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Biomedical subjects

J B Jansen

Publications and source records attributed to J B Jansen.

At least 289 records · Page 16Linked to original sources
PubMed1984

Plasma cholecystokinin concentrations in patients with pancreatic insufficiency measured by sequence-specific radioimmunoassays.

It has been claimed that plasma cholecystokinin (CCK) concentrations are raised in patients with pancreatic insufficiency. We have measured plasma CCK concentrations in 32 patients with pancreatic insufficiency (22 alcoholic pancreatitis and 10 cystic fibrosis) and in 30 normal subjects by radioimmunoassays using antibodies with different specificities. Antibody 1703 binds to COOH-terminal forms of CCK containing at least 14 amino acid residues and does not cross-react with gastrins. Antibody T204 binds to all CCK-peptides containing the sulfated tyrosyl region and shows low cross-reactivity with sulfated gastrins but no binding to nonsulfated gastrins. Antibody 5135 binds to all COOH-terminal CCK-peptides and shows full cross-reactivity with gastrins. In patients with pancreatic insufficiency, plasma CCK concentrations (1.2 +/- 0.1 pmol/liter, antibody 1703; 2.0 +/- 0.2 pmol/liter, antibody T204; 12.5 +/- 1.4 pmol/liter, antibody 5135) were not significantly different from those in normal subjects (1.1 +/- 0.1 pmol/liter, antibody 1703; 2.2 +/- 0.3 pmol/liter, antibody T204; 10.5 +/- 0.9 pmol/liter, antibody 5135). Furthermore, plasma CCK concentrations in patients with pancreatic insufficiency due to alcoholic pancreatitis (1.2 +/- 0.1 pmol/liter, antibody 1703; 1.9 +/- 0.2 pmol/liter, antibody T204; 14.0 +/- 1.9 pmol/liter, antibody 5135) were not significantly different from those in patients with cystic fibrosis (1.2 +/- 0.2 pmol/liter, antibody 1703; 2.4 +/- 0.4 pmol/liter, antibody T204, 9.1 +/- 1.0 pmol/liter, antibody 5135). Cross-reactivity with gastrin accounted for almost all CCK-like-immunoreactivity measured with antibody 5135.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Effect of equimolar amounts of long-chain triglycerides and medium-chain triglycerides on plasma cholecystokinin and gallbladder contraction.

The present study was undertaken to compare the effects of equimolar amounts of long-chain triglycerides (LCT) and medium-chain triglycerides (MCT) on plasma cholecystokinin (CCK) concentrations and gallbladder contraction in man. On separate mornings and in random order six healthy volunteers ingested either 60 mmol LCT or 60 mmol MCT. Plasma CCK concentrations were measured by a sensitive and specific radioimmunoassay and gallbladder contraction by ultrasonography. Ingestion of LCT induced significant increases in plasma CCK from 2.8 +/- 0.5 to 6.5 +/- 0.7 pmol/l (p less than 0.005) and decreases in gallbladder volume from 33.4 +/- 5.9 to 13.2 +/- 4.2 cm3 (p less than 0.005). On the other hand, no significant changes in plasma CCK and gallbladder volume were found after MCT. Ingestion of MCT was followed by abdominal cramps and diarrhea, while LCT were without side effects. It is concluded that, in contrast to LCT, MCT do not induce CCK release and gallbladder contraction.

Adult↗
PubMed1984

Plasma cholecystokinin response to oral fat in patients with Billroth I and Billroth II gastrectomy.

