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  • 1
    ISSN: 1432-0428
    Keywords: C-peptide ; insulin secretion ; effect of insulin ; alloxan-diabetic rats ; C-peptide effect in vivo ; somatostatin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of synthetic rat C-peptide 1 and C-peptide 2 on plasma insulin and blood glucose concentrations in the rat were studied. Infusion of rat C-peptide (500μg·h-1· kg-1) diminished glucose induced increase of plasma insulin by 56% (15.2±0.9 versus 6.6± 0.6 ng/ml, p〈0.01, mean±SEM). Somatostatin infused at a rate of 50 μg·h-1·kg-1 body weight inhibited glucose-induced insulin secretion by 33%. In the presence of a mixture of both C-peptides or somatostatin, blood glucose after intravenous glucose was higher than in the control experiments. In alloxan-diabetic rats, C-peptide (160 μg/kg) significantly increased and prolonged the hypoglycaemic effect of exogenous insulin. It is suggested that C-peptide may not be a biologically inert substance.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Diabetic mice ; isolated perfused pancreas ; high insulin levels ; hyperglucagonemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diabetes mellitus is held to be accompanied by inappropriately high levels of plasma glucagon relative to blood glucose concentrations. This has been interpreted as indicating lack of insulin. To establish glucagon release in presence of high levels of endogenous insulin, the effects of both glucose and arginine were studied in the isolated perfused pancreas of genetically diabetic mice (db/db). Stimulation with glucose 2.75 mM or glucose plus arginine 8.25 mM exhibited a pronounced hyperglucagonemia. Following glucose 8.25 mM, however, there was no depression of glucagon secretion. Despite excessive high levels of endogenous insulin, there was a pattern of rather non-suppressible glucagon release. Lack of insulin per se, therefore, is unlikely to be the sole cause of hyperglucagonemia in this type of genetic animal diabetes mellitus.
    Type of Medium: Electronic Resource
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