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Am J Physiol Endocrinol Metab 257: E127-E132, 1989;
0193-1849/89 $5.00
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AJP - Endocrinology and Metabolism, Vol 257, Issue 2 E127-E132, Copyright © 1989 by American Physiological Society

ARTICLES

Plasma membrane-specific deficiency in cardiac beta-adrenergic receptor in streptozocin-diabetic rats

A. Kashiwagi, Y. Nishio, Y. Saeki, Y. Kida, M. Kodama and Y. Shigeta
Third Department of Medicine, Shiga University of Medical Science, Japan.

Cell surface [3H]CGP 12177 binding sites in 10-wk streptozocin-diabetic rats decreased by 41% (P less than 0.01) compared with that in the control rats. In contrast, there was no difference in the total cell receptor concentration between the control and the diabetic rats, which was measured by hydrophobic antagonist [125I]-iodocyanopindolol binding. Forty-eight-hour in vivo insulin treatment significantly (P less than 0.05) increased cell surface beta-adrenergic receptor concentration by 37% above that in diabetic rats without any change in total receptor concentration in the cells. However in vitro treatment of 8 nM insulin, 33 mM glucose, or 10 mM 3-hydroxybutyrate for 2 h showed no effect on [3H]CGP 12177 binding. In contrast, 10 microM isoproterenol-dependent decrease and the recovery of cell surface receptors after the removal of the agonist were significantly (P less than 0.01) impaired in diabetic rats compared with those of control rats. These results indicate that only cell surface beta-adrenergic receptors decrease in diabetic rats, which may be associated with abnormalities in the receptor distribution. The decrease in cell surface receptor number closely associates with the diabetic state and is reversed by the short-term insulin treatment.


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