The present study was undertaken to determine whether bypassing the duodenum in patients with Billroth II gastrectomy affects plasma cholecystokinin (CCK) release in response to ingestion of fat. Plasma CCK concentrations were measured by radioimmunoassay using two antibodies; antibody 1703 binds to all carboxyl-terminal CCK-peptides containing at least 14 amino acid residues, while antibody T204 is specific for the sulphated tyrosine region of CCK. There were no significant differences among fasting plasma CCK concentrations in seven patients with Billroth II gastrectomy (1.3 +/- 0.4 fmol/ml, antibody 1703; 2.6 +/- 0.4 fmol/ml, antibody T204), six patients with Billroth I gastrectomy (0.6 +/- 0.3 fmol/ml, antibody 1703; 2.9 +/- 0.5 fmol/ml, antibody T204), and nine normal subjects (0.7 +/- 0.1 fmol/ml, antibody 1703; 1.9 +/- 0.3 fmol/ml, antibody T204). Ingestion of 250 ml 20% Intralipid induced similar increases in plasma CCK in patients with Billroth II gastrectomy (11.2 +/- 2.0 fmol/ml, antibody 1703; 10.1 +/- 2.4 fmol/ml, antibody T204) as in patients with Billroth I gastrectomy (11.8 +/- 2.0 fmol/ml, antibody 1703; 8.4 +/- 1.1 fmol/ml, antibody T204). However, the increments in plasma CCK in patients with gastrectomy (11.5 +/- 1.4 fmol/ml, antibody 1703; 9.3 +/- 1.4 fmol/ml, antibody T204) were significantly (p less than 0.01) greater than those in normal subjects (4.7 +/- 0.8 fmol/ml, antibody 1703; 4.1 +/- 0.7 fmol/ml). Similarly, the integrated plasma CCK secretion in patients with Billroth II gastrectomy (510 +/- 58 fmol/ml X 120 min, antibody 1703; 458 +/- 69 fmol/ml X 120 min, antibody T204) and in patients with Billroth I gastrectomy (457 +/- 143 fmol/ml X 120 min, antibody 1703; 365 +/- 61 fmol/ml X 120 min, antibody T204) were significantly (p less than 0.05) greater than in normal subjects (230 +/- 49 fmol/ml X 120 min, antibody 1703; 162 +/- 24 fmol/ml X 120 min, antibody T204). It is concluded that the plasma CCK response to oral fat is significantly greater in patients with partial gastrectomy than in normal subjects, and that patients with Billroth I and Billroth II gastrectomy have similar increases in plasma CCK after ingestion of fat.

Administration, Oral↗
PubMed1984

Plasma cholecystokinin response to a liquid fat meal in vagotomized patients.

Since previous studies have suggested that in patients with truncal vagotomy (TV) the plasma cholecystokinin (CCK) secretion in response to nutrients is impaired, we have measured the plasma CCK response to a liquid fat meal (250 ml 20% Intralipid) in six patients with TV and pyloroplasty. We have compared the results with those obtained in eight normal subjects, six patients with duodenal ulcer, and eight patients with highly selective vagotomy (HSV). Plasma CCK concentrations were measured by a sensitive and specific radioimmunoassay employing antibody T204 directed against the sulphated tyrosine region of CCK. Basal plasma CCK concentrations were not significantly different among the four groups studied (2.1 +/- 0.4 pmol/l in normal subjects, 2.8 +/- 0.5 pmol/l in duodenal ulcer patients, 3.1 +/- 0.5 pmol/l in patients with TV, and 2.7 +/- 0.5 pmol/l in patients with HSV). The increments in plasma CCK after ingestion of the fat meal in patients with TV (15.7 +/- 3.1 pmol/l) and HSV (14.9 +/- 1.6 pmol/l) were significantly higher (p less than 0.01) than those in normal subjects (4.8 +/- 0.9 pmol/l) and in patients with duodenal ulcer (5.5 +/- 0.6 pmol/l). Similarly, the integrated plasma CCK secretions in patients with TV (554 +/- 139 pmol/l, 120 min) and in patients with HSV (876 +/- 132 pmol/l, 120 min) were significantly increased (p less than 0.05) compared to those in normal subjects (187 +/- 29 pmol/l, 120 min) and in patients with duodenal ulcer (264 +/- 35 pmol/l, 120 min). It is concluded that patients with TV and HSV show an increased plasma CCK secretion in response to a liquid test meal.

Adult↗
PubMed1984

Cholinergic regulation of pancreatic polypeptide secretion in chronic renal failure.

