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Biomedical subjects

B Petersen

Publications and source records attributed to B Petersen.

At least 91 records · Page 5Linked to original sources
PubMed1985

Complete sulfation of jejunal gastrin in the human fetus.

The degree of tyrosine-O-sulfation and the ratio between large (gastrin-34 and component I) and small (gastrin-17 and -14) molecular forms of gastrin were studied in extracts of human fetal (n = 14) and adult (n = 9) antrum, duodenum, jejunum and pancreas. Boiled water extracts were applied to gel- and ion-exchange chromatography before and after treatment with trypsin and arylsulfatase. The fractions were monitored with sequence-specific radioimmunoassays that distinguish sulfated from non-sulfated gastrins. In antrum and duodenum about half the gastrins were sulfated at all stages of development. In the fetal jejunum gastrin occurred in sulfated form only while in the adult 72% (range, 64-88%) of the jejunal gastrins were sulfated. The larger molecular forms of gastrin predominated in the fetal compared with the adult antrum. In duodenum and jejunum, however, the ratio between small and large forms was the same in fetus and adult. Gastrin was undetectable in both fetal and adult pancreas. The results show that the degree of sulfation of gastrin varies substantially in the different parts of the gut at different stages of development. The differences may have functional significance, since sulfation increases the pancreozyminic and cholecystokinetic potency of gastrin.

Adult↗
PubMed1985

Is somatostatin a humoral regulator of the endocrine pancreas and gastric acid secretion in man?

The effect of low dose infusions of somatostatin on meal stimulated gastric acid secretion was studied in eight healthy volunteers by intragastric titration after a peptone test meal with radioimmunoassay control of the plasma concentrations of somatostatin and the pancreatic hormones glucagon and insulin. Infusion of somatostatin in a dose of 100 ng/kg/h, resulting in a plasma concentration of 13.4 +/- 2.1 pmol/l, inhibited acid secretion significantly, and in a dose of 800 ng/kg/h, with corresponding plasma concentration of 66.5 +/- 12.0 pmol/l the acid secretion was virtually abolished. Plasma concentrations of insulin and pancreatic glucagon decreased significantly during infusion of 200 ng/kg/h (24.5 +/- 7.5 pmol/l) and glucose concentrations increased. Serum gastrin was only significantly decreased during the highest dose of somatostatin. The range of plasma somatostatin concentrations obtained with the lower doses correspond to reported physiological variations. The results support the concept that somatostatin participates in the hormonal control of the pancreatic endocrine and the acid secretion.

Adult↗
PubMed1985

Decreased sulfation of serum and tissue gastrin in hypergastrinemia of antral origin.

The sulfation of gastrin in serum, antrum and duodenum was studied in 22 normo- and 20 hypergastrinemic patients. The ratio between gastrin-17 and gastrin-34 was measured in antrum and duodenum. The degree of sulfation was reduced in the antrum of hypergastrinemic patients (35.3 +/- 1.3%, mean +/- SEM) compared with 48.0 +/- 2.1% in normo-gastrinemic patients (p less than 0.001). The degree of sulfation in serum and duodenum was similar to that of the antral gastrins in all patients. The percentage of gastrin-34 in antrum was increased (7.3 +/- 0.7%) in hypergastrinemic compared with 4.9 +/- 0.3% in normogastrinemic patients (p less than 0.01). In the duodenum the percentage of gastrin-34 was similar in normo- and hypergastrinemia. When classified according to clinical diagnosis, sulfation of antral gastrin was normal in duodenal ulcer (47.6 +/- 4.5%) but decreased in gastric ulcer (36.7 +/- 1.6%, p less than 0.01) and pernicious anemia (31.3 +/- 1.9%, p less than 0.001) compared with 48.2 +/- 2.2% in control patients. In pernicious anemia a larger proportion of antral gastrins occurred as gastrin-34 (8.2 +/- 0.9%) compared with 4.8 +/- 0.4% in control patients (p less than 0.01). Our study suggests that both sulfation and proteolytic processing of the gastrin precursor is diminished in hypergastrinemia of antral origin.

Anemia, Pernicious↗
PubMed1985

A glucose-dependent mechanism in jejunum inhibits gastric acid secretion: a response mediated through enteroglucagon?

