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Biomedical subjects

F Stadil

Publications and source records attributed to F Stadil.

At least 91 records · Page 5Linked to original sources
PubMed1976

Pancreatic-polypeptide response to food in duodenal-ulcer patients before and after vagotomy.

In 21 normal fasting subjects basal serum-pancreatic-polypeptide (H.P.P.), as measured by a specific radioimmunoassay, was 43 +/- 4 pmol/l (mean +/- S.E.M). This basal concentration was of the same magnitude as that of other gastrointestinal peptide hormones. In normal subjects the H.P.P. response to food was bisphasic. A rapid eightfold increase, reaching a maximum 20--30 min after beginning of the meal, was followed by a secondary, prolonged increase. H.P.P. did not return to basal concentration within five hours. 14 duodenal-ulcer (D.U.) patients were studied before and after truncal vagotomy. Before operation the D.U. patients had higher basal H.P.P. concentrations than the normal group (110 +/- 40 pmol/l) whereas their H.P.P. response pattern to food was similar to that of the normal subjects. After vagotomy the primary rapid increase in H.P.P. concentration was eliminated and the secondary, prolonged response was significantly reduced (P less than 0-005). The results indicate that H.P.P. is a digestive hormone under vagal control.

Adult↗
PubMed1976

The heterogeneity of gastrin, with reference to conversion of gastrin-17.

High-resolution gel chromatography monitored by a sensitive radioimmunoassay for gastrin has disclosed that gastrin circulates in twenty different components. Since the assay is specific for the biological active sequence of gastrin (-Trp-Met-Asp-PheNH2), we conclude that all the twenty circulating molecular forms of gastrin encountered in this study may participate in the regulation of gastric acid secretion. There are two dominating forms of gastrin in serum: gastrin-34-like components and gastrin-17-like components. The former constituted 60% and the latter constitutes approximately 30% of the immunoreactive gastrins. We suggest that extragastrointestinal conversion of gastrin-17, released from tissue, is an important source of gastric-34-like components. Such conversion has been observed in intact man and pig. Studies with the isolated perfused porcine liver indicate that the liver is important in the metabolism of gastrin-17, and that conversion may be a hepatic function.

Animals↗
PubMed1976

Serum-gastrin in cirrhosis.

Fifty patients with cirrhosis of the liver had gastrin concentrations in serum above normal when measured in the fasting state. Hypergastrinaemia predominated in non-alcoholic cirrhosis. In both groups of patients, serum gastrin levels were higher in patients with inactive cirrhosis than when cirrhosis was slightly active.

Aged↗
PubMed1976

Disappearance of gastrin heptadecapeptide in the isolated perfused pig liver.

To elucidate the role of the liver in gastrin metabolism three liver perfusions and two control experiments were performed; 2,5, 5 and 250 microgram of porcine nonsulphated gastrin-17 were injected into a perfusate of pig blood circulated through an isolated perfused liver. A significant decrease of gastrin concentration was observed during liver perfusions, concentration being halved in 35 minutes with all doses. It is suggested that this decrease is due to hepatic degradation and that the liver may play an important role in metabolism of gastrin-17.

Animals↗
PubMed1976

Insulin secretion in the Zollinger-Ellison syndrome.

The insulin response to oral glucose ingestion was measured in six patients with the Zollinger-Ellison (ZE) syndrome, five patients with partial gastrectomy (antrectomy for duodenal ulcer) and six matched normal subjects. The blood glucose curves were similar in ZE-patients and gastrectomized controls and significantly above the glucose concentrations in normal controls. The insulin response was three-doubled in ZE-patients, whereas gastrectomized controls only doubled their response in comparison with the normal subjects. Treatment of a hepatic gastrinoma by streptozotocin infusion into the hepatic artery in a patient with diabetes mellitus and hyperinsulinism almost normalized his glucose tolerance and insulin secretion. The results demonstrate that the ZE-syndrome is associated with increased insulin release. We suggest that the hyperinsulinism partly is a consequence of previous gastric surgery and partly due to the insulinogenic effect of gastrin.

Adult↗
PubMed1976

Gastrin content and gastrin release. Studies on the antral content of gastrin and its release to serum during stimulation by food.

To examine the release of gastrin by food from antral mucosa eight patients were stimulated for 30 minutes by instillation of bovril during gastroscopy. Bovril caused a steady increase in serum concentrations of gastrin and an acute fall in the antral content of gastrin to 42+/-8.4 per cent after 10 minutes. After 10 minutes the antral content increased again towards the basal values. No change in gastrin components could be detected; component III (gastrin-17) constituted more than 95 per cent of the antral gastrins throughout the 30-minute period. The serum gastrin response to a steak meal was higher in 22 duodenal ulcer patients than in nine young normal subjects and it was higher postoperatively in eight patients studied before and after truncal vagotomy. In the duodenal ulcer patients whith the highest antral content of gastrin, the serum response to food was higher only during the early phase of the feeding response. It is concluded that the gastrin content of the antral mucosa represents an acute releasable pool of gastrin-17, which contributes only to the first 10-15 minutes of the feeding response. It does not reflect the total amount of gastrin released into the circulation during feeding.

