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)

The action of acute and chronic administration of ethanol on pancreatic exocrine secretion in humans and several animal species is reviewed. If the data concerning the secretory action of ethanol on the pancreas are to the property assessed, several experimental variables have to be considered. Acute intravenous administration of ethanol inhibits basal and hormonally stimulated pancreatic secretion of bicarbonate and protein in nonalcoholic humans and most species of animals tested. Oral or intraduodenal ethanol causes moderate stimulation of pancreatic bicarbonate and enzyme secretion. Since anticholinergic agents and truncal vagotomy diminish the ethanol-induced inhibition of pancreatic secretion in the intact animal, it is possible that the action of ethanol on the pancreas is at least partly mediated by inhibitory cholinergic mechanisms. The action of ethanol on the pancreas may also be mediated by release of gastrointestinal hormones. Intravenous and oral administration of ethanol releases gastrin in dogs but not in humans. Pancreatic polypeptide is unlikely to be the hormonal mediator of the ethanol-induced inhibition of exocrine pancreatic secretion in humans and dogs, since ethanol does not release pancreatic polypeptide. The main secretory changes induced by chronic alcoholism in humans and dogs are increased basal secretion of pancreatic enzymes and decreased basal bicarbonate output, and these secretory changes may favour the occurrence of protein precipitates which are believed to be the first lesion of chronic pancreatitis in man. A decrease in the concentration of "pancreatic stone protein" in pancreatic juice may favour the development of protein precipitates in chronic alcoholic patients.
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PMID:[The pancreas and alcohol]. 390 Dec 51

The basal concentrations of sulfated and non-sulfated gastrins in serum were measured radioimmunochemically in healthy subjects and in normo- and hyper-gastrinemic diseases. The degree of sulfation in patients with duodenal and gastric ulcer, chronic pancreatitis, gallstone disease, and chronic renal failure were similar to that of healthy controls, in whom 37.7 +/- 1.9% (mean +/- SEM) of serum gastrins were sulfated. In eight patients with the Zollinger-Ellison syndrome 57 +/- 5.4% of the gastrins were sulfated (p less than 0.005, compared with controls). In patients with pernicious anemia (no. = 20) only 24.4 +/- 2.0% of the gastrins were sulfated (p less than 0.005, compared with controls). An inverse correlation (r = -0.63, p less than 0.01) was found between the degree of sulfation and the total gastrin concentration in pernicious anemia but not in gastrinoma patients. The results indicate that diseases with increased synthesis of gastrin are accompanied by an abnormal degree of sulfation.
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PMID:Variations in the sulfation of circulating gastrins in gastrointestinal diseases. 666 33

Pancreatic and gut hormones have been measured in 39 patients with chronic pancreatitis, 16 of whom had severe pancreatic insufficiency. Patients with pancreatic insufficiency had significantly diminished fasting levels and postprandial rises of pancreatic polypeptide which were less than 20% of normal. Patients with chronic pancreatitis, with or without exocrine insufficiency, had two- to threefold higher plasma levels of motilin and enteroglucagon than controls. Plasma levels of insulin, pancreatic glucagon, gastric inhibitory polypeptide and gastrin were similar to normal in these patients. The pattern of response of these hormones to a test breakfast differs markedly from those seen in other gut disease states and may reflect pathophysiological mechanisms.
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PMID:Pancreatic and gastrointestinal hormones in chronic pancreatitis. 675 14

