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)

In order to study the effects of a physiologic meal on calcitonin (CT) secretion we studied 6 normal male volunteers (aged 28-34 yr). Each subject was given, on two separate days, either a mixed meal or 200 ml of distilled water, in random order. Gastrin (G) was effectively stimulated by the meal (F = 8.82; p less than 0.001) and reached a peak (with an average 100% increase) 30 min after the end of the meal, slowly decreasing thereafter; no increase was seen after water ingestion. On the other hand, CT levels remained stable throughout the observation period on both occasions. Ionized and total calcium did not show significant variations either after the meal or after water ingestion. These findings suggest that G alone, at the concentrations usually reached after a physiologic meal, is unable to stimulate CT secretion, at least in the absence of calcium increases.
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PMID:Meal-stimulated gastrin release and calcitonin secretion. 276 61

This study was designed to test the effects of pentagastrin and epidermal growth factor (EGF) on stress-induced ulceration and on the antral content of gastrin and somatostatin (SLI) in rats. Four groups of 14 to 15 rats had been prepared for 7 days by one of the following methods: saline injection (control); injection of pentagastrin (250 micrograms/kg, 3 times/day); injection of EGF (10 micrograms/kg, 3 times/day); or injection of EGF plus pentagastrin. At the end of the treatment period, half of each group of rats were sacrificed (nonstress group). There were no ulcers in the nonstress control groups of rats. Stress was applied by water immersion in the remaining half of the rats. The injections of pentagastrin and/or EGF resulted in substantial increase in antral content of SLI. After 20 hours of stress, the ulcer index was 40.5 +/- 3.3 in the controls, compared to 6.4 +/- 1.2 and 16.2 +/- 2.3 in rats that received pentagastrin or EGF, respectively. Injections of both pentagastrin and EGF resulted in an ulcer index of 26.2 +/- 2.0, which was significantly lower than that in controls, but higher than that in rats treated with either peptide alone. The stress resulted in significant decrease in antral SLI in all groups of rats, whereas SLI content in rats treated with pentagastrin and/or EGF remained significantly higher than that of controls. Antral content of gastrin did not differ significantly in the four groups tested. The ulcer index was inversely correlated with antral SLI content. We confirm and extend previous observations that pentagastrin and EGF prevent stress ulcer formation, and suggest that endogenous SLI may account, at least in part, for their antiulcer activity.
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PMID:Cytoprotective effect of pentagastrin and epidermal growth factor on stress ulcer formation. Possible role of somatostatin. 285 83

The effect of three concentrations of high-methoxy apple pectin (5, 10, and 15 g), on solid-liquid meal digestion was studied in 12 healthy men by the gastrointestinal intubation technique. The gastric emptying of water and carbohydrates is significantly reduced only after 10 and 15 g pectin. The changes in gastric pH are similar for pectin-free and pectin-containing meals. Cumulative lipase and trypsin outputs are not significantly different with and without pectin. When gastric uronic acid concentration is above 6 g/l, the duodenal absorption of carbohydrates is significantly reduced (p less than 0.001). The mean blood glucose levels with 10 and 15 g pectin are significantly higher than the control values at 180 min (p less than 0.05). Pectin does not modify serum concentrations of secretin, cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP), gastric inhibitory polypeptide (GIP), and somatostatin but serum motilin and gastrin levels are below the control values after high fiber meal.
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PMID:Effect of increased amounts of pectin on a solid-liquid meal digestion in healthy man. 286 75

The effects of various biologically active peptides on net jejunal water and electrolyte fluxes were studied in dogs in vivo. Vasoactive intestinal peptide (VIP), gastric inhibitory polypeptide (GIP), glucagon, gastrin, bombesin and neurotensin all had secretagogue activity, while methionine enkephalin stimulated net absorption. Somatostatin had no effect on net basal water and electrolyte transport, but inhibited glucagon-stimulated secretion. Secretin, calcitonin, substance P and pancreatic polypeptide (PP) did not have any effect on net water and electrolyte transport in the doses used in these experiments. The precise role played by these peptides in the control of intestinal transport has still to be determined. Studies in man have confirmed that food in the proximal small bowel stimulates secretion at sites remote from the application of food, and abnormal secretion of some peptides (e.g. VIP) has been associated with diarrhoea. Somatostatin has been used successfully to reduce the volume of certain types of secretory diarrhoea. Methods used in these experiments have been applied to the study of the composition and absorption characteristics of solutions used for oral rehydration in diarrhoea and in exercise-induced dehydration. Glucose polymers have been shown to be absorbed as rapidly as glucose from the jejunum.
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PMID:The effect of luminal and hormonal factors on small intestinal water and electrolyte transport. 287 15

Chronic treatment with rGRF for 14 days with or without a specific antibody against somatostatin-14 were performed on 24-day old male Sprague-Dawley rats. Serum GH concentrations were significantly increased at the time of sacrifice while growth was not affected. rGRF, possibly through its effect on GH release, stimulated lung and kidney weights, increasing water content of the latter. Muscle and testes remained insensitive to GRF while the heart showed signs of reduced growth. Liver growth responded positively to the combined rGRF and ASS treatments whereas the pancreas exhibited loss of weight; on both of these organs, GH may act directly. The increased weights of gastric fundus and duodenum may result from an indirect action of GH on serum levels of gastrointestinal hormones such as gastrin. The results of this study stress the specific response of each organ to increased GH serum levels and indicate that their respective growth control factors cannot be generalized.
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PMID:Effects of somatocrinin and a somatostatin antiserum on body and organ growth in the rat. 287 76

