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Endocrinology Vol. 138, No. 9 3624-3629
Copyright © 1997 by The Endocrine Society

ARTICLES

Thyrotropin Regulation by Thyroid Hormone in Thyroid Hormone Receptor ß-Deficient Mice1

Roy E. Weiss, Douglas Forrest2, Joachim Pohlenz3, Kevin Cua, Tom Curran and Samuel Refetoff

Departments of Medicine (R.E.W., J.P., K.C., S.R.) and Pediatrics (J.P., S.R.) and the J. P. Kennedy, Jr. Mental Retardation Research Center (S.R.), The University of Chicago, Chicago, Illinois 60637; Department of Human Genetics (D.F.), Mount Sinai Medical Center, New York, New York 10029; St. Jude Children’s Research Hospital (T.C.), Department of Developmental Neurobiology, Memphis, Tennessee 38105

Address all correspondence and requests for reprints to: Roy E. Weiss, M.D., Ph.D., Thyroid Study Unit, MC 3090, University of Chicago, 5841 South Maryland Avenue, Chicago, Illinois 60637-1470. E-mail: rweiss{at}medicine.bsd.uchicago.edu

Thyroid hormone responsive genes can be both positively and negatively regulated by thyroid hormone. TSH is down-regulated by thyroid hormone and rises during thyroid hormone deprivation. Because both thyroid hormone receptor (TR) {alpha} and ß genes are expressed in the pituitary gland, it is unclear what the relative roles of TR{alpha} and TRß are in TSH regulation. Experiments using over expression of artificial genes have yielded conflicting results. The TRß knock-out mouse that lacks both TRß1 and TRß2 isoforms provides a model to examine the role of these receptors in TSH regulation. TRß deficient (TRß-/-) and wild-type (TRß+/+) mice of the same strain were deprived of thyroid hormone by feeding them a low iodine diet containing propylthiouracil and were then treated with different doses of L-T3 and L-T4. Thyroid hormone deprivation rapidly increased the serum TSH level in both TRß+/+ and TRß-/- mice, reaching a similar level in the absence of thyroid hormone. In contrast, the decline of serum TSH by treatment with both L-T3 and L-T4 was severely blunted in TRß-/- mice, and full suppression was not achieved with the maximal L-T3 dose of 25 µg/day·mouse. These data indicate that TRß is not required for the up-regulation of TSH in thyroid hormone deficiency. However, although TR{alpha} alone can mediate thyroid hormone induced TSH suppression, TRß enhances the sensitivity of TSH down-regulation and may be essential for the complete suppression of TSH.




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