Controversial data have been reported on gastric acid secretion in patients with chronic pancreatitis. Moreover, studies on gastroduodenal morphological changes in patients with this disease and with other alcohol-related conditions have given different results. Basal and penta-gastrin-stimulated gastric secretion, histological changes of gastric and duodenal mucosa, and basal and meal-stimulated gastrin were measured in 21 patients with chronic alcoholic pancreatitis and in the following pair-matched groups: 21 chronic alcoholics and 21 control subjects (nonulcer dyspepsia), and in 19 patients with proven liver cirrhosis of alcoholic origin. No patient suffered from peptic ulcers. Moreover, gastric secretion was also measured in 51 patients with proven duodenal ulcers and in 34 healthy subjects. Basal acid output in patients with chronic pancreatitis was significantly higher (p less than 0.05) than in the other groups, except for the patients with duodenal ulcers. Peak acid output values in patient with chronic pancreatitis were similar to those measured in patients with duodenal ulcer, and they were higher than in the healthy subject group and in patients with liver cirrhosis, but statistical significance was not attained for patients with nonulcer dyspepsia. An increased frequency of duodenitis was found in patients with chronic pancreatitis, whereas an increased frequency of gastric metaplasia in the duodenal bulb was observed in all the patients with alcohol-related conditions considered. No relevant differences among the considered groups were found relating to gastric histological changes. Basal and meal-stimulated gastrin were similar in all the studied groups. This study suggests that in patients with chronic pancreatitis there is increased gastric secretion and probably an increased capacity for secretion of acid. Moreover, in patients with chronic pancreatitis, duodenitis seems to be frequent, but it probably is not directly related to chronic alcohol consumption.
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PMID:Gastric secretion, gastroduodenal histological changes, and serum gastrin in chronic alcoholic pancreatitis. 707 77

Pancreatic secretion and pancreatic enzyme contents were studied in rats given orally methadone for six months (10 to 50 mg . kg-1 . day-1 in drinking water). The main results were as follows: 1. In conditions of acute pancreatic fistula under urethane anesthesia: (a) basal concentration of total protein increased in the juice (+23 p. 100, p less than 0,05). The increase in trypsinogen appeared larger than that of other enzymes; (b) under conditions of maximal stimulation by 2 deoxy-glucose (2 DG), all secretory parameters were increased (protein x 2.7, p less than 0.05; sodium x 1.7, p less than 0.02; bicarbonate x 1.8, p less than 0.05); (c) under conditions of maximal electrical stimulation of the vagus, pancreatic response was unsignificantly increased; (d) dose-response curves to secretin and CCK-PZ were unsignificantly changed. 2. Pancreatic weight was not changed. In the pancreatic tissue: (a) total protein decreased (-10 p. 100, p less than 0.01) as well as amylase (-30 p. 100 p less than 0.001), lipase (-19 p. 100, p less than 0.01) and trypsinogen (-9 p. 100, NS); (b) concentrations of DNA and RNA were unsignificantly increased; (c) histological structure was normal in optical microscopy. 3. Antral gastrin cell numbers were not changed. 4. In conclusion, a decrease in pancreatic enzymatic contents, associated with an increase of total protein in basal secretion and after maximal stimulation by 2DG are consistent with the hypothesis of an increase in synthesis and a decrease in turnover time of exportable proteins in the pancreatic tissue of methadone treated rats. No chronic pancreatitis was observed in these conditions. Endogenous gastrin was probably not involved in pancreatic changes observed.
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PMID:[Responses of exocrine pancreas to a six month oral treatment by methadone in rats (author's transl)]. 720 31

Of 114 patients with chronic pancreatitis, 19 (16.7%) has gastric or duodenal ulcers. Patients with moderate pancreatic exocrine dysfunction tended to show high acid output and low serum gastrin levels, while those with severe dysfunction had slightly lower acid output and higher serum gastrin levels. The higher the degree of pancreatic fibrosis, the higher tended to be the acid output and serum gastrin levels. Not all patients with ulcers developed hypergastrinemia. The mechanism of acid hypersecretion and ulcer formation in patients with chronic pancreatitis cannot be explained solely by pancreatic deterioration, fibrosis or gastrin release; a decrease in the production and release of gastric inhibitory hormone should be taken into consideration.
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PMID:Gastric acid secretion and serum gastrin levels in chronic pancreatitis. 722 67