Secretion of pancreatic polypeptide (PP) is regulated mainly by cholinergic mechanisms and we have studied this in patients with chronic renal failure (CRF). Basal serum PP concentrations in 25 patients with CRF (401 +/- 80; 116-2100 pmol/l; mean +/- SEM and range) were significantly higher than in 65 normal subjects (33 +/- 2; 21-120 pmol/l, P less than 0.001). Ingestion of a standard test meal induced significantly larger increases in serum PP in 11 patients with CRF (304 +/- 45; 155-640 pmol/l) than in 11 normal subjects (140 +/- 33; 51-440 pmol/l, P less than 0.005). Insulin-hypoglycaemia (0.1 U/kg i.v.) provoked similar increases in serum PP in five patients with CRF (404 +/- 79; 170-665 pmol/l) as in five normal subjects (449 +/- 92; 180-706 pmol/l). Administration of atropine (1 mg i.v.) did not normalize the elevated basal serum PP concentrations in five patients with CRF. On the other hand, administration of the same dose of atropine 60 min after ingestion of food decreased postprandial serum PP levels to basal values within one hour both in five patients with CRF and in six normal subjects. Sephadex G-50 column chromatography of basal, postprandial and post-atropine sera from three patients with CRF revealed at least three different molecular forms. The PP peak coeluting with the 4200 molecular weight human PP standard comprised more than half of total PP immunoreactivity and was the only peak to be influenced by feeding or atropine. We conclude that in patients with CRF, PP secretion stimulated by cholinergic mechanisms is normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Effect of atropine on the plasma cholecystokinin response to intraduodenal fat in man.

The present study was undertaken to determine whether atropine inhibits the plasma cholecystokinin (CCK) response to intraduodenal fat. Plasma CCK concentrations were measured by radioimmunoassay using two sequence-specific antibodies. Antibody 1703 bound to all COOH-terminal CCK peptides containing at least 14 amino acid residues, while antibody T204 was specific for the sulphated tyrosine region of CCK. Intraduodenal instillation of 60 ml corn oil in 6 normal subjects induced significant increases in plasma CCK. Intravenous administration of atropine (0.015 mg/kg as bolus followed by 0.005 mg/kg X h over 3 h) resulted in significant inhibition of plasma CCK concentrations at 10, 20 and 30 min (antibody 1703) and at 20 and 30 min (antibody T204 ) after instillation of fat. However, the peak increments in plasma CCK during atropine (8.6 +/- 1.9 pmol/l, antibody 1703; 5.4 +/- 1.1 pmol/l, antibody T204 ) were not different from those found without atropine (6.3 +/- 0.8 pmol/l, antibody 1703; 3.9 +/- 0.9 pmol/l, antibody T204 ). Similarly, the integrated plasma CCK secretion after intraduodenal fat was not significantly different when measured during atropine (461 +/- 119 pmol/l X 3 h, antibody 1703; 269 +/- 97 pmol/l X 3 h, antibody T204 ) and without atropine (428 +/- 62 pmol/l X 3 h, antibody 1703; 188 +/- 66 pmol/l X 3 h). It is concluded that administration of atropine delays but does not inhibit the CCK response to intraduodenal corn oil in man.

Adult↗
PubMed1984

The glucagonoma syndrome: stimulus-induced plasma responses of circulating glucagon components IRG9000 and IRG3500.

Plasma responses of the major immunoreactive glucagon (IRG) components have been investigated in a case of glucagonoma syndrome. Fasting plasma IRG was 4155 pg/ml. Gel chromatography of plasma revealed that 66% of immunoreactivity was present as IRG9000, while IRG3500 accounted for an additional 26%. The appearance in peripheral plasma of these two glucagon fractions was examined after administration of a number of compounds. IRG levels were clearly elevated after arginine and tolbutamide. Both calcium and calcitonin induced a biphasic rise of IRG, the increase being slower after calcium administration. Somatostatin suppressed plasma IRG levels. All tests induced changes in both IRG3500 and IRG9000. In general, relative changes were more pronounced in IRG3500 than in IRG9000, while absolute changes were greater in IRG9000. The shape of the response curves of IRG3500 and IRG9000 was quite similar after arginine, calcium and somatostatin. After tolbutamide the IRG9000 response was delayed as compared to the IRG3500 component. During the latter part of the calcitonin infusion, IRG9000 remained elevated while IRG3500 was back at its starting level.

