Abnormality in intracellular distribution of .BETA.-adrenergic receptor and impaired respones of .BETA.-adrenergic agonist in cardiomyocytes isolated from streptozocin-induced diabetic rats.
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The number of cell-surface β-adrenergic receptors on cardiomyocytes isolated from diabetic rats, as determined by the hydrophilic ligand [<SUP>3</SUP>H] CGP-12177, decreased significantly to 59% of that in control rats (p<0.01), while the number of total cell β-adrenergic receptors, as determined by the hydrophobic ligand [<SUP>125</SUP>I] ICYP, did not differ between the two groups. Adenylate cyclase activity in cardiac plasma membrane isolated from diabetic rats also decreased significantly to 48% of the control level (p<0.05). Forty-eight hour in vivo insulin treatment improved the decrease in the number of cell-surface β-adrenergic receptors without causing any changes in serum T3 level or urinary catecholamine excretion rate. Insulin, high levels of glucose, and 3-hydroxybutyrate levels did not affect [<SUP>3</SUP>H] CGP-12177 binding to cardiomyocytes. Furthermore, diabetic cardiomyocytes showed significant (p<0.05) impairment in their recovery from agonist-induced down-regulation as compared with the control level.<BR>These results indicate that the decrease in the number of β-adrenergic receptors in cardiac plasma membrane, which is associated with abnormalities in the receptor distribution, played an important role in the cardiac unresponsiveness to a β-adrenergic agonist in diabetic rats. The decrease in the number of receptors in plasma membrane is closely associated with the diabetic state and is reversed by short-term insulin treatment.
- 一般社団法人 日本糖尿病学会の論文
一般社団法人 日本糖尿病学会 | 論文
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