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Biomedical subjects

B Petersen

Publications and source records attributed to B Petersen.

At least 109 records · Page 6Linked to original sources
PubMed1983

Increased concentrations of the NH2-terminal fragment of gastrin-17 in acute duodenal ulcer and acute gastritis.

The concentration of the NH2-terminal fragment of gastrin-17 in serum was determined by radioimmunochemistry. Two antisera were used, one specific for the COOH-terminus and the other for the NH2-terminus of gastrin-17. The NH2-terminal gastrin-17 immunoreactivity in unfractionated serum correlated well with the amount of fragment found after gel filtration of the same sera (p less than 0.001). In healthy subjects (no. = 100), the NH2- and COOH-terminal gastrin immunoreactivity was 8 +/- 1 and 20 +/- 1 pmol/l (mean +/- SEM), respectively. In patients with acute duodenal ulcer (no. = 30) and acute gastritis (no. = 10) the NH2-terminal immunoreactivity was fourfold increased compared with in healthy subjects (p less than 0.001), whereas the COOH-terminal was identical, the NH2- and COOH-terminal concentrations being 33 +/- 7 and 22 +/- 2 pmol/l in duodenal ulcer and 35 +/- 6 and 21 +/- 1 pmol/l in acute gastritis. Other groups of patients had NH2- and COOH-terminal gastrin concentrations in serum similar to those measured in healthy subjects. The results suggest that gastrin cells process gastrin-17 abnormally during the acute phase of duodenal ulcer and gastritis.

Acute Disease↗
PubMed1983

The effect of vasoactive intestinal polypeptide on meal-stimulated gastric acid secretion in man.

The effect of vasoactive intestinal polypeptide (VIP) on meal-stimulated gastric acid secretion was studied in six healthy volunteers. Acid secretion was stimulated by instillation of a 10% solution of peptone, which was adjusted to pH 5.5, circulated through the stomach via a double-lumen gastric tube by a peristaltic pump. The acid secretion was estimated by continuous titration by a pH-stat. The subjects were studied twice on separate days, receiving an intravenous infusion of either VIP (1 microgram/kg/h) or saline. No effect on acid secretion was found. Mean serum gastrin concentration rose from 42 pmol/l to 150 pmol/l during meal stimulation and was unaffected by infusion of VIP. Plasma VIP concentration during infusion of saline was 6.8 pmol/l and during VIP infusion, 82.8 pmol/l. Plasma VIP concentration was unaffected by the peptone meal.

Adult↗
PubMed1983

Variations in the release of the NH2-terminal fragment of gastrin-17 in the course of duodenal ulcer disease.

Fasting and meal-stimulated NH2-terminal gastrin concentrations in serum were significantly higher in patients with active duodenal ulcer than in control subjects and in patients with inactive duodenal ulcer (p less than 0.05). In contrast, the COOH-terminal gastrin concentrations (the bioactive gastrins) did not differ among the groups. Parallel variation in the NH2- and COOH-terminal gastrin concentrations occurred both during meal stimulation and as response to adrenaline or secretin infusion. In a longitudinal study of duodenal ulcer patients, higher NH2- than COOH-terminal gastrin concentrations were associated with the active phase of the disease, whereas this seldom occurred during the inactive phase (p less than 0.001). These data suggest that abnormally large amounts of the NH2-terminal fragment of gastrin-17 are released to the circulation during the active phase of duodenal ulcer.

Adolescent↗
PubMed1983

Significance of the molecular heterogeneity of gut hormones.

Molecular heterogeneity is a fundamental feature of ribosomally synthesized proteins and polypeptides. The heterogeneity reflects gene duplications with subsequent differences in mutation of the genes, different post-transcriptional and post-translational processings and different amino acid modifications. Gut hormones are also heterogeneous, but the degree of heterogeneity reported so far for each hormone has varied. The most extensively studied (i.e. cholecystokinins, gastrins, opioid peptides and glucagons) have displayed a high degree off heterogeneity. Similar degrees will probably emerge for the remaining gut hormones when they have been studied in greater detail. In accordance with the nature of the molecular difference, a distinction between macro- and microheterogeneity is proposed. Macroheterogeneity is caused by variations in peptide chain length; microheterogeneity by derivatizations or substitutions in single amino acid residues. The molecular heterogeneity has profound implications for measurement and study of a gut hormone. Thus, measurement in biological fluids requires careful evaluation of the number and affinity of different molecular forms. Understanding of the function and pathophysiology of gut hormones requires full clarification of their molecular heterogeneity.