Duodenal Ulcer↗
PubMed1976

The vagus and gastrin components in peripheral blood.

To study the role played by vagal activity for the gastrins in peripheral blood, the mean pattern during feeding was studied in 16 duodenal ulcer patients before and after selective (n=8), or truncal vagotomy (n=8). Two normal subjects were studied with and without atropine during hypoglycaemic activation of the vagus. Gastrins were fractionated by gel chromatography. Serum gastrin was almost exclusively made up of gastrin component II (gastrin 34-like) and III (gastrin 17-like). Both components rose after feeding but the major increase was incomponent III. Total gastrin concentrations rose after vagotomy but no qualitative changes were seen. During hypoglycaemia a marked increase in gastrin component III and a lesser increase in component II was found. This pattern was not changed by atropine. It is concluded that the vagus plays little or no role for a selective release of the various gastrins. Furthermore there is no indication that the higher serum levels after vagotomy consist of gastrins of a lesser biological activity.

Atropine↗
PubMed1976

On the beta-adrenergic contribution to the gastric acid and gastrin responses to hypoglycaemia in man.

To study the beta-adrenergic contribution to the hypoglycaemic stimulation of gastric acid and gastrin release the effect of an equal and extensive beta-adrenergic blockade with three drugs was studied. Propranolol was investigated in 12, pindolol in 22, and practolol in 11 patients. Fasting concentration of gastrin serum and spontaneous acid secretion were not reduced by the drugs. Propranolol eliminated the gastrin response to hypoglycaemia, pindolol reduced it, and practolol caused no alteration. The hypoglycaemic acid response was reduced by all three drugs, propranolol reduced the response to one-half and was the strongest inhibitor, practolol the weakest. It is concluded that beta-adrenergic receptors may be of major importance for the hypoglycaemic stimulation of the stomach, but the receptors respond differently from the receptors in the heart.

Adult↗
PubMed1976

Effect of epinephrine and norepinephrine on gastrin release and gastric secretion of acid in man.

To study the physiological importance of epinephrine and norpinephrine for gastrin release and gastric secretion of acid the effect of intravenous infusions was investigated. Two doses were used (5 and 50 mg per kg per minute in one hour), the low dose of epinephrine and both doses of epinephrine (n=20) stimulated gastrin release and acid secretion, whereas the high dose (n=8) stimulated the gastrin release strongly, but did not change acid secretion. Norepinephrine in the low dose (n=11) caused a very small increase in gastrin release and no change in acid secretion, whereas the high dose (n=11) inhibited acid secretion without any change in gastrin concentration. No postoperative change was observed in the release of gastrin by both doses of epinephrine after truncal vagotomy in sex and seven patients with duodenal ulcer. It is concluded that epinephrine and norepinephrine both may be of importance in the physiological regulation of gastrin release and gastric acid secretion.

Dose-Response Relationship, Drug↗
PubMed1976

Gastrin response to food after three types of intestinal shunt operations for obesity.

In a retrospective study the basal and food-stimulated serum concentrations of gastrin and gastric secretion of acid were studied in 28 patients following three types of intestinal shunt operation for obesity. In each type 48 cm of functioning small intestine was preserved, but the ratio between functioning jejunum and ileum was different. The basal and stimulated concentrations of gastrin in serum were significantly higher in patients with the shortest jejunum in function. There was no difference in the gastric acid output. The study suggests that gastrin participates in evoking the gastric hypersecretion of acid which follows massive bowel resection or bypass. Deprivation of a hormonal inhibitory substance from the upper jejunum may be responsible for the increased serum gastrin concentration.

Adult↗
PubMed1976

Effect of streptozocin on gastrin release.

As streptozocin has a toxic effect on gastrin producing cells in some patients with gastrinomas, the action of the drug upon normal gastrin release was evaluated in patients with carcinoid tumours (n=6) and malignant insulinomas (n=2). No acute effects were recorded in 22 instances where gastrin levels were followed during the first 24 hours after infusion of streptozocin. When gastrin levels were compared throughout a course of repeated infusions during months a significant increase was noted. Concentrations were doubled after 6 g streptozocin given during a four months period, and tripled after 10 g in nine months period. One patients developed bleeding duodenal ulcer after a total dose of 6 g. It is concluded that streptozocin does not damage normal G cells, but by some action seems to stimulate gastrin relase. Peptic ulceration may be an important side effect during a long term treatment.

Adenoma, Islet Cell↗
PubMed1976

Gastrins in tissue. Concentration and component pattern in gastric, duodenal, and jejunal mucosa of normal human subjects and patients with duodenal ulcer.

