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  • gastrin  (4)
  • Gastrin  (3)
  • HPLC  (2)
  • Lung  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Characterization of glucagon-like peptide-I(7-36)amide receptors of rat lung membranes by covalent cross-linking
    Amsterdam : Elsevier
    FEBS Letters 280 (1991), S. 247-250 
    Details
    ISSN: 0014-5793
    Keywords: Covalent cross-linking ; GLP-I(7-36)amide ; Lung ; Receptor
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0014-5793(91)80303-K
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  • 2
    Electronic Resource
    Electronic Resource
    Characterization of receptors for glucagon-like peptide-1(7-36) amide on rat lung membranes
    Amsterdam : Elsevier
    FEBS Letters 267 (1990), S. 78-80 
    Details
    ISSN: 0014-5793
    Keywords: Adenylate cyclase ; GLP-1(7-36)amide ; Guanine nuclcotide ; Lung ; Receptor
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0014-5793(90)80292-Q
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  • 3
    Electronic Resource
    Electronic Resource
    Characterization of phospholipase A2 activity in aspirates of human pancreatic pseudocysts after isolation by reversed-phase high performance liquid chromatography (1989)
    Springer
    Journal of molecular medicine 67 (1989), S. 131-135 
    Details
    ISSN: 1432-1440
    Keywords: Phospholipase A2 ; Pancreatic pseudocysts ; HPLC
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Phospholipase A (PLA) is able to attack membrane phospholipids and thereby plays a putative role in the pathogenesis of pancreatic pseudocysts. We looked for PLA2-like activity in aspirates from human pancreatic pseudocysts. In material originating from one cyst which occurred shortly after an acute pancreatitis attack, hydrolyzing enzymatic activity measured by a sensitive bioassay system for PLA2 activity was found without prior trypsin activation (67×103 U/min/100 µl). A biochemical characterization of this hydrolyzing enzymatic activity was provided after resolution of the respective proteins contained in the cyst fluid by HPLC. High hydrolyzing activities were found in correspondence to one specific, early eluting peak. The purified enzyme had pH optima at 3.5 and 6. Addition of EDTA (5 mM) to the test system abolished the enzymatic activity which mirrored the requirement for calcium ions. The activity was optimal at calcium concentrations ranging from 1–2 mM. Higher calcium concentrations reduced the enzymatic activity. The enzyme showed high heat stability. SDS-gel analysis of the peak showed one single band with a molecular weight of about 20,000 Daltons. Our findings demonstrate the possibility of activated, PLA-like activity in human pancreatic pseudocyst fluid. We speculate that an inappropriate activation of this enzyme in peri- or intrapancreatic “fluid collections” could account for pseudocyst formation after an acute pancreatitis attack.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01711338
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  • 4
    Electronic Resource
    Electronic Resource
    Influence of chronic omeprazole treatment on gastric endocrine function (1987)
    Springer
    Journal of molecular medicine 65 (1987), S. 169-173 
    Details
    ISSN: 1432-1440
    Keywords: Gastrin ; Insulin ; Omeprazole ; Somatostatin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of a 4-week treatment with the substituted benzimidazole omeprazole (20 mg daily) or placebo on gastric endocrine function was tested in healthy male volunteers. Compared with placebo-treated subjects basal serum gastrin levels were slightly but significantly increased after treatment with omeprazole from 10 to 22 pg/ml (medians;P〈0.05) but returned to pretreatment values after 2 weeks recovery (9 pg/ml). Antral gastrin tissue concentration increased and was still elevated after recovery; however, antral gastrin concentrations also increased in placebo controls, and increments immediately after cessation of omeprazole treatment (2.58 µg/g; median) were not significantly over control values (1.92 µg/g;P〉0.1). Postprandial gastrin release, basal and food-stimulated insulin release, antral somatostatin concentration, and volume densities of antral G and D cells were unaffected. It is concluded that, due to incomplete inhibition of gastric acid secretion at the omeprazole dose studied, only slight effects on the endocrine stomach are to be expected after 4 weeks of administration of omeprazole.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01728228
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  • 5
    Electronic Resource
    Electronic Resource
    Effect of starvation on endocrine cells in the rat stomach
    Amsterdam : Elsevier
    Regulatory Peptides 14 (1986), S. 33-39 
    Details
    ISSN: 0167-0115
    Keywords: gastrin ; parietal cells ; rat ; somatostatin ; starvation ; stomach
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0167-0115(86)90203-X
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  • 6
    Electronic Resource
    Electronic Resource
    Elimination of the low-molecular weight proteinase inhibitor camostate (FOY 305) and its degradation products by the rat liver (1987)
    Springer
    Research in experimental medicine 187 (1987), S. 401-406 
    Details
    ISSN: 1433-8580
    Keywords: Camostate (FOY 305) ; Degradation ; Rat liver ; HPLC
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The elimination of the low molecular weight proteinase inhibitor camostate (FOY 305) was studied in rats after oral administration and in the the situ perfused rat liver. After feeding of camostate (400 mg/kg b. w.) only the metabolites (FOY 251, GBA) were detected in blood samples withdrawn from the portal and hepatic vein. This indicated a rapid degradation of FOY 305 after absorption from the gut lumen. The hepatic extraction of the anti-proteolytic active metabolite FOY 251 during a single liver passage was 23%. It remained almost constant over the period of 120 min. In the perfused rat liver, FOY 305 was given in concentrations comparable to the in vivo studies. It was eliminated by 20%. In these experiments, the compound was metabolized to FOY 251 and in minor amounts to guanidino-benzoate (GBA), the latter being an anti-proteolytic ineffective degradation product. In conclusion, a low hepatic extraction of FOY 305 led to pharmacologically effective concentrations of the active metabolite FOY 251 in the circulation after oral ingestion of the proteinase inhibitor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01852177
