Normal men and women were infused with the π-adrenergic receptor stimulator, isoproterenol (isopropylnorepinephrine, Isuprel). At a low dose (2 μg./min.), immunoreactive insulin (IRI) and free fatty acid (FFA) concentrations rose without a measurable change in plasma glucose. The rise in IRI was not blocked by pretreatment with nicotinic acid to prevent FFA mobilization by isoproterenol. Higher doses of isoproterenol (6 μg./min.) caused larger increments of IRI and FFA concentrations but also elevated plasma glucose. All effects of isoproterenol were the β-adrenergic receptor DlocKing agent y propranolol. Propranolol had no effect on glycogenolysis or IRI stimulation by glucagon. It is concluded that isoprotenol inereases IRI levll by direet seimnlation of β-adrenergic receptors. The ability of glucagon to stimulate the pancreatic islet and to elevate IRI appears to be mediated by a different mechanism.
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Original contribution|
March 01 1967
Beta Adrenergic Stimulation of Insulin Release in Man
Daniel Porte, Jr, MD
Daniel Porte, Jr, MD
Department of Medicine, University of Washington School of Medicine, and Veterans Administration Hospital
Seattle, Washington
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Daniel Porte; Beta Adrenergic Stimulation of Insulin Release in Man. Diabetes 1 March 1967; 16 (3): 150–155. https://doi.org/10.2337/diab.16.3.150
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