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Stimulation of Creatine Kinase Activity in Rat Organs by Human Growth Hormone in Vivo and in Vitro^*

A. GOLANDER, I. BINDERMAN, A. M. KAYE, A. NIMROD and D. SÖMJEN

Department of Pediatrics, Tel Aviv Medical Center Tel Aviv, 65211, Israel
The Hard Tissues Unit, Tel Aviv Medical Center Tel Aviv, 65211, Israel
Department of Hormone Research, The Weizmann Institute of Science Rehovot 76100, Israel
Biotechnology General Rehovot 76326, Israel

Address all correspondence and reprint requests to: A. Golander, Department of Pediatrics, Tel Aviv Medical Center, Rokach Hospital, P.O. Box 51, Tel Aviv, 65211, Israel.

Abstract

Intraperitoneal injection of human GH (hGH) (4 µg/g BW) into 21-day-old rats causes, 24 h later, an increase in creatine kinase (CK) specific activity in kidney (1.7-fold), liver (1.6-fold), and in epiphyseal cartilage (1.8-fold). Similar stimulation was obtained when tissue explants were incubated for 24 h with hGH (1 µg/ml); CK activity rose 1.8-fold in kidney, 1.9-fold in the liver, and 2.6-fold in epiphyseal cartilage. Highly significant stimulation of CK specific activity was obtained in these same organs in hypophysectomized rats. The increase in CK specific activity in the kidney, to some extent in the liver, but not in the epiphyseal cartilage, was also obtained on in vivo treatment with either human placental lactogen or ovine PRL. Stimulation of CK in these three organs by hGH is followed by a parallel increase in DNA synthesis. Dexamethasone, which was also found to increase CK activity in rat kidney and liver, did not affect the increase of CK by hGH in the kidney, stimulated the effect of hGH in the liver, and partially inhibited the effect of hGH in the epiphyseal cartilage. Diethylaminoethyl cellulose chromatography revealed that the basal and induced activity of CK in all cases was due to the brain type isozyme. On the basis of this evidence for a direct effect of hGH on CK brain type activity, we suggest that its stimulation is potentially a convenient and sensitive assay for biological activity of GH. (Endocrinology 118: 1966–1970, 1986)

Footnotes

^* This work was supported in part by a grant from the Rockefeller Foundation, New York.

Incumbent of the Joseph Moss Professorial Chair in Molecular Endocrinology at the Weizmann Institute of Science.

Received August 28, 1985.