In healthy subjects iso- and hyper-tonic glucose or saline was instilled intrajejunally and the effect on gastric acid secretion determined. Iso- and hyper-tonic glucose (100 ml; 300, 600, 900, 1200 mosm) reduced acid secretion dose-dependently (p less than 0.05), whereas iso- and hyper-tonic saline (100 ml; 300, 1000, 1500 mosm) was without influence. The enteroglucagon plasma levels increased during intrajejunal glucose but not during saline infusion. Gastrin and pancreatic glucagon levels were not affected. Hence, our results substantiate the concept of a non-osmosensitive, glucose-specific inhibitory mechanism of acid secretion located in the jejunum. Furthermore, enteroglucagon could be a possible humoral mediator of the inhibition.

Adult↗
PubMed1985

Effects of a fixed combination of low dose nifedipine and acebutolol on essential hypertension: comparison with standard dose acebutolol.

114 patients from four clinics participated in a double blind study designed to assess the efficacy of a nifedipine-acebutolol fixed combination -10 mg + 100 mg - as compared with acebutolol -200 mg- in essential hypertension. During the ten week study the mean blood pressure readings (s.d.) 1-3 h after treatment decreased from 179.2/104.8 (10.2/6.2) to 150.3/87.7 (9.8/7.7) in the combination group and from 181.7/106.5 (14.4/7.0) to 150.4/89.0 (15.0/10.4) in the acebutolol group. The mean systolic and diastolic blood pressures were also decreased after exertion (load) and 24 hours after treatment at the end of the 6th week of the study. A doubling of the dose from week 7 to 10 did not change these figures. These results reveal the possibility of treating essential hypertension with a low dose of beta-adrenergic blocking agents in combination with 10 mg nifedipine. Both drugs were well tolerated. 3 patients (5%) in the combination group and 3 patients in the acebutolol group were withdrawn from the study because of headache and dizziness.

Acebutolol↗
PubMed1985

Aminophenylboronic acid affinity chromatography and thiobarbituric acid colorimetry compared for measuring glycated albumin.

Two techniques originally developed for measurement of glycated ("glycosylated") hemoglobin but also applicable to determination of glycated albumin are the thiobarbituric acid colorimetric technique (I) and the aminophenylboronic acid affinity chromatographic procedure (II). The latter reliably distinguishes diabetics from nondiabetics, and concentrations of glycated hemoglobin and glycated albumin are linearly correlated. I is nonspecific; it neither correlates with diabetic status nor with values derived via the affinity technique. Most of the chromogenic material is present in the fraction of albumin that does not bind to aminophenylboronic acid. Glucose interferes significantly with I but only slightly with II. Prolonged incubation of plasma with glucose dramatically increases the II-determined glycated albumin. Reactivity with thiobarbituric acid increases much less, and mainly in the II-bound fraction. This fraction contains a high proportion of nonspecifically reactive material. The percentage of glycated albumin determined in crude plasma samples by II differs only slightly from the value determined by purifying the albumin from the plasma. This technique appears more promising than I for eventual clinical applications.

Blood Glucose↗
PubMed1985

Use of aminophenylboronic acid affinity chromatography to measure glycosylated albumin levels.

A simple technique for the measurement of glycosylated albumin by affinity chromatography on m-aminophenylboronic acid agarose columns is presented. The technique relies on bromcresol green determination of albumin in the nonbound and bound fractions. There is a linear correlation between albumin concentration of the bound fraction and glycohemoglobin values in individuals. A control nondiabetic plasma pool with a glycohemoglobin value of 7.10% +/- 0.05% (mean +/- SEM) had a glycoalbumin value of 1.64% +/- 0.06%, while a diabetic control plasma pool with a glycohemoglobin value of 13.63% +/- 0.07% had a glycoalbumin value of 4.02% +/- 0.12%. Compared with results from the affinity technique, the preponderance of colorimetric reaction determined with the thiobarbituric acid procedure is nonspecific, in that it does not correlate with diabetic status or with values derived by the affinity procedure. The bulk of thiobarbituric acid-reactive material is present in the fraction of albumin that does not bind to aminophenylboronic acid. This nonbound fraction contains plasma glucose, which significantly interferes with thiobarbituric acid determinations but only very slightly interferes with the affinity procedure. Prolonged incubation of plasma with 500 mg/dl glucose dramatically increases affinity-determined glycosylated albumin. Thiobarbituric acid reactivity increases much less, the increase being mainly in the fraction bound to aminophenylboronic acid. The percentage glycosylated albumin determined by the affinity technique in crude plasma samples differs very slightly, if at all, from that determined by purification of the albumin from plasma. The affinity technique appears very promising for eventual clinical applications in the management of diabetes.

Blood Glucose↗
PubMed1984

The stability of gastric acid secretion during prolonged pentagastrin stimulation in man.