Adenoma, Islet Cell↗
PubMed1984

Effect of bombesin on plasma cholecystokinin in normal persons and gastrectomized patients measured by sequence-specific radioimmunoassays.

Since bombesin is known to stimulate pancreatic enzyme secretion and gallbladder contraction, we have measured plasma cholecystokinin (CCK) concentrations during bombesin infusion using sequence-specific radioimmunoassays. Antibody 1703 binds to COOH terminal CCK peptides containing at least 14 amino acid residues, while antibody T204 is specific for the sulfated tyrosine region of CCK. In nine normal persons infusion of increasing doses of bombesin (2.4, 6, 18, and 60 pmol/kg X 20 min) induced dose-related integrated plasma CCK responses (58.5 +/- 9.7, 70.5 +/- 12.2, 79.5 +/- 11.1, and 101.4 +/- 15.4 pmol/L X 20 min [antibody 1703] and 50.4 +/- 11.9, 62.0 +/- 13.4, 74.7 +/- 9.2, and 116.1 +/- 11.3 pmol/L X 20 min [antibody T204]). Infusion of 60 pmol bombesin/kg X 20 min in eight patients with partial gastrectomy resulted in similar increases in plasma CCK (8.1 +/- 1.8 pmol/L, antibody 1703; 9.5 +/- 2.0 pmol/L, antibody T204) as in eight normal control subjects (6.5 +/- 0.9 pmol/L, antibody 1703; 8.8 +/- 1.0 pmol/L, antibody T204). During infusion of bombesin, plasma gastrin levels increased from 16.7 +/- 1.4 to 49.6 +/- 8.1 pmol/L (P less than 0.005) in the normal persons, while there was no significant change in plasma gastrin levels in gastrectomized patients. Bombesin did not significantly influence gastric acid secretion in three patients with partial gastrectomy studied. It is concluded that infusion of bombesin releases CCK in humans by a gastrin-independent mechanism.

Adult↗
PubMed1983

Molecular forms of cholecystokinin in human plasma during infusion of bombesin.

Bombesin is a tetradecapeptide with stimulatory actions on several gastrointestinal functions. Infusion of bombesin (60 pmol/kg. 20 min) into 7 normal subjects induced significant increases in plasma cholecystokinin (CCK) as measured with 2 sequence-specific radioimmunoassays. Employing antibody 1703, specific for carboxyl-terminal CCK-peptides containing at least 14 amino acid residues, plasma CCK concentrations rose from 0.8 +/- 0.2 pmol/l to 9.9 +/- 1.7 pmol/l (p less than 0.005), while using antibody T204, specific for the sulfated tyrosine region of CCK, plasma CCK levels increased from 2.9 +/- 0.5 pmol/l to 12.4 +/- 1.3 pmol/l (p less than 0.005). Plasma samples obtained from 3 subjects during bombesin infusion were fractionated by Sephadex column chromatography. Fractionation revealed 4 molecular forms of CCK: peak I eluted in the void volume and comprised 0-7% of CCK-like immunoreactivity, peak II eluted at 35% and comprised 8-41% of CCK-like immunoreactivity, peak III eluted at 50% and comprised 44-61% of CCK-like immunoreactivity, and peak IV eluted at 75% and comprised 15-27% of CCK-like immunoreactivity. Radioimmunoassay with a carboxyl-terminal CCK-antibody fully cross-reacting with gastrin did not reveal additional molecular forms of CCK. Since both the carboxyl-terminus and the sulfated tyrosine region are required for biological activity of CCK, it is likely that all these molecular forms of CCK possess biological activity.

Adult↗
PubMed1983

Radioimmunoassay of cholecystokinin in human tissue and plasma.

