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Thyroid Hormone-Induced Expression of Specific Somatostatin Receptor Subtypes Correlates with Involution of the TtT-97 Murine Thyrotrope Tumor¹

Department of Medicine, Division of Endocrinology, University of Colorado Health Science Center (R.A.J., V.D.S., J.M.D., D.F.G., W.M.W., E.C.R.), Denver, Colorado 80262; Sandoz Pharma (C.B., F.R.), Basel, Switzerland; and the Department of Medicine, Division of Endocrinology, University, of Newcastle-upon-Tyne (R.A.J.), Newcastle-upon-Tyne, United Kingdom

Address all correspondence and requests for reprints to: Dr. William M. Wood, Department of Medicine, Division of Endocrinology, Campus Box B151, University of Colorado Health Science Center, 4200 East Ninth Avenue, Denver, Colorado 80262. E-mail: Andy.James{at}btinternet.com

Following the protracted hypothyroid state, treatment with thyroid hormone will induce a decline in TSH and reduce thyrotrope hyperplasia. Somatostatin is a hypothalamic peptide that has been implicated in the negative regulation of TSH secretion in the thyrotrope. Moreover, analogs of native somatostatin have potent TSH-reducing and growth-retarding effects on human thyrotropinomas. The TtT-97 tumor is an in vivo murine thyrotropic model that has retained its physiological response to thyroid hormone. This study investigates the regulation of somatostatin receptor subtypes in this tumor. TtT-97 tumors, actively growing in hypothyroid mice, did not express any significant somatostatin receptor messenger RNA (mRNA) or protein. T₄ administration resulted in a reduction in TSHß mRNA expression and a marked degree of tumor involution. Analysis of residual tumors from thyroid hormone-treated mice showed the specific up-regulation of SSTR1 and SSTR5 mRNA subtypes and the appearance of abundant, high affinity SSTR receptor-binding sites within the tumor. Thus, the TtT-97 tumor provides a thyrotrope-specific model in which to study the regulation of somatostatin receptor subtypes by thyroid hormone and correlate this expression with both antisecretory and antiproliferative effects.

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