The total concentration of gastrin and distribution of gastrin components were examined in mucosal biopsies from corpus, antrum, duodenum, and jejunum from normal subjects and patients with duodenal ulcer. The concentration was highest in the antrum, being 12.1+/-1.9 nmol per g of mucosa (mean +/-SEM) for normal subjects, and 9.0 +/-1.6 nmol per g of mucosa for duodenal ulcer patients (P eaual to 0.03). A steep gradient was found distally: in the proximal duodenum the concentration was 0.1; in the distal duodenum, 0.02 to 0.01; and in the proximal jejunum, less than 0.01 of the antral concentration. In corpus of the stomach, the concentrations were similar to those found in the jejunum. Gel filtrations showed that most gastrin immunoreactivity was eluted in positions corresponding to serum component II (gastrin-34-like) and III (gastrin-17-like), but immunoreactivity corresponding to all the components present in serum was found. No interference from cholecystokinin was observed in duodenal biopsies. In corpus, antrum, and jejunum component III was the predominant form, whereas component II made up half of immunoreactive gastrin in the duodenum. No major differences were observed between normal subjects and duodenal ulcer patients. There was no simple relationship between acid secretion and mucosal gastrin concentration, but ulcer patients with the highest acid secretion had the lowest antral content and the highest duodenal content.

Animals↗
PubMed1976

Effect of intrajejunal fat on meal-stimulated acid and gastrin secretion in man.

The effect of intrajejunal fat infusion on meal-stimulated gastric acid and gastrin secretion was studied in 8 healthy volunteers. Intrajejunal fat significantly reduced the acid response to a meal, measured by intragastric titration, as compared to intrajejunal infusion of saline. While serum gastrin concentrations rose from fasting levels to a constant plateau after the meal when saline was infused, fat infusion resulted in a transitory decrease in serum gastrin concentration followed by a significant increase. It is concluded that inhibition of gastrin release only plays a minor role, if any, in the observed fat-induced jejuanl inhibition of meal-stimulated acid secretion.

Adult↗
PubMed1975

The glucose-induced gastrointestinal stimulation of insulin secretion in man: relation to age and to gastrin release.

An oral 50 g glucose tolerance test and a simple intravenous glucose infusion test were performed in 20 young (20 - 32 years), 20 middle-aged (42 -55 years), and 20 old (65 - 81 years) normal subjects. Blood glucose, serum insulin, and serum gastrin concentrations were measured during all tests. The intravenous glucose infusion duplicated the oral blood glucose curve in young, middle-aged, and half of the old subjects. In the remaining old subjects the intravenous blood glucose curve was below the oral blood glucose curve. Glucose and insulin concentrations were of similar magnitude in all groups, but maximum concentrations were reached later in the old subjects. Glucose per os induced a rapid rise in serum gastrin concentrations of the order of 10 pmol/1 and a subsequent decrease of about 20 pmol/1 in all groups. The intravenous glucose infusion induced no significant changes in serum gastrin concentrations. The non-glycaemic (i.e. enteral) stimulation of insulin secretion was expressed as the difference between the integrated incremental areas of the oral and intravenous insulin curves in subjects with identical glucose curves during the two tests. This stimulation was of similar magnitude in all age groups, and it was not correlated to variations in gastrin concentrations. However, in the young subjects the enteral stimulation was greater during the first 30 minutes and smaller during the two last hours when compared to the old subjects. The results suggest that: 1. A simple intravenous glucose infusion test can be used to copy the oral blood glucose curve. 2. The size of the enteral stimulation of insulin secretion during the whole test is independetn of age. 3. The action of the glucose-induced enteral stimulation is delayed with age, and closely linked to the dynamics of the glycaemic stimulus. 4. The glucose-induced gastrin release is probably too small to affect insulin secretion significantly.

Adult↗
PubMed1975

The enteral insulin-stimulation after Whipple's operation.

The insulin response to oral and intravenous glucose was measured in ten patients after resection of antrum, duodenum, proximal jejunum, and the head of pancreas (Whipple's operation). Compared to matched normal subjects the operation reduced neither the total nor the gut hormone induced part of the insulin response to oral glucose. The results suggest, that hormones from the first part of the intestinal tract are not necessary as incretins.

Blood Glucose↗
PubMed1975

Activation of histidine decarboxylase by H2-receptor blockade: mechanism of action.

1 Treatment with histamine H2-receptor antagonists, which inhibit basal acid secretion was found to activate rat stomach histidine decarboxylase. At the same time the serum gastrin concentration was greatly increased. 2 In antrectomized rats neither the enzyme activity nor the serum gastrin concentration was affected by the treatment. 3 In analogy with previous observations on other inhibitors of acid secretion we suggest that the H2-receptor antagonists stimulate gastrin release through their effect on acid secretion and that the raised serum gastrin level is responsible for the enzyme activation.

Animals↗