A highly sensitive radioimmunoassay for cholecystokinin (CCK) without any cross-reactivity with gastrin is described. The antibody was raised in a rabbit by immunisation with 30% CCK and bound to all COOH-terminal CCK-peptides containing at least 14 amino acid residues. The affinity constant of the antibody was 59.4 X 10(10) l/mol. CCK 33 conjugated to [125I]hydroxyphenylpropionic acid-succinimide ester was used as label. The binding between label and antibody was inhibited by 50% (ID50) at a concentration of 2.8 pmol/l cholecystokinin 33. The detection limit of the assay was between 0.5 and 1.0 pmol/l plasma. Concentrations of CCK in aqueous acid extracts of human upper small intestine were 36.5 +/- 9.8 pmol/g and of human cerebral cortex 28.2 +/- 2.5 pmol/g tissue. Plasma samples were extracted in 96% ethanol prior to assay. No advantage was obtained by adding aprotinin to the tubes. When frozen at -20 degrees C plasma CCK was stable for at least 6 months. Basal plasma CCK concentrations in 30 normal subjects were very low, 0.9 +/- 0.1 pmol/l, range 0.5 to 3.1 pmol/l. Intraduodenal administration of fat induced significant increases in plasma CCK from 1.1 +/- 0.1 to 8.2 +/- 1.3 pmol/l (p = 0.01). Infusion of exogenous CCK, resulting in plasma CCK levels slightly lower than those measured during administration of fat, induced pancreatic enzyme secretion and gallbladder contraction. The reliability of this radioimmunoassay for measurements of CCK in human plasma was extensively evaluated.

Adult↗
PubMed1983

Immunological evidence of cholecystokinin-39 in porcine brain.

Using a sensitive and specific radioimmunoassay for cholecystokinin-39 (CCK-39), CCK-39 was demonstrated in aqueous-acid extracts of procine brain. The highest concentration of CCK-39 was found in the cortex (6.1 +/- 1.5 pmol/g). In the cortex CCK-39 comprised 21% of total CCK-immunoreactivity and 51% of large CCK-immunoreactivity.

Animals↗
PubMed1983

The effect of a gastrin-receptor antagonist on gastric acid secretion and serum gastrin in the Zollinger-Ellison syndrome.

We studied the effect of intravenous administration of a gastrin-receptor antagonist (proglumide) on gastric acid secretion and serum gastrin in three patients with Zollinger-Ellison syndrome. Proglumide administered as a bolus injection (50 mg/kg) or as an infusion (50 mg/kg hour and 100 mg/kg hour) or as a combination of bolus injection and infusion (50 mg/kg I.V. followed by 50 mg/kg hour) inhibited gastric acid secretion by 13-62%. Cimetidine (2 mg/kg I.V. followed by 2 mg/kg hour) inhibited gastric acid secretion by 83-86%. Neither proglumide nor cimetidine significantly influenced serum gastrin concentrations. We conclude that proglumide is a relatively weak inhibitor of gastric acid secretion in patients with the Zollinger-Ellison syndrome.

Adult↗
PubMed1983

Effect of acarbose, pectin, a combination of acarbose with pectin, and placebo on postprandial reactive hypoglycaemia after gastric surgery.

In a double-blind study we have compared the effect of 50 mg acarbose, 100 mg acarbose, 4.2 g pectin, a combination of 50 mg acarbose with 4.2 g pectin, and placebo on plasma glucose, plasma insulin, breath hydrogen and hypoglycaemic symptoms after a normal carbohydrate rich meal in nine patients with previous gastric surgery. Fifty milligrams acarbose, 100 mg acarbose and the combination of 50 mg acarbose with 4.2 g pectin significantly inhibited the postprandial peak glucose concentration (p less than 0.01). The lowest plasma glucose concentration, observed 60-150 minutes after ingestion of the meal, was significantly increased by the addition of 50 mg acarbose (p less than 0.01) and the combination of acarbose with pectin (p less than 0.05). The combination of acarbose with pectin was the only treatment that significantly inhibited the plasma insulin peak (p less than 0.05). Eight of nine patients had symptoms of hypoglycaemia on placebo, two on 50 mg acarbose (p less than 0.05), two on 100 mg acarbose (p less than 0.05), five on pectin (ns), and two on the combination of acarbose and pectin (p less than 0.05). All treatments with acarbose induced significant increases in breath hydrogen excretion (p less than 0.05).

Acarbose↗
PubMed1982

Low binding of Bolton-Hunter-labelled cholecystokinin-33 to carboxyl-terminal CCK-antibodies.