Prolonged stimulation with pentagastrin in doses of 100 and 500 ng h-1 kg-1 was performed in nine healthy subjects. A plateau in gastric secretion was reached after 90 min with 100 ng h-1 kg-1 and 500 ng h-1 kg-1 resulted in a secretory plateau after 60 min. When the plateau was reached the acid secretion rate was constant for the rest of the study, that is 4 h after beginning the pentagastrin infusion. Medians and interquartile ranges of acid output were 4.9 (3.7-5.2) and 8.1 (5.8-9.5) mmol of H+/30 min. We conclude that no 'fade' of gastric acid secretion occurs during 4 h of submaximal pentagastrin stimulation in normal subjects, and that the time required for reaching a secretory plateau is dependent on the dose of pentagastrin.

Adult↗
PubMed1984

Abnormal processing of antral gastrin in active duodenal ulcer disease.

The concentrations of gastrins containing the active C-terminal tetrapeptide amide (mainly gastrin-34 and gastrin-17) and the N-terminal tridecapeptide fragment of gastrin-17 were measured in antral and duodenal biopsy specimens. The antral concentration of the N-terminal gastrin fragment was much higher in patients with active duodenal ulcer (33.4 +/- 6.8 nmol g-1, mean +/- SEM, n = 15) than in controls (5.6 +/- 2.9 nmol g-1, n = 10), patients with gastric ulcer (5.6 +/- 1.8 nmol g-1, n = 10) or patients with pernicious anaemia (7.7 +/- 2.5 nmol g-1, n = 6). No differences were found between the groups regarding gastrin-34 and gastrin-17 concentrations. In duodenal extracts, the N- and C-terminal gastrin concentrations were similar in all groups of patients. These data suggest that the posttranslational processing of antral gastrin is abnormal in patients with active duodenal ulcer disease.

Adult↗
PubMed1984

Interaction of calcium and gastrin on gastric acid secretion in duodenal ulcer patients.

A dose response study of the effect on gastric acid secretion of synthetic human gastrin-17 in doses of 50,200, and 500 ng/kg/h was performed in eight healthy volunteers and in eight patients with duodenal ulcer. The study was repeated on a separate day during intravenous infusion of calcium gluconate (0.1 mmol Ca2+/kg/h). In healthy subjects the acid response to the combined infusion of synthetic human gastrin and calcium did not significantly exceed the response to synthetic human gastrin alone, in contrast with patients with duodenal ulcer in whom the combined infusion did significantly improve acid output compared with infusion of synthetic human gastrin alone. The dose of synthetic human gastrin required for half maximal acid response (D50) was reduced in both groups but significantly more in patients with duodenal ulcer. No difference in serum gastrin concentrations or in serum calcium concentrations were found. It is hypothesised that extracellular calcium plays a role in gastrin stimulated acid secretion in man and that patients with duodenal ulcer are more sensitive to this calcium dependent mechanism than non-duodenal ulcer subjects.

Adult↗
PubMed1984

Gastrin-releasing peptide: pharmacokinetics and effects on gastro-entero-pancreatic hormones and gastric secretion in normal men.

Gastrin-releasing peptide (GRP) was infused at two dose levels [GRP I (0-30 min): bolus dose of 1.41 pmol kg-1, followed by 0.12 pmol kg-1 min-1; GRP II (30-60 min): bolus dose of 5.67 pmol kg-1, followed by 1.50 pmol kg-1 min-1] to six normal men to study the pharmacokinetics of GRP using a newly developed RIA and the effect of GRP on gastro-entero-pancreatic hormones and gastric acid secretion. The half-life of disappearance of GRP was 2.8 +/- 0.4 min (+/- SEM). The MCR and the apparent space of distribution were 33.0 +/- 4.0 ml kg-1 min-1 and 133 +/- 31 ml kg-1, respectively. GRP stimulated the secretion of gastrin, pancreatic polypeptide, insulin, glucagon, and glucose-dependent insulinotropic polypeptide in a dose-dependent manner. Gastric acid secretion was stimulated 15 min after the increase in gastrin secretion, suggesting that GRP stimulated gastric acid secretion via release of gastrin. GRP had no significant effect on the secretion of enteroglucagon or neurotensin. In the mammalian gastrointestinal tract, GRP is localized exclusively to nerve tissue. This fact and its potent effects demonstrated here make it a likely candidate for peptidergic nervous control of gastrointestinal function.

Adult↗
PubMed1984

Abnormally processed gastrins in active duodenal ulcer disease.

