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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 38 (1993), S. 28-32 
    ISSN: 1573-2568
    Keywords: cysteamine ; somatostatin ; insulin ; exocrine pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cysteamine is known to deplete somatostatin from pancreatic D cells. In the isolated perfused rat pancreas we investigated its effects on somatostatin and insulin release as well as exocrine pancreatic secretion in the presence of 16.7 mM glucose and 180 pM CCK-8. At a concentration of 0.1 mM, cysteamine had no significant effect on pancreatic endocrine and exocrine functions. At 10 mM, however, cysteamine released somatostatin (380±70 vs 100±20 fmol/20 min), inhibited insulin output (890±120 vs 13210±3260 μunits/20 min) and reduced exocrine pancreatic secretion (volume: 12±2 vs 20±2 μl/20 min; lipase: 31±3 vs 60±7 units/20 min). We conclude that the complex changes induced by cysteamine are consistent with a physiological role of endogenous somatostatin in the regulation of insulin release. The reduction of exocrine pancreatic secretion, however, was at least in part, if not completely, mediated via the insuloacinar axis rather than a direct effect of cysteamine-released somatostatin on pancreatic acinar cells.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 38 (1993), S. 1537-1542 
    ISSN: 1573-2568
    Keywords: somatostatin ; cysteamine ; pancreas ; insular-acinar axis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cysteamine is known to deplete somatostatin from pancreatic D cells. In the isolated perfused rat pancreas we investigated its effects on somatostatin and glucagon release as well as exocrine pancreatic secretion in the presence of 1.8 mM glucose. Cysteamine, 10 mM, released somatostatin, but had no effect on CCK-stimulated amylase secretion. Arginine-stimulated glucagon release, however, was significantly inhibited by cysteamine. Concomitantly we still observed stimulation of somatostatin secretion, but also a potentiation of CCK-stimulated amylase secretion. Our results are consistent with a role of somatostatin in the regulation of exocrine pancreatic secretion via its effect on pancreatic A and B cells.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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