The effect of food on gastrin secretion was examined in 62 patients with various diseases of the alimentary system (chronic gastritis, chronic cholecystitis, chronic pancreatitis) and in 16 normal subjects. In normal persons, the initial gastrin level in the blood was 55.4 +/- 5.2 ng/ml, while in patients with chronic gastritis and chronic pancreatitis, it was increased and in chronic cholecystitis diminished. Development of atrophic gastritis led to the delay of gastrin secretion irrespective of the food irritant type. The patients suffering from chronic cholecystitis manifested a paradoxical reaction (a decrease in gastrin concentration) to fat intake. The patients with chronic pancreatitis showed a decrease in the gastrin content in response to glucose and absence of substantial changes in response to fat.
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PMID:[Gastrin secretion during food stimulation in digestive system diseases]. 729

Fasting serum gastrin and gastrin response to a protein meal were measured in a group of patients with chronic pancreatitis and in controls. No significant differences were found between the two groups of subjects. In patients with chronic pancreatitis no relation was found between gastrin release and the severity of pancreatic exocrine insufficiency.
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PMID:Serum gastrin in chronic pancreatitis. 737 71

Plasma gastrin levels were measured by radioimmunoassay before and after a test meal associated with 40 ml ethanol in 21 patients presenting with chronic calcifying pancreatitis, in 10 apparently normal subjects drinking since at least 5 years 100 g alcohol a day, in 14 subjects presenting hepatic alcoholic cirrhosis and in 18 apparently normal non alcoholic controls. Post-stimulation gastrin concentration were higher in chronic pancreatitis patients or in normal alcoholics (peak post-stimulation value: 74 +/- 41 and 74 +/- 43 pg/ml respectively) than in cirrhotics or non alcoholic controls (45 +/- 26 and 41 +/- 15 pg/ml respectively) (m +/- SD).
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PMID:Increased gastrin release in chronic calcifying pancreatitis and in chronic alcoholism. 740 35

Given an indication for surgery in patients with chronic pancreatitis, such as distal common bile duct obstruction, duodenal stenosis, or dilated pancreatic duct with stones and congestion, the surgeon must decide the type of operation to perform. A duodenopancreatectomy, the Whipple procedure, is widely considered to be the gold standard. It is highly effective in relieving pain and eliminating the structural abnormalities noted above. Duodenum-preserving resection of the head of the pancreas (DPRHP) seems to be an attractive alternative to pancreaticoduodenectomy (PD) in the treatment of chronic pancreatitis. In a clinical prospective randomized trial the efficiency of both operative methods was investigated. Between 7/1987 and 12/1993 43 patients were randomly assigned to undergo either a Whipple procedure (n = 21) or DPRHP (n = 22). Data on postoperative course, mortality, and postoperative morbidity were compiled. As concerns long-term results, postoperative hormonal status (insulin, neurotensin, cholecystokinin, gastrin) was checked, basal and stimulated with a standardized meal, using standard hormonal assay kits. All patients with PD survived, whereas one with DPRHP died from peritonitis. Patients with DPRHP had a significant more rapid convalescence (16.5 vs. 21.7 days). The range for postoperative follow-up is from 36 months to 5.5 years. In the DPRHP group 18 patients are in good condition. Two had diabetes and one developed carcinoma. In the PD group one died from hepatic coma, 14 are in good condition and 6 developed diabetes. All gained body weight with an average of 6.4 vs. 4.9 kg, DPRHP vs. PD. A difference between DPRHP and PD was obvious for the postoperative hormonal status. Results are satisfactory in both groups. For patients with DPRHP however, we see a quicker convalescence and a significant benefit as concerns postoperative hormonal status.
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PMID:[Pancreatic function and quality of life after resection of the head of the pancreas in chronic pancreatitis. A prospective, randomized comparative study after duodenum preserving resection of the head of the pancreas versus Whipple's operation]. 763 46


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