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)

Epidermal growth factor (EGF) has been shown to stimulate the growth of adult rat gastric mucosa and to increase DNA synthesis of mouse small and large intestinal mucosa. This study examines whether EGF affects the functional and structural development of the rat gastric mucosa. Rats were injected with 20 micrograms/kg EGF three times/day for 5 days beginning on the 10th day after birth. A control group of animals received saline injections of identical volume. All rats were killed on day 15. EGF significantly increased the weight of the whole stomach and the DNA, RNA, and protein content of the oxyntic gland mucosa, but had no effect on the RNA/DNA ratio, or antral and serum gastrin levels. Two groups of similarly treated rats, were anesthetized with ether, pylorus-ligated, and injected with either saline or pentagastrin (250 micrograms/kg) after they had recovered from anesthesia. EGF-treated rats had significantly higher rates of basal acid secretion and pentagastrin-stimulated acid secretion than the saline-treated controls. EGF, however, did not alter basal or pentagastrin-stimulated pepsin secretion nor did it change mucosal pepsinogen content. These results indicate that EGF stimulates oxyntic mucosal growth in unweaned rats but that it does not lead to precocious maturation or functional development.
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PMID:Effect of epidermal growth factor on the development of rat gastric mucosa. 257 37

Metabolic effects of a trickle challenge with the equivalent of 10,000 infective Ostertagia ostertagi larvae per day were investigated in 12 calves allocated to infected, pair-fed control or ad libitum-fed control groups. Changes in hormone levels reflecting abomasal, pituitary and pancreatic function were monitored using radioimmunoassay techniques previously validated for use in cattle. A range of metabolic profile parameters and blood metabolites was also measured. Feed intake of the infected calves began to decline as blood gastrin and pepsinogen levels reached a peak. The depression in appetite recorded in this group was responsible for significant increases in plasma urea and non-esterified fatty acid levels and associated with an increase in growth hormone/insulin ratio. No significant difference in glucagon levels was recorded between groups. A decline in blood albumin values was also shown in the infected group and associated with a drop in nitrogen digestibility. A significant depression in circulating calcium levels was related to either the hypoalbuminaemia or impaired mineral absorption in the intestine. A decrease in plasma cholesterol values in the infected group was associated with changes in digestive function.
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PMID:Ostertagia ostertagi infection in the calf: effects of a trickle challenge on the hormonal control of digestive and metabolic function. 259 87

To investigate whether hypergastrinemia and low serum levels of pepsinogen I are associated with gastric hypoacidity in cirrhosis with capillary ectasia of gastric mucosa and whether this alteration is secondary to the presence of atrophic gastritis, two groups of patients were studied: 1) 12 cirrhotic patients with diffuse gastric red spots at the endoscopic examination, and 2) 12 cirrhotic patients with endoscopically normal mucosa. Vascular ectasia of the gastric mucosa was histologically confirmed in all patients with gastric red spots. The study of base-line and stimulated acid gastric secretion showed that 9 of 12 (75%) cirrhotics with gastric vascular ectasia had achlorhydria and that 8 of these 9 patients had high base-line gastrin serum levels (greater than 130 pg/ml) and low base-line pepsinogen I serum levels (less than 20 ng/ml). Base-line gastrin and pepsinogen I serum levels were significantly greater and lower, respectively, in patients with gastric vascular ectasias than in cirrhotics without these lesions. None of the patients of either group had complete atrophy in the corpus of the stomach, and only 4 of the 9 cirrhotics with gastric vascular ectasia and achlorhydria had moderate atrophy. These results show that achlorhydria is frequently associated with hypergastrinemia and low pepsinogen I serum levels in patients with cirrhosis and gastric vascular ectasias and suggest that this disturbance is not secondary to a morphologic abnormality of the gastric mucosa.
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PMID:Gastric vascular ectasias in cirrhosis: association with hypoacidity not related to gastric atrophy. 259 68