Labelling of cholecystokinin-33 (CCK33) with [125I]hydroxyphenylpropionic acid-succinimide ester (Bolton-Hunter-reagent) results in labels with excellent immunoreactivity when tested with non-carboxyl-terminal CCK-antibodies but extremely low binding to carboxyl-terminal CCK-antibodies. This finding might explain some of the difficulties experienced with production of immunoreactive CCK33 labels prepared by the Bolton-Hunter method.

Animals↗
PubMed1982

Serum gastrin responses to bombesin and food in patients with hypergastrinemia.

Serum gastrin responses to bombesin and to food were studied in patients with hypergastrinemia. Nine unoperated patients with hypergastrinemia of antral origin (seven achlorhydria by two idiopathic G-cell hyperfunction) had significantly higher serum gastrin responses to bombesin (P less than 0.001) and to food (P less than 0.001) than eight unoperated patients with Zollinger-Ellison syndrome. Three gastrectomized Zollinger-Ellison patients showed large serum gastrin responses to bombesin, and two of them had large postprandial increases in serum gastrin. Serum gastrin in a single patient with retained excluded antrum in the duodenal stump after partial gastrectomy with Billroth II anastomosis responded to bombesin but not to food. In nonoperated patients with hypergastrinemia of antral origin, the serum gastrin responses to bombesin and to food were significantly correlated (r = 0.786; P less than 0.02) while in unoperated Zollinger-Ellison patients no such correlation was found (r = 0.095; P greater than 0.10). It is concluded that determination of the serum gastrin response to bombesin does not provide more information than measurement of postprandial serum gastrin concentrations in the differential diagnosis of patients with basal hypergastrinemia.

Adult↗
PubMed1982

Effect of changes in serum calcium on secretin-stimulated serum gastrin in patients with Zollinger-Ellison syndrome.

This study was undertaken to determine whether or not the serum gastrin response to secretin in patients with Zollinger-Ellison syndrome is influenced by changes in serum calcium. After infusion of 50 mg/kg disodium ethylenediaminetetraacetate over 90 min in 7 patients with Zollinger-Ellison syndrome, increases in serum gastrin following administration of 1 CU/kg (Cu-clinical unit) secretin GIH (118 +/- 46 pg/ml) were lower than the response before the infusion (755 +/- 90 pg/ml; p less than 0.01). Before infusion of disodium ethylenediaminetetraacetate all 7 patients with Zollinger-Ellison syndrome had gastrin increases after secretin administration above 100 pg/ml, while after the infusion 4 of 7 patients had secretin-stimulated increases in serum gastrin below 100 pg/ml. Subsequent normalization of serum calcium by infusion of 3 mg/kg calcium over 15 min resulted in gastrin responses to secretin of greater than 100 pg/ml. Infusion of 10 mg/kg calcium over 120 min in 4 Zollinger-Ellison syndrome patients induced significant increases in secretin-stimulated serum gastrin from 660 +/- 180 to 1339 +/- 286 pg/ml (p = 0.005). This dose of calcium did not increase the gastrin response to secretin in 5 normogastrinemic and 2 hypergastrinemic control subjects. It was concluded that serum gastrin response to secretin in patient with Zollinger-Ellison syndrome is influenced by serum calcium concentrations.

Adult↗
PubMed1982

Serum pancreatic polypeptide responses to food and secretion in patients with Billroth I and Billroth II gastrectomies and in normal subjects.

Serum pancreatic polypeptide (PP) responses to food and to secretion were measured in 7 patients with antrectomy and gastroduodenostomy (Billroth I gastrectomy), 11 patients with antretectomy and gastrojejunostomy (Billroth II gastrectomy), and 12 normal subjects. The integrated postprandial serum PP secretion was significantly lower in the patients with Billroth II gastrectomy (4.4 +/- 0.9 nmol/L X 120 min) than in the patients with Billroth I gastrectomy (9.3 +/- 2.3 nmol/l X 120 min; P less than 0.05) and the normal subjects (10.9 +/- 1.3 nmol/L X 120 min; P less than 0.001). The serum PP response to food in the patients with Billroth I gastrectomy was not significantly different from the response in the normal subjects. The serum PP responses to intravenous injection of 1 CU/kg of secretin GIH were similar in the three groups studied. These studies point to an important role of the duodenum in the postprandial secretion of PP.

Adult↗