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  • 1975-1979  (3)
  • insulin release  (3)
  • glucose  (1)
  • 1
    ISSN: 1432-0428
    Keywords: Isolated islets ; insulin release ; glucagon ; glucose ; cyclic adenosine monophosphate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Glucose stimulation increased the cAMP content of collagenase-isolated rat pancreatic islets fourfold above baseline values. The elevation was transient, lasting about 5 min, and was dose-dependent. Insulin release continued at a constant rate throughout the incubation. — Glucagon, in the absence of glucose, increased cAMP for about 1 min, but only slightly, and had no effect on insulin release. In the presence of glucose, however, glucagon enhanced islet cAMP content 15-fold and increased the release of insulin. Glucagon was most effective at high glucose concentrations (16.6 and 25 mM). — This indicates that glucagon is critically dependent on the presence of glucose in order to increase the islet cAMP content and to stimulate insulin release. The inability of glucagon to generate sufficient cAMP in the absence of glucose might be one of the reasons why the hormone is a potentiator rather than an initiator of insulin release.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Islet hyperplasia ; islet DNA ; islet protein ; insulin release ; tolbutamide treatment ; theophylline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Following prolonged administration of tolbutamide the DNA- and protein content per islet was enhanced but the IRI content per islet was diminished. Glucose-induced (2.0,8.0 or 16.6 mM) and leucine-induced (12.5 or 25.0 mM) IRI release from isolated islets, as well as 14CO2-production from U-14C glucose, were decreased. Theophylline (5.0 mM) restored the glucose sensitivity of the islets towards normal. The results indicate that tolbutamide-induced islet cell hyperplasia does not entail islet hyperfunction, as previously thought. Decreased IRI release may partially be explained by a tolbutamide-induced alteration of the adenylate cyclase/phosphodiesterase system of the B-cell.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Gastric inhibitory polypeptide ; insulin release ; isolated rat islets ; enteroinsular axis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Gastric Inhibitory Polypeptide (GIF; 1 or 10 μg/ml) potentiated glucose-induced (8 or 16.6 mM) insulin (IRI) release from isolated rat pancreatic islets. Basal release was unaffected. The threshold concentration of glucose necessary for GIF to modulate IRI release was between 6 and 8 mM. GIP had no effect on IRI release from islets submitted to a maximal glucose stimulus (25 mM).
    Type of Medium: Electronic Resource
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