An intravenous bolus injection of nicotine (1 mg/kg) markedly elevated gastric acid secretion; oral administration of ethanol (40%, 10 ml/kg) significantly increased arterial serum gastrin and somatostatin levels. Chronic pretreatment with oral nicotine (5 or 25 micrograms/ml in drinking tap water, for 10 days), but not acute pretreatment with a single oral dose of nicotine (2 or 4 mg/kg), inhibited the nicotine-induced gastric acid secretion and ethanol-induced gastrin and somatostatin release. Pretreatment subcutaneously with a ganglion-blocking dose of hexamethonium (10 mg/kg), however, inhibited nicotine-stimulated acid output and ethanol-evoked somatostatin secretion but not ethanol-induced gastrin release. It is concluded that ethanol-evoked gastrin secretion could be due to activation of specific sites which are not nicotinic receptors, but which are depressed by chronic nicotine pretreatment. On the other hand, the release of somatostatin by ethanol appears to be controlled by ganglionic receptors in the gut.
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PMID:Effects of ethanol and nicotine on gastrin and somatostatin release in rats. 288 3

Systemic cholecystokinin (CCK) suppresses food intake in various species and has therefore been proposed to act as a satiety factor. Because CCK is also present in the hypothalamus and furthermore meets neurotransmitter criteria, the hypothesis was tested whether CCK participates in the transmission of satiety messages at the lateral hypothalamic (LH) level. The results of this study demonstrate that in halothane-anesthetized cats, neurons located in the LH will indeed release CCK-like material after a carbohydrate-protein meal in a time-dependent fashion. This release, as water loads demonstrate, is most likely due to volumetric distension rather than to the nutrient content. The releasable CCK does not originate from peripheral sources, since intravenously infused CCK octapeptide (CCK-8) does not appear in the perfusate. The release occurs only in discrete neurons and is not universal to CCK-releasing systems within the LH, and also, CCK-releasing systems are not present at all locations. The molecular form of CCK in feline hypothalamus is the COOH-terminal octapeptide (CCK-8) as shown by high-performance liquid chromatography. No gastrin-17 is present. CCK-8 is also the predominant form found in meal-induced as well as in KCl-induced CCK released from hypothalamic neurons. These results suggest a correlated role for hypothalamic CCK in the termination of food intake.
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PMID:Release of hypothalamic cholecystokinin in cats: effects of nutrient and volume loading. 291 18

The effects of inhibiting polyamine synthesis on the functional development of the gastric mucosa were studied in rats from 5 to 40 days old. They were treated from day 14 after birth with alpha-difluoromethylornithine (DFMO) at a concentration of 2% in the drinking water of mothers and pups. The rats were weaned on day 18. Basal acid and pepsin secretion, oxyntic gland mucosal pepsinogen content, and antral gastrin content followed similar developmental patterns in control animals. Levels of these parameters remained measurable but low until around the time of weaning, when dramatic log linear rises were observed. DFMO failed to delay the onset of the rises in any of these maturational indices. Ornithine decarboxylase (ODC) activity in the oxyntic gland mucosa was low but discernible in rats of every age studied. DFMO significantly reduced ODC activity at every age except 40 days, where there was no difference from control values. Our results suggest that ODC activity in the rat gastric mucosa does not change appreciably during neonatal development and that inhibiting putrescine synthesis from its precursor ornithine by DFMO treatment does not prevent or delay gastric mucosal maturation.
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PMID:Role of ornithine decarboxylase in functional development of rat gastric mucosa. 310 30

The effect of long-term administration of an antacid preparation on the gastric mucosa was investigated in rats, special attention was directed towards hypergastrinaemia and density of argyrophil cells. One ml of an Al (OH)3- and Mg (OH)2-containing antacid (in vitro neutralization capacity 28 mmol/die) or water was administered intragastrically 4 times daily. An additional group of rats remained untreated. Twelve hours after the final dose serum gastrin levels were significantly (p less than 0.001) elevated (113 +/- 28 pg/ml) compared to the control groups (33 +/- 1 and 22 +/- 2 pg/ml). Antral gastrin (G)-cell density was also increased after antacids by 58% whereas the somatostatin (D)-cell density and the somatostatin concentration in antral tissues were decreased. The number of fundic D- and argyrophil cells were not altered by antacid treatment. The number of parietal cell declined significantly in response to antacids. The foveolar gland region was almost doubled after antacids. It is concluded that in the rat 1. despite persistent hypergastrinaemia due to chronic antacid administration increases in argyrophil cell densities are not to be found; 2. long-term administration of antacids exert a trophic effect on the corpus mucosa predominantly by an increase of mucus neck cells.
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PMID:Influence of prolonged antacid administration on rat gastric mucosa. 314 98

Using commercially available diagnostic reagents, serum immunoreactive gastrin activity was measured in five normal horses that were starved of food and water for 24 hours. Blood samples were taken every 15 minutes for two hours. The horses were then fed a pelleted diet for 15 minutes and samples were taken every 15 minutes for a further two hours. Three further samples were taken at hourly intervals. The total sampling period was seven hours. Basal immunoreactive gastrin activity was lower than that reported in other mammals, ranging from a mean of 7.0 pg/ml to 13.8 pg/ml. At 30, 60 and 75 minutes after feeding, mean gastrin immunoreactivity was significantly elevated at 17.4, 19.8 and 18.2 pg/ml respectively. A late significant elevation occurred also five hours after feeding reading 19.4 pg/ml. This low activity may reflect a lower concentration of serum gastrin in the horse than in other mammals, or the methods used in the study may have failed to detect equine serum gastrins.
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PMID:Serum immunoreactive gastrin activity in horses: basal and postprandial values. 345 68


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