To assess the functional and morphological characteristics of the gastric mucosa of patients with fundic hyperplastic polyps (FP), the determination of gastric acid secretion, serum gastrin levels, serum pepsinogen 1 (PG1) levels and histological examination were undertaken in 24 patients with FP, 34 with foveolar hyperplastic polyps (HP) and 62 controls, who had no gastric lesions. The following were the results of our investigation. 1) There were no differences between the patients with FP and the controls as to gastric acid secretion, serum gastrin levels, and serum PG1 levels. On the other hand, hypochlorhydria, hypergastrinemia and hypopepsinogenemia were common in those with HP. 2) Histological examination using gastric biopsy specimens showed almost normal gastric mucosa in patients with FP. However, severe atrophic gastritis of the fundus was common in patients with HP. 3) It was shown that there were definite differences between the patients with FP and those with HP with regard to the gastric function and morphology, although both types of gastric polyp were histologically classified as hyperplastic.
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PMID:[Gastric mucosa in patients with fundic hyperplastic polyps]. 275 38

In isolated guinea pig gastric chief cells, gastrin-I and cholecystokinin-hexapeptide (CCK-4) stimulated pepsinogen release. However, the efficacies of these two peptide were 51% of that observed with CCK-octapeptide (CCK8). CR1409 and L-364718, both of which are new CCK receptor antagonists in pancreatic acinar cells, also inhibited 10(-8) M CCK8-stimulated pepsinogen release with a half-maximal inhibitory concentration (IC50) observed at 3 x 10(-9) M, respectively. The dose response curve to CCK8 for pepsinogen release shifted to the right in the presence of CR1409 or L-364718. The IC50 of these two antagonists for the CCK8-stimulated increase in cytosolic Ca2+ concentration monitored by Fura-2 were equal to those for CCK8-stimulated pepsinogen release. By contrast, the IC50 of dibutyryl cyclic GMP, a well-known CCK receptor antagonist, for CCK8-stimulated pepsinogen release was less than that for CCK8-stimulated increase in cytosolic Ca2+ concentration. Results suggested that CCK receptors in gastric chief cells are unique and may be different from CCK receptors in other tissues previously reported.
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PMID:[Characterization of cholecystokinin receptors in gastric chief cells--effect of CCK analogs and CCK receptor antagonists on chief cells]. 281 Aug 48

Female rats were treated orally for 3 mo with omeprazole (40 and 400 mumol/kg). Both doses caused total inhibition of gastric acid secretion and recovery was parallel to that of H+-K+-ATPase activity (30-50 and 60-80% inhibition 24 h after doses, respectively). The H+-K+-ATPase activity returned to control levels within 1 wk after the last dose. Plasma gastrin levels were dose-dependently increased during treatment but reversed to control levels within 9 days after the last dose. Parallel with a general increase in corpus mucosal mass, both pepsinogen and H+-K+-ATPase total content increased. However, their tissue concentrations did not differ from control values, suggesting that neither parietal nor chief cell density are changed by omeprazole treatment and also that their growth is parallel to the general hyperplasia. In contrast, the oxyntic mucosal histamine concentration was increased, indicating an increase in the enterochromaffin-like (ECL) cell density. Maximal capacity of the mucosa to secrete acid increased in parallel with the increase in mucosal mass and total H+-K+-ATPase content. However, basal acid secretion did not differ between treatment groups. Increased capacity slowly declined toward control levels over the 70-day recovery period after withdrawal of omeprazole. These results suggest that hypergastrinemia, induced in the rat by pharmacological inhibition of gastric acid secretion, causes a hyperplasia of oxyntic mucosal cells, ECL cells growing faster than the others. The hyperplastic mucosa has an increased capacity to produce acid and is functionally normal.
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PMID:Rat parietal cell function after prolonged inhibition of gastric acid secretion. 282 15

