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Thyroid Hormone Is Essential for Pituitary Somatotropes and Lactotropes¹

Department of Human Genetics, University of Michigan Medical School (J.H.S., S.K.K., M.L.B., T.L.G., D.E.W.-C., S.A.C.), Ann Arbor, Michigan 48109; the Department of Human Genetics, Mount Sinai School of Medicine (A.C.-B.), New York, New York 10029-6514; and the Department of Laboratory Medicine and Pathology, Mayo Clinic (R.V.L.), Rochester, Minnesota 55905

Address all correspondence and requests for reprints to: Dr. Sally Camper, 4301 MSRB III, 1500 West Medical Center Drive, Department Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan 48109-0638. E-mail: scamper{at}umich.edu

Mice homozygous for a disruption in the -subunit essential for TSH, LH, and FSH activity (Gsu^-/-) exhibit hypothyroidism and hypogonadism similar to that observed in TSH receptor-deficient hypothyroid mice (hyt) and GnRH-deficient hypogonadal mutants (hpg). Although the five major hormone-producing cells of the anterior pituitary are present in Gsu^-/- mice, the relative proportions of each cell type are altered dramatically. Thyrotropes exhibit hypertrophy and hyperplasia, and somatotropes and lactotropes are underrepresented. The size and number of gonadotropes in Gsu mutants are not remarkable in contrast to the hypertrophy characteristic of gonadectomized animals. The reduction in lactotropes is more severe in Gsu mutants (13-fold relative to wild-type) than in hyt or hpg mutants (4.5- and 1.5-fold, respectively). In addition, T₄ replacement therapy of Gsu mutants restores lactotropes to near-normal levels, illustrating the importance of T₄, but not -subunit, for lactotrope proliferation and function. T₄ replacement is permissive for gonadotrope hypertrophy in Gsu mutants, consistent with the role for T₄ in the function of gonadotropes. This study reveals the importance of thyroid hormone in developing the appropriate proportions of anterior pituitary cell types.

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