In contrast to healthy subjects, duodenal ulcer patients in the active phase contain large amounts of a peptide in serum and antrum which react with antiserum specific for the N-terminus, but not the C-terminus of gastrin-17. The immunochemical and chromatographic properties were similar to that of the N-terminal tridecapeptide sequence of gastrin-17. The peptide follows the clinical course of duodenal ulcer disease, as it disappears when the ulcer heals. The N-terminal tridecapeptide - lacking the bioactive tetrapeptide of gastrin-17 - is a potent inhibitor of gastric acid secretion, presumably by way of competitive antagonism to gastrin. It is suggested to participate in the regulation of gastric acid secretion in patients with active duodenal ulcer disease. To confirm the chemical structure of the peptide, antral and gastrinoma extracts were used for isolation, purification and amino acid analysis. We found two different peptides with the same N-terminus as gastrin-17, namely the previously known N-terminal tridecapeptide fragment of gastrin-17 and a new gastrin component, identical with a C-terminal glycine extended gastrin-17. Furthermore, a C-terminal glycine extended component, corresponding to each of the other molecular forms of gastrin were present. Thus, a variety of abnormally processed gastrins are synthesized and released to the circulation during the active period of duodenal ulcer disease.

Amino Acid Sequence↗
PubMed1984

Effect of intravenous and intrajejunal fat infusion on gastric acid secretion and plasma neurotensin-like immunoreactivity in man.

The effects of intrajejunal and intravenous infusion of fat (100 ml Intralipid 20%) on pentagastrin-stimulated gastric acid secretion and on the concentrations of plasma neurotensin-like immunoreactivity (p-NTLI) were studied in eight healthy subjects. Gastric acid secretion was studied for a 1.5-h period at 15-min intervals after fat administration. Acid secretion was reduced by 58% and 36%, respectively, after intrajejunal and intravenous administration. The concentration of p-NTLI rose significantly from 29 to 177 pmol/l at 45 min after intrajejunal administration but did not change after intravenous infusion. The results indicate that large volumes of fat inhibit gastric acid secretion by a neurotensin-independent postabsorptive mechanism and by an intestinal mechanism that may in part be mediated by neurotensin.

Adult↗
PubMed1983

The N-terminal tridecapeptide fragment of gastrin-17 inhibits gastric acid secretion.

After a meal the serum concentrations of the N-terminal tridecapeptide-like fragment of gastrin-17, (1-13)G-17, increased markedly in patients with active duodenal ulcer, but less so in healthy subjects. Consequently the synthetic (1-13)G-17 was infused intravenously in doses that resulted in concentrations similar to those measured in duodenal ulcer patients in order to examine whether the N-terminal fragment influences gastric acid secretion. Doses of 125 and 400 pmol (1-13)G-17/kg per h inhibited the meal-stimulated acid secretion by 36% (P less than 0.05) and 66% (P less than 0.05) respectively. The release of endogenous C-terminal gastrin immunoreactivity was not influenced. The infusion of (1-13)G-17 also inhibited the acid response to exogenous gastrin-34, gastrin-17 and Peptavlon, but not to gastrin-4. The results suggest that the N-terminal gastrin-17 fragment--although devoid of the hitherto considered only active site of gastrin--plays a significant role in the regulation of the gastric acid secretion in patients with active duodenal ulcer.

Adult↗
PubMed1983

Variations in the sulfation of circulating gastrins in gastrointestinal diseases.

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.

Adult↗
PubMed1983

Metabolism of the NH2-terminal tridecapeptide of gastrin-17 in normal subjects and duodenal ulcer patients.

The metabolism of the NH2-terminal tridecapeptide fragment of gastrin-17 (1-13)G-17) was examined in normal subjects and duodenal ulcer patients. A dose of 65 pmol synthetic human (1-13)G-17/kg/h was infused intravenously for 90 min. After cessation of infusion the disappearance curve was similar in the two groups. The mean half-life, volume of distribution, and clearance rate were, for normal and duodenal ulcer subjects, 6.3 and 6.3 min, 100 and 93 ml/kg, and 11.0 and 10.2 ml/kg/h, respectively. The gastric acidity decreased during the infusion in duodenal ulcer patients (54 +/- 11 to 40 +/- 10 meq/l (p less than 0.02] but not in normal subjects. The results suggest that the increased serum concentrations of the NH2-terminal fragment of gastrin-17 in duodenal ulcer patients are not caused by a decreased metabolism of (1-13)G-17. Moreover, the data show that (1-13)G-17 reduces gastric acid secretion.

Adult↗