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  • 7
    Electronic Resource
    Electronic Resource
    Somatostatin-gastrin interactions in the rat stomach (1988)
    Springer
    Research in experimental medicine 188 (1988), S. 115-121 
    Details
    ISSN: 1433-8580
    Keywords: Gastrin ; Rat ; Somatostatin ; Stomach
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Low concentrations of somatostatin and gastrin within or slightly above the range of physiologically circulating levels were perfused in the isolated, vascularly perfused rat stomach preparation. Somatostatin at 10 and 50 pg/ml significantly inhibited acetylcholine-stimulated gastrin secretion by 26% and 45%, respectively, whereas perfusion of 50 and 500 pg/ml exogenous gastrin did not modify gastric somatostatin secretion. Perfusion of somatostatin-antiserum significantly increased gastrin release by 235%. It is concluded that (1) somatostatin is a powerful inhibitor of the gastrin cell under in vitro conditions; the data are in accordance with a concept that endogenous somatostatin could act as a true hormone; (2) the secretory activity of the somatostatin cell is not significantly affected by circulating gastrin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01852267
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  • 8
    Electronic Resource
    Electronic Resource
    Role of circulating catecholamines in the control of pancreatic polypeptide and gastrin release (1989)
    Springer
    Research in experimental medicine 189 (1989), S. 181-187 
    Details
    ISSN: 1433-8580
    Keywords: Catecholamines ; Gastrin ; Man ; Pancreatic polypeptide ; Physical exercise
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of circulating catecholamines on the release of pancreatic polypeptide (PP) and gastrin was studied in volunteers. Physical exercise increased plasma epinephrine by 374 ± 123% and plasma norepinephrine by 167 ± 30%, but plasma PP concentrations remained unchanged during standardized bicycle ergometry. Immediately after cessation of exercise catecholamine levels decreased rapidly, whereas PP concentrations increased by 55%. In a second series, epinephrine infusion (5, 25, and 75 ng · kg−1 · min−1) increased epinephrine levels by 38 ± 12, 331 ± 69, and 1229 ± 131%, respectively, whilst norepinephrine was unaffected. Neither during nor after catecholamine infusion PP secretion was affected. Gastrin release increased by a maximum of 85 ± 38% (at epinephrine 75 ng · kg−1 · min−1). It is concluded, that (1) changes in circulating adrenaline do not significantly influence PP secretion in man; (2) the PP increase immediately following physical exercise cannot be attributed to a rapid fall of catecholamine levels; (3) endogenous catecholamines are of minor importance in the control of gastrin secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01852166
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  • 9
    Electronic Resource
    Electronic Resource
    Response of gastric inhibitory polypeptide (GIF) to test meal in chronic pancreatitis — Relationship to endocrine and exocrine insufficiency (1976)
    Springer
    Diabetologia 12 (1976), S. 609-612 
    Details
    ISSN: 1432-0428
    Keywords: GIP ; gastrin ; insulin ; incretin ; chronic pancreatitis ; test meal ; malassimilation of fat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Twenty-nine patients with chronic pancreatitis had a significantly greater IR-GIP response to a test meal than 15 controls. This increased response was not related to the degree of steatorrhoea or glucose intolerance. It was most marked in a group of patients with moderately impaired IRI release and medium steatorrhoea. From this is concluded that the IR-GIP response to a test meal is determined by at least two factors: 1. feedback control via insulin secretion, 2. assimilation of fat. In chronic pancreatitis endocrine insufficiency may induce an exaggerated GIP response and severe exocrine insufficiency may prevent fat induced GIP release. Gastrin is not involved in the different GIP response in patients with chronic pancreatitis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01220638
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  • 10
    Electronic Resource
    Electronic Resource
    Gastric inhibitory polypeptide (GIP), gastrin and insulin: Response to test meal in coeliac disease and after duodeno-pancreatectomy (1976)
    Springer
    Diabetologia 12 (1976), S. 279-286 
    Details
    ISSN: 1432-0428
    Keywords: GIP ; gastrin ; insulin ; incretin ; coeliac disease ; duodeno-pancreatectomy ; chronic pancreatitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The response of serum immunoreactive gastric inhibitory polypeptide (IR-GIP), gastrin (IRG) and insulin (IRI) to a mixed standard meal was measured in 15 controls, 6 patients with coeliac disease, 26 patients with chronic pancreatitis and 6 patients with chronic pancreatitis and partial duodenopancreatectomy (Whipple's procedure). Serum levels of IR-GIP, IRG and IRI were significantly reduced in patients with coeliac disease. The serum glucose increase was significantly smaller only during the first hour after the meal. Since small intestinal GIP- and G-cells are situated mainly in the glands of duodenal and jejunal mucosa their absolute number is not significantly reduced in coeliac disease. It is suggested that the release of IR-GIP and duodenal IRG is influenced by the rate of absorption of nutrients. In patients with chronic pancreatitis the IR-GIP release is significantly greater than in controls, the IRG release normal and the IRI response delayed. After Whipple's procedure the IR-GIP response is increased significantly while the IRG secretion is abolished. This demonstrates that the duodenum is not necessary for GIP release and that pancreatic and jejunal gastrin are without clinical significance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00422096
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