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Thyrotropin Increases Malic Enzyme Messenger Ribonucleic Acid Levels in Rat FRTL-5 Thyroid Cells

Laboratory of Biochemistry and Metabolism, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health Bethesda, Maryland 20892
Clinical Endocrinology Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health Bethesda, Maryland 20892
CEOS/Dipartimento di Biologia e Patologia Cellulare e Molecolare, University of Naples Naples, Italy

Address requests for reprints to: Dr. Leonard D. Kohn, Laboratory of Biochemistry and Metabolism, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Section of Cell Regulation, Building 10, Room 9B-13, Bethesda, Maryland 20892.

Abstract

The addition of TSH to FRTL-5 thyroid cells induces a 7- to 8-fold increase in the steady state level of malic enzyme [L-malate-NADP⁺ oxidoreductase (decarboxylating); EC 1.1.1.40] mRNA, but does not alter β-actin mRNA levels. Insulin alone or together with TSH has no effect on malic enzyme mRNA. The effect of TSH is not the result of thyroid hormone formation, since the addition of T₃ in the presence or in the absence of TSH and the addition of 5% serum (which includes T₃ and T₄) have no effect. Forskolin (10^–6 M) reproduces the TSH effect, suggesting that cAMP is involved.

Received for publication July 13, 1988. Revision received November 2, 1988. Accepted for publication November 29, 1988.

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