Amino Acid Sequence↗
PubMed1982

Effect of naloxone on met-enkephalin-induced gastric acid secretion and serum gastrin in man.

It has previously been demonstrated that met-enkephalin, and endogenous opiate, stimulates gastric acid secretion in man, while naloxone inhibits meal-stimulated acid secretion. In seven healthy subjects the opiate receptor antagonist naloxone was infused in a dose of 10 microgram/kg/h during stimulation of gastric acid secretion with pentagastrin 100 ng/kg/h and met-enkephalin 0.1 microgram/kg/h. Naloxone had no effect on pentagastrin-induced acid secretion, whereas met-enkephalin-induced acid secretion was completely abolished in both studies without affecting serum gastrin levels, suggesting that the acid inhibitory effect of naloxone is specifically directed towards met-enkephalin-induced acid secretion. The results support the assumption that met-enkephalin participates in the physiological stimulation of gastric acid secretion.

Adult↗
PubMed1982

Calcium and stimulus-secretion coupling in gastric fundic mucosa. Effect of inhibition of calcium transport by verapamil on gastric acid secretion in the isolated guinea pig fundic mucosa and in healthy subjects.

The effect on gastric acid secretion of blocking transmembrane Ca2+ influx into the parietal cells has been studied in the isolated guinea pig fundic mucosa and in healthy volunteers. Verapamil inhibited in a dose-related manner histamine-stimulated acid secretion in the guinea pig mucosa, whereas stimulation with theophylline and dibutyryl cyclic-AMP was unaffected. The effect of verapamil (Isoptin, 2.0 mg/h) on acid secretion stimulated by increasing doses (50, 200, 500 ng/kg-h) of 15-leucine synthetic human gastric I was studied in seven healthy volunteers, alone and in combination with infusion of calcium gluconate (1.0 meq Ca2+/kg-h). Verapamil inhibited the acid response to the lowest dose of gastrin, resulting in a significant increase of D50 of 15-leucine synthetic human gastrin I. This effect was partly reversed by calcium infusion. It is concluded that one of the mechanisms by which extracellular calcium concentration influences acid secretion is by transmembrane influx of Ca2+ during stimulation.

Adult↗
PubMed1981

Effect of endogenous pancreatic glucagon on gastric acid secretion in patients with duodenal ulcer before and after parietal cell vagotomy.

The effect of endogenous pancreatic glucagon on submaximal pentagastrin stimulated gastric acid secretion was studied by infusion of 1-arginine in patients with duodenal ulcer before and after parietal cell vagotomy without drainage (PCV). Preoperatively infusion of 1-arginine resulted in a marked inhibition of acid secretion, whereas no effect was found postoperatively. Plasma glucagon concentrations were identical pre- and postoperatively, fasting as well as during arginine infusion. Serum gastrin concentration rose after PCV but not unaffected by arginine infusion both pre- and postoperatively. The study demonstrates that intact vagal innervation of the fundic glands is a condition of inhibition of pentagastrin induced acid secretion by pancreatic glucagon released by infusion of 1-arginine.

Adult↗
PubMed1981

Removal of endogenous gastrin in man.

The concentration of gastrin was determined in arterial and venous serum from the head, lung, liver, kidney, and legs in six fasting patients with mild hepatic parenchymatous disease. Extraction of gastrin could not be demonstrated in any of the vascular beds examined. The results indicate that gastrin degradation is not confined to certain specific organs but takes place in many organs or perhaps in the total volume of distribution for gastrin.

Adult↗
PubMed1981

Infusion of vasoactive intestinal polypeptide in man: pharmacokinetics and effect on gastric acid secretion.

Elimination and effect on acid secretion of vasoactive intestinal polypeptide (VIP) were studied in six healthy volunteers. On a background infusion of pentagastrin, 100 ng/kg-h, VIP was administered as stepwise intravenous infusions in doses of 0.5, 0.9, and 2.7 micro/g/kg-h, each dose being give for 1 h. Mean plasma VIP concentrations rose from 5.7 pmol/l to 28, 106 and 336 pmol/l during the VIP infusions. No significant changes in acid secretion occurred during VIP infusion as compared to infusion of pentagastrin alone, and no duodeno-gastric reflux was registered. Serum gastrin concentrations were unaltered during VIP infusion. Elimination of VIP was bi-exponential with half-lives of 2 and 21 min, respectively. Metabolic clearance rate was 42 ml/kg-min and the estimated volume of distribution 135 ml/kg.

