Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Induction of the fed pattern of human exocrine pancreatic secretion by nutrients: role of cholecystokinin and neurotensin (1992)
    Springer
    Journal of molecular medicine 70 (1992), S. 902-908 
    Details
    ISSN: 1432-1440
    Keywords: Cholecystokinin ; Gastrointestinal hormones ; Human ; Interdigestive pattern ; Fed pattern ; Pancreatic secretion ; Neurotensin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of the present study was to assess the role of cholecystokinin and neurotensin in converting the cyclical interdigestive pattern of pancreatic secretion into the non-cyclical fed pattern. Six healthy male volunteers were studied on 4 separate days. During each experiment a mixed liquid meal or solutions of individual nutrients were perfused intraduodenally for 180 min at 2 ml/min. The mixed meal contained 4.3 g glucose, 2.0 g fractionated soya oil, and 1.7 g casein hydrolysate per 100 ml, which delivered a caloric load of 0.9 kcal/min into the duodenum. The isocaloric and isotonic solutions of individual nutrients contained 44.5 g glucose, 17.8 g fractionated soya oil, or 44.5 g hydrolysed serum bovine albumin per liter and delivered 0.36 kcal/min into the duodenum. Duodenal aspirates and blood samples were collected at regular intervals for determination of pancreatic enzyme outputs and plasma levels of cholecystokinin and neurotensin, respectively. The mixed meal converted the cyclical interdigestive secretory pattern into the noncyclical fed pattern whereas none of the three individual nutrients abolished the interdigestive pattern. Not only the mixed meal but also lipid and protein perfusion consistently stimulated cholecystokinin release. Integrated incremental cholecystokinin release amounted to 32.3±9.9 pg/ml × 180 min with the mixed meal, 23.2±6.5 with lipid perfusion (P〈 0.05 versus mixed meal) and 13.4±3.8 with protein perfusion (P〈0.05 versus mixed meal). The carbohydrate solution did not significantly release cholecystokinin. None of the duodenal perfusates raised neurotensin plasma levels. We conclude that (a) intraduodenal delivery of a mixed meal at 0.9 kcal/min converts the interdigestive pattern of pancreatic secretion, (b) cholecystokinin but not neurotensin is involved in converting this pattern in response to low-caloric meals, and (c) a threshold amount of CCK release must be exceeded to convert the secretory pattern.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00180436
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    General and selective inhibition of pancreatic enzyme discharge using a proteinase inhibitor (FOY-305) (1984)
    Springer
    Journal of molecular medicine 62 (1984), S. 406-411 
    Details
    ISSN: 1432-1440
    Keywords: Pancreatic secretion ; Intracellular transport ; Proteinase inhibitor ; Two-dimensional gel electrophoresis ; FOY-305
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The guanidino acid esters (FOY, FOY-305) represent a new class of potent proteinase inhibitors and are thought to have a beneficial effect on the course of acute pancreatitis. Because of their structure and low molecular size they might enter cells and interfere with cellular processes. To test this possibility in the case of the exocrine pancreas a series of in vivo and in vitro studies was carried out to analyse intracellular transport and discharge of pancreatic enzymes in the presence of FOY-305. The infusion of FOY-305 to conscious rats led to a transient inhibition of protein and enzyme discharge from the cannulated pancreas accompanied by lower serum enzyme levels and increased enzyme content in the pancreas. An identical inhibition of discharge of newly synthesized proteins was observed in vitro in the presence of 1 µM FOY-305. The analysis of the release of individual enzymes using separation on two-dimensional gels showed a pronounced inhibition of mainly the release of acidic proteins. FOY-305 not only interfered with discharge of serine proteinases (trypsinogen, chymotrypsinogen, proelastase) but also with procarboxypeptidases and lipase. It was concluded that FOY-305 enters the acinar cell and due to an unspecific binding to acidic proteins interferes with the intracellular transport of individual enzyme proteins during their passage through the membrane-bound cellular compartments. This charge-dependent effect is independent of the inhibitory effect on enzymatic activity of serine proteinases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01742297
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...