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Cell Regulation Section, Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA

(Requests for offprints should be addressed to K Suzuki; Email: koichis{at}nih.go.jp.)

(K Suzuki is now at Department of Bioregulation, Leprosy Research Center, National Institute of Infectious Diseases, 4-2–1 Aoba-cho, Higashimurayama, Tokyo 189-0002, Japan)
(L D Kohn is now at Ohio University School of Osteopathic Medicine and Edison Biotechnology Institute, Athens, Ohio 45701, USA)

We have shown that thyroglobulin (Tg) is a potent autocrine regulator of thyroid-specific gene expression, and proposed that the accumulated follicular Tg within the colloid is a major factor in determining follicular function. In the present report, we examined the effect of Tg on the action of TSH/cAMP and iodine with special focus on the regulation of basolateral and apical iodide transporters; the sodium/iodide symporter (NIS) and the pendred syndrome gene (PDS) by Tg. We show that expression of NIS and PDS are differentially regulated by Tg concentration and exposure time. In addition, we found that PDS gene was induced by TSH/cAMP and iodide in the presence of Tg. Based on these results, we propose a model for the physiological turnover of follicular function that is dynamically regulated by Tg.

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