Caerulein, gastrin, and C-terminal fragments of cholecystokinin (CCK) varying in length from eight (CCK-8) to four (CCK-4) amino acids stimulate pepsinogen secretion from dispersed chief cells prepared from guinea pig stomach. C-terminal fragments of CCK containing fewer than four amino acids, even when tested at concentrations as high as 3 mM, do not stimulate pepsinogen secretion. The efficacies of gastrin and the various CCK-related peptides, coupled with the pattern of action of CCK receptor antagonists, indicate that chief cells from guinea pig stomach possess two functionally distinct classes of receptors, C-receptors and G-receptors. The C-receptors can be occupied by caerulein, CCK-8, CCK-7, des(SO3)CCK-8, or des(SO3)CCK-7, and occupation of C-receptors causes full stimulation of pepsinogen secretion. G-receptors can be occupied by gastrin I, gastrin II, CCK-6, CCK-5, or CCK-4, and occupation of G-receptors causes stimulation of pepsinogen secretion that is 60% of maximal.
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PMID:Functionally distinct receptors for cholecystokinin and gastrin on dispersed chief cells from guinea pig stomach. 283 29

We defined duodenal ulcers (DUs) not healed within 3 months with H2-antagonists as "intractable", because the recurrence rate of these DUs is higher than that of DUs healed within the same periods, and etiological differences are suggested to exist among these two groups. To verify the pathophysiological differences, gastric analysis including modified sham-feeding (MSF) were performed in 12 intractable, 10 tractable DUs and 5 healthy controls. By MSF stimulation, acid output increased in all subjects and the mean acid output of MSF amounted to about 60% of the tetragastrin maximum. Mean acid output of intractable DU cases was significantly higher than the controls in any stimulatory state and was different only in MSF with tractable DU. No significant changes of serum gastrin were recognized during MSF and both serum pepsinogen I and II are higher in DU cases than the control in basal state, but the two DU groups show no significant difference or increase by MSF or gastrin stimulation. These data suggest that vagal activity of intractable DUs is higher than not only healthy subjects, but tractable DUs and participation of gastrin in the increase of acid output by MSF might be denied.
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PMID:Gastric acid, serum gastrin and pepsinogen I and II responses to modified sham-feeding in tractable and intractable duodenal ulcers. 288 82

Of 86 cases of aged patients with chronic gastritis treated with Trimebutine or Flutazolam, we evaluated the changes of serum pepsinogen-I and gastrin levels in their clinical courses from the points of the correlation with severity of chronic gastritis, aging phenomenon and the changes of symptom and endoscopic findings. In order to elucidate the multidimensional interrelation among these items, we used Hayashi's quantification theory II as a conventional analysis method. In aged patients, generally, although the serum gastrin levels were rather high compared with younger generation, the serum pepsinogen-I levels were consistently low throughout their clinical courses. There were some correlation between the levels of serum gastrin and the severity of chronic gastritis. When the drugs were effective on improving the condition of the disease, the level of gastrin revealed gradual decrease. These changes of gastrin were more typical in patients treated with Trimebutine.
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PMID:[Studies on the clinical significance concerning the changes in serum pepsinogen-I and gastrin levels in aged patients with chronic gastritis]. 289 25

The gastric pepsin output by the totally isolated, vagally denervated, and both luminally and vascularly perfused rat stomach was studied. Basal release of pepsin was 3% of total gastric mucosal stores per hour. Topical (luminal) administration of 0.001 M HCl was without effect. Graded concentrations of pentagastrin, gastrin, histamine, and impromidine in the vascular perfusate were tested. Pentagastrin induced only a slight increase in pepsin release (15% of total content per hour). Gastrin had a more pronounced effect and elicited a significant increase in the pepsin output, reaching a maximum of 28% of total pepsin content per hour. The CD50 of gastrin was 0.061 nM. Histamine and impromidine likewise produced significant increases in the pepsin secretion (maximum, 40% and 35% of total stores per hour, respectively). When the CD50 of histamine (0.718 microM) was compared with that of impromidine (0.011 microM), impromidine on molar basis had 65 times higher potency than histamine as a pepsin secretagogue. When the pepsin and acid responses during gastrin, histamine, and impromidine stimulation were compared, the pepsinogen secretion was shifted to the left and thus was more sensitive to stimulation than the acid secretion.
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PMID:Pepsin secretion by the totally isolated, vascularly perfused rat stomach. 295 63


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