Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.4 (trypsin)
42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Complete sulfation of jejunal gastrin in the human fetus. 400 48

We studied the effect of hydrochloric acid (HCl) in the proximal small intestine on release of cholecystokinin (CCK) and secretin and on exocrine pancreatic secretion in conscious dogs with gastric cannulas and modified Herrera pancreatic cannulas. Intraduodenal administration of HCl in a concentration of 50 or 100 mM at rates of 0.05, 0.1, 0.2, and 0.4 mmol/min significantly increased plasma concentration of CCK in a dose-dependent manner, whereas plasma gastrin levels decreased. The increased plasma CCK level paralleled a significant increase in pancreatic trypsin output. Plasma secretin concentration and pancreatic bicarbonate output also increased in response to the acid, and the increase was dependent on the acid loads delivered in the duodenum. Thus, in dogs, HCl in the duodenum releases both CCK and secretin to stimulate pancreatic secretion of bicarbonate as well as enzymes.
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PMID:Duodenal acidification releases cholecystokinin. 401 65

Sera from 15 patients with the Zollinger-Ellison syndrome were subjected to gel filtration on Sephadex G-50 superfine columns (10 x 2000 mm). The concentration of gastrin in the effluent was determined by a sensitive radioimmunoassay. Immunoreactive gastrin was eluted in four components in 14 sera. (1) Component I, eluted in the same position as proinsulin, constituted 9.7 +/- 1.2 (mean +/- SEM)% of the total immunoreactivity. (2) Component II (;big gastrin') eluted between proinsulin and insulin constituted 57.8 +/- 4.1% (mean +/- SEM) of immunoreactive gastrin. In three sera with the highest concentration of gastrin, component II appeared biphasic. (3) Component III (;little gastrin') was distributed in two peaks; the first one eluted in the same position as the heptadecapeptide gastrin II made up 17.4 +/- 2.7 (mean +/- SEM)% of the total immunoreactivity; the second one eluted in the same position as gastrin I constituted 9.5 +/- 1.3 (mean +/- SEM)%. (4) Component IV (;minigastrin') was eluted immediately before the salt peak and constituted 5.6 +/- 1.4 (mean +/- SEM)%. In one serum only components I and II were present. After incubation with trypsin all immunoreactivity in components I and II was converted to heptadecapeptide-like gastrins.The findings suggest that immunoreactive gastrin in serum from Zollinger-Ellison patients is circulating in at least four components of different molecular size.
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PMID:Gel filtration studies on immunoreactive gastrin in serum from Zollinger-Ellison patients. 419 48

The apparent molecular size and charge of immunoreactive gastrin components were studied in sera from patients with pernicious anaemia or gastrinomas (the Zollinger-Ellison syndrome) by Sephadex gel filtration and aminoethylcellulose chromatography. The following serum components were distinguished: (1) a monophasic component I similar in size to proinsulin which was converted into ;little' gastrin I by trypsin digestion; (2) a biphasic component II, corresponding to ;big' gastrins I and II (Gregory and Tracy); (3) a biphasic component III corresponding to ;little' gastrins I and II (Gregory and Tracy); and (4) a biphasic component IV, corresponding to ;minigastrins' I and II (Gregory and Tracy). ;Big, big' gastrin, a plasma component found in the void volume of the Sephadex G-50 column by Yalow and Berson (1972) was undetectable in the sera investigated. A component in gastrinoma and antral mucosa extracts corresponding in size to ;big big' gastrin was detectable by the assay; the ;big big' gastrin fraction from gastrinoma tissue was heterogenous, with components of apparent MW 30 000-100 000. It is concluded that serum gastrin circulates in the form of at least four components, of which the three smaller ones are in pairs.
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PMID:Immunoreactive gastrin components in human serum. 482 Jun 33

