and disease. 619 37

Selective upper abdominal sympathectomy increased basal acid output in rats but was without effect on stimulated acid output, serum gastrin concentration, and gastric mucosal histidine decarboxylase activity. The sympathectomy was verified by fluorescence histochemistry and determination of tissue catecholamines. A drastic reduction in tissue noradrenaline, adrenaline, and dopamine levels occurred after sympathectomy, and fluorescence microscopy showed a complete loss of adrenergic nerve fibers. Vagotomy reduced catecholamine levels in the stomach wall by 50% but did not affect the catecholamine content in the pancreas and small bowel. Surprisingly, combined vagotomy and upper abdominal sympathectomy resulted in lower catecholamine levels than sympathectomy alone in extragastric but not in gastric tissues.
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PMID:Effects of upper abdominal sympathectomy on gastric acid, serum gastrin, and catecholamines in the rat gut. 651 11

In the rat nephrectomy raises the serum gastrin concentration but makes the parietal cells refractory to gastrin. Pylorus ligation stimulates the gastric acid output by a long vago-vagal reflex in innervated animals and by an intramural reflex in chronically vagotomized animals. Nephrectomy reduced the acid response to pylorus ligation in vagally intact rats but enhanced it in vagotomized rats. The acid response to pylorus ligation in all the experimental groups was inhibited by a muscarinic blocker, atropine, and by an H2-antagonist, metiamide. The serum gastrin concentration was raised by nephrectomy and by vagal denervation. Histamine mobilization from gastric endocrine cells is reflected in the activity of gastric histidine decarboxylase. The enzyme activity in pylorus-ligated innervated rats was raised by pentagastrin, atropine, and metiamide. In nephrectomized rats the basal enzyme activity was high, and it was raised further, slightly but significantly, by pentagastrin. The basal enzyme activity in pylorus-ligated rats was also quite high after vagotomy, and it was raised further by pentagastrin. After vagotomy + nephrectomy the basal enzyme activity was very high; it was not raised further by pentagastrin. It appears that both vago-vagal and intramural reflexes involve a cholinergic and a histaminergic pathway, that gastrin is not important for the neurally mediated acid response elicited by pylorus ligation, and that the postulated histaminergic pathway does not involve histamine derived from the gastric endocrine-like cells.
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PMID:Mechanism of gastric acid response to pylorus ligation: effects of nephrectomy. 666 25

Diets containing egg white, casein, menhaden fish meal, soy protein or wheat gluten were fed to rats to assess the impact of dietary protein (and other nutrients) on gastric functions. The menhaden fish meal group exhibited increases in stomach histidine decarboxylase (HDC) activity, histamine concentration, as well as acid secretion when compared with the control, casein group. When rats were fed amino acid-supplemented casein or fish meal diets to simulate each other's amino acid profile, a small increase in gastric HDC activity, histamine content and acid secretion was observed in comparison with the unsupplemented casein or fish meal groups. The high mineral content of menhaden fish meal (15%) was thought to be a potential inducing factor for gastric histamine metabolism and acid secretion. Adding fish meal ash to the casein diet or to a cod fillet diet elevated stomach HDC activity and histamine concentration significantly. Furthermore, when calcium (Ca) was added to the casein diet to simulate its high content in menhaden fish meal (7.8%), similar elevated levels of gastric histamine were obtained for the Ca-supplemented casein group as for the fish meal group. The role of Ca could be due to release of gastrin, which results in release of stomach histamine, or by facilitating mast cell histidine incorporation with subsequent histamine synthesis.
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PMID:Gastric histamine metabolism and acid secretion in rats as influenced by diet and nutrient content. 682 9

Acid and pepsin secretion and gastric mucosal histidine decarboxylase activity were measured in rats of various ages between 5 and 40 days after injection of saline, pentagastrin, histamine, or carbachol. Basal acid secretion first appeared on day 15. At this time carbachol significantly stimulated both acid and pepsin secretion. Gastrin and histamine did not stimulate acid or pepsin secretion until day 20. Histidine decarboxylase activity first appeared on day 10 and was first increased by pentagastrin on day 18. Injection of 8-day-old rats with corticosterone prematurely induced acid secretion on day 12 in response to all three stimulants and pepsin secretion in response to carbachol only. These studies provide a comprehensive picture of the development of gastric mucosal sensitivity to the three naturally occurring stimulants and indicate that adrenal glucocorticoids play an important role in that development.
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PMID:Development of sensitivity to different secretagogues in the rat stomach. 682 87


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