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Section on Cell Regulation, Laboratory of Biochemistry and Metabolism, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health Bethesda, Maryland 2089
Address requests for reprints to: Dr. Leonard D. Kohn, Department of Biochemistry/Metabolism, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Building 10, Room 9B13, Bethesda, Maryland 20892.
Abstract
Insulin enhances the ability of TSH to induce iodide uptake in FRTL-5 rat thyroid cells maintained in 5% serum; however, in cells maintained in 0.2% serum, insulin inhibits the ability of TSH to induce iodide uptake. Since the inhibitory action of insulin is duplicated by 100-fold lower concentrations of insulin-like growth factor-I (IGF-I), inhibition appears to be mediated by the IGF-I receptor. Insulin and IGFI inhibit the action of a cAMP analog to induce iodide uptake in a manner identical to TSH, but do not inhibit basal or TSHincreased cAMP levels; inhibition, thus, results from regulation of cAMP signal action rather than cAMP signal generation. Inhibition is associated with a more than 2-fold decrease in the maximum velocity of iodide influx, a less than 15% change in the rate of iodide efflux, and no change in the Km for iodide influx, i.e. inhibition effectively results from a decrease in the number of iodide porters. The inhibitory action of insulin/IGFI is not additive with hydrocortisone, which, under the same conditions, also inhibits TSH- or cAMP-induced iodide porter activity. Actinomycin-D, given 24 h after TSH, superinduces TSH-induced iodide porter activity and abolishes the inhibition by insulin, IGF-I, and/o:r hydrocortisone; a similar paradoxical effect of actinomycin-D under these conditions has been explained by its ability to inhibit the action of a cAMP-induced factor that increases mRNA degradation. The inhibitory actions of insulin, IGF-I, and hydrocortisone on cAMP-induced iodide porter activity contrast with their simultaneous and synergistic stimulation of the transcriptional action of cAMP on DNA and thyroglobulin synthesis under these conditions. (Endocrinology 128: 1136–1143,1991)
Received August 8, 1990.
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