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Concise Publication Free access | 10.1172/JCI107064
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: JCI | 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: JCI | 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: JCI | PubMed | Google Scholar
Published September 1, 1972 - More info
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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