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Endocrinology, Vol 99, 988-995, Copyright © 1976 by Endocrine Society

ARTICLES

Compensatory thyroid