Adult↗
PubMed1981

Acid secretory potency and elimination of the 15-leucine gastrin-17 analogue in man.

The effect on gastric acid secretion and the elimination of a commercially available synthetic human gastrin analogue (15-Leucine Synthetic Human Gastrin I, 15-LSG) were studied in six healthy human subjects. On a molar basis acid secretory efficacy was approximately four times greater than pentagastrin and secretory potency ten times greater. Elimination of 15-LSG was bi-exponential, with half-lives of 5.2 +/- 0.8 and 25.9 +/- 7.0 min. Metabolic clearance rate was 6.9 +/- 0.4 ml/kg-min and volume of distribution 52 ml/kg.

Adult↗
PubMed1981

The effect of a synthetic met-enkephalin analogue (FK 33-824) on gastric acid secretion and serum gastrin in man.

A synthetic met-enkephalin analogue was infused into seven healthy human subjects on a background infusion of pentagastrin to study the effect on gastric acid secretion and serum gastrin concentration. Gastric acid secretion rose from 4.2 meq H+/15 min to 7.8 meq H+/15 min during infusion of met-enkephalin, 0.1 micrograms/h. Met-enkephalin in a dose of 1 microgram/kg/h had no effect on pentagastrin-stimulated acid secretion. Serum gastrin concentration remained unchanged throughout the study. It is suggested that met-enkephalin could be a partial agonist on the parietal cell. The possible role of met-enkephalin in the cephalic phase of gastric acid secretion is discussed.

Adult↗
PubMed1980

The NH2-terminal tridecapeptide fragment of gastrin-17 in serum from duodenal ulcer patients.

The concentration of gastrin in serum from 47 fasting patients with duodenal ulcer was measured with two radioimmunoassays, one specific for the COOH- and the other specific for NH2-terminal sequence of gastrin-17. The COOH-terminal assay measured 13 +/- 2 pmol and the NH2-terminal 42 +/- 7 pmol-equivalent gastrin-17 per litre (mean +/- S.E.M.). This result, corroborated by gel chromatography, shows that an NH2-terminal fragment of gastrin-17, presumably the tridecapeptide, circulates in concentrations higher than those of the four known gastrin components. The abundance of NH2-terminal fragment in serum suggests that the complementary COOH-terminal tetrapeptide fragment of gastrin-17 is also produced in large quantities.

Amino Acid Sequence↗
PubMed1978

Hormone receptors. 7. Characteristics of insulin receptors in a new line of cloned neonatal rat hepatocytes.

1. A new line of cloned, differentiated rat hepatocytes (RL-PR-C) was evaluated for its usefulness as an in vitro system for studying the regulation of the insulin receptor. 2. Insulin rapidly reversibly and specifically bound to RL-PR-C hepatocytes. Binding of tracer 125I-labeled insulin, which was competitively inhibited by native insulin as well as by proinsulin and analogs of insulin and proinsulin in proportion to their biological activity, was not influenced by glucagon, corticotropin, or human growth hormone. Anti-insulin receptor serum from a patient with Acanthosis Nigricans Type B competed with 125I-labeled insulin for binding to cell surface sites. 3. Trypsinization destroyed insulin binding sites, but these were restored by incubation under growth conditions; a 75% restoration of binding sites was achieved by one cell population doubling. 4. RL-PR-C hepatocytes responded to insulin binding by an increase in glycogen synthesis from glucose. The insulin effect was maximal at 85 nM, but was detectable at lower, more physiological, concentrations. 5. Chronic exposure (for at least 3h) of hepatocytes to insulin (10(-10)--(10(-8) M) reduced by up to 60% the number of binding sites for insulin (down-regulation). Down-regulation was prevented by cycloheximide at concentration (10 micron) sufficient to inhibit markedly protein synthesis from tracer isoleucine. Recovery from down-regulation induced by native insulin at 10(-7 M or lower concentrations was complete by 18 h under growth conditions. 6. Although RL-PR-C hepatocytes spontaneously transform after about 90 population doublings, no significant differences between normal and transformed cells were observed in insulin binding characteristics and in interaction of cells with anti-insulin receptor serum. However, transformed cells exhibited a substantially reduced (maximum of 20%) down-regulation response to insulin. 7. RL-PR-C rat hepatocytes appear, for these reasons, to be a useful model system for studying the regulation of the insulin receptor.

Animals↗