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Concise Publication Free access | 10.1172/JCI107064

Rat liver adenyl cyclase activity in various thyroid states

Judith K. Jones, Faramarz Ismail-Beigi, and Isidore S. Edelman

Cardiovascular Research Institute, University of California School of Medicine, San Francisco, California 94122

Department of Medicine, University of California School of Medicine, San Francisco, California 94122

Department of Biochemistry and Biophysics of the University of California School of Medicine, San Francisco, California 94122

Find articles by Jones, J. in: PubMed | Google Scholar

Cardiovascular Research Institute, University of California School of Medicine, San Francisco, California 94122

Department of Medicine, University of California School of Medicine, San Francisco, California 94122

Department of Biochemistry and Biophysics of the University of California School of Medicine, San Francisco, California 94122

Find articles by Ismail-Beigi, F. in: PubMed | Google Scholar

Cardiovascular Research Institute, University of California School of Medicine, San Francisco, California 94122

Department of Medicine, University of California School of Medicine, San Francisco, California 94122

Department of Biochemistry and Biophysics of the University of California School of Medicine, San Francisco, California 94122

Find articles by Edelman, I. in: PubMed | Google Scholar

Published September 1, 1972 - More info

Published in Volume 51, Issue 9 on September 1, 1972
J Clin Invest. 1972;51(9):2498–2501. https://doi.org/10.1172/JCI107064.
© 1972 The American Society for Clinical Investigation
Published September 1, 1972 - Version history
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Abstract

Thyroidectomized and euthyroid rats were injected with three doses of triiodothyronine (T3) or of the diluent over a 6 day period, and liver homogenates were assayed for basal, epinephrine-stimulated, and NaF-stimulated adenyl cyclase activity. Based on NaF-stimulated levels, total adenyl cyclase activity, expressed per milligram of liver protein, was increased after thyroidectomy. Administration of T3 to either hypothyroid or euthyroid rats, however, had no effect on the NaF-stimulated levels. Basal and epinephrine-stimulated enzyme activities were the same in hypothyroid, euthyroid, and hyperthyroid (euthyroid + T3) liver homogenates. In contrast, injections of T3 in hypothyroid rats increased the activities of basal and epinephrine-stimulated adenyl cyclase. In view of the findings in euthyroid and hyperthyroid liver, it is possible that this effect is transient. In general, no correlation was found between the effects of thyroid hormone on respiration and on adenyl cyclase activity of the rat liver. These results imply that the hepatic thermogenic response to thyroid hormone is not mediated by stimulation of adenyl cyclase activity with the possible exception of the early effects of T3 in the athyroid rat.

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