Immunoreactive cholecystokinin (CCK) levels in human and rat plasma are described using a radioimmunoassay specific for the biologically active sulfated end of CCK. This assay detected significant changes in plasma cholecystokinin levels during intrajejunal administration of amino acids and intravenous infusions of CCK-8 which were followed by increased pancreatic secretion. In humans, the concentration (pg/ml) of plasma cholecystokinin increased from 10.8 to 18.9 following intrajejunal amino acid instillation and from 15.4 to 31.1 during CCK infusion, while pancreatic trypsin secretion increased more than 15 fold. Ingestion of a test meal also caused a rapid and significant elevation (P less than 0.05) in both plasma CCK (14.5-21.7 pg/ml) and gastrin (50-160 pg/ml) levels. In the rat, an injection of 46 ng of CCK-8 produced a 300% increase in immunoreactive plasma CCK levels (2 min) and caused peak pancreatic protein secretion within 5 min; 4 fold lower doses (11.5 ng) elevated plasma CCK by 38% and pancreatic protein secretion to a small but significant extent. The ability of this assay to detect various forms of sulfated CCK in human plasma was also determined. Following gel chromatography on Sephadex G-50, at least three different immunoreactive peaks were found in plasma from fasted subjects and after intrajejunal amino acid stimulation. While the lower molecular weight CCK peptides (CCK-8 and CCK-12) were detected in plasma from both fasted and stimulated subjects, the larger form (CCK-33) was only present in measurable concentrations after amino acid infusion. The simultaneous measurement of increased plasma CCK levels and pancreatic secretion and the changes in the distribution of CCK peptides following amino acid infusion provides strong support that this assay detects physiologically relevant changes in biologically active CCK peptides.
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PMID:Immunoreactive cholecystokinin in human and rat plasma: correlation of pancreatic secretion in response to CCK. 609 73

Many small biologicaly active peptides are derived from larger precursor forms which fulfil a variety of roles in the synthesis, segregation and intracellular migration of secretory products. Limited proteolysis may occur at several stages during this process, giving rise to products that are either degraded (e.g. the prepeptides) or discharged coordinately from their cells of origin during exocytosis (e.g. insulin and C-peptide). Molecular defects have recently been found to occur at cleavage sites in proinsulin as well as in other proproteins, and these point mutations may, in some instances, be responsible for familial metabolic disorders. The nature and cell specificity of the proteolytic enzymes involved in the conversion of the various precursor forms remains unresolved. Recent studies in our laboratory have led to the identification of precursors of glucagon and somatostatin in rat islets of Langerhans. Analysis of tryptic maps of these precursors has shown that a trypsin-like enzyme would be sufficient to cleave the C-terminally located somatostatin sequence from its precursor (relative molecular mass 12,500), but that both trypsin-like and carboxypeptidase B-like enzymes would be necessary to cleave the internal glucagon sequence from its prohormone (relative molecular mass 18,000). Molecular cloning techniques have provided valuable new approaches to analysing the structures of a variety of precursor forms, including those for insulin, gastrin, growth hormone, adrenocorticotropic hormone and the endorphins, and in the future will undoubtedly shed more light on the structures of their chromosomal genes, the mechanisms regulating their expression, and their evolutionary origins.
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PMID:Formation of biologically active peptides. 610 30

It has been shown previously that trypsinogen and its activation peptide but not trypsin decreased gastric secretion. The purpose of this work was to study the dose-action relation between the intraduodenal infusion of trypsinogen and gastric secretion. Three dogs provided with gastric and duodenal Thomas fistulae were stimulated by continuous i.v. perfusion of porcine gastrin I-II (6 microgram kg-1 h-1). Pancreatic juice was diverted to the exterior and gastric secretion was collected. Upon reaching a gastric secretory plateau, porcine trypsinogen was infused intraduodenally at doses of 5, 10, 20, 40, 80 and 160 mg. Each test was continued for a further 60 min. Control was made with isotonic saline. There was a dose-related inhibition of the gastrin-stimulated gastric acid output. This inhibition reached a maximum of 50% with 40 mg of intraduodenal trypsinogen, showing no increase with higher doses.
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PMID:Dose-related inhibition of gastric secretion by intraduodenal trypsinogen in dogs. 615 84

Methods are described for obtaining antisera specific for the NH2-terminal regions of human and porcine big gastrin (G34) that can be used in radioimmunoassays. Three antisera have been characterized in detail: one (L66) raised to human 1--15 (Tyr7-Pro8-Ser9) G34 has an antigenic determinant in the 1--6 region of human G34; a second (L107) raised to 1--19 hG34 has an antigenic determinant in the 1--12 region. Both these antisera react weakly with porcine G34. A third antiserum (L33) raised to porcine G34 has an antigenic determinant in the 1--12 region of this peptide, and reacts weakly with human G34. In human antral extracts fractionated on Sephadex G50, L66 and L107 revealed a minor peak of immunoreactivity corresponding to G34, and a major peak corresponding to the NH2-terminal tryptic peptide of G34. Concentrations of the latter peptide were closely similar to those of G17 (i. e.) the COOH-terminal tryptic peptide of G34), consistent with the idea that G34 is cleaved within G-cells by a trypsin-like enzyme to yield G17. Antiserum L33 revealed small amounts of immunoreactivity in antral extracts of dog and cat, but did not reveal significant immunoreactivity in rat antral extracts. In contrast, L66 reacted with rat antral extracts, but not dog or cat. The sequences of G34 in these species are not known, but the results suggest significant differences compared with human and porcine G34, and indicate a high degree of species-specificity with NH2-terminal G34 antisera.
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PMID:Immunochemical studies on big gastrin using NH2-terminal specific antisera. 616 51

The effect of highly selective vagotomy on pancreatic exocrine function and the release of gastrin and cholecystokinin was studied in 10 patients with endoscopically-proven duodenal ulceration. Cholecystokinin and gastrin concentrations in serum both increased significantly after highly selective vagotomy. Amylase concentration in the duodenal aspirate increased significantly after vagotomy, but trypsin concentration remained unchanged. The expected reductions in gastric acid secretion were noted. Thus highly selective vagotomy reduces acid secretion effectively in patients with duodenal ulcer without impairing the exocrine function of the pancreas.
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PMID:Effect of highly selective vagotomy on pancreatic exocrine function and on cholecystokinin and gastrin release. 617 87

The CCK- and secretin stimulated pancreatic volume, bicarbonate and enzyme secretion was investigated before and during fasting for 20 days in 12 obese subjects. Pancreatic function tests were performed at the start of the fasting period and on the 10th and 20th day. In an additional and comparable group of 8 obese patients plasma concentrations of cholecystokinin (CCK), gastrin and insulin as well as metabolic parameters (bicarbonate, beta-OH-butyrate and free fatty acids) have been measured before and during total fasting. During three weeks of total fasting the average overweight of the patients undergoing pancreatic function tests was reduced from 49 to 31% (-11.5 +/- 1,5 kg). A significant reduction of volume, bicarbonate, trypsin and amylase secretion occurred already after 10 days of total fasting. After 20 days these parameters were further significantly reduced compared to the 10th day. All mentioned parameters were found at the lower limit of the normal range at the end of the fasting period at 20 days. The only exception being lipase secretion; the decrease of this enzyme was not significant at the 5% level. No significant reduction of basal plasma concentrations could be observed for CCK and gastrin during the course of total fasting. The plasma insulin levels were significantly reduced after 7 days whereas at 10 and 20 days insulin concentration was not significantly lowered compared to day 1. A small but significant decrease in the blood bicarbonate concentration could be observed after 7 days of fasting which remained constant up to the end of the study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of long-term fasting of obese patients on pancreatic exocrine function, gastrointestinal hormones and bicarbonate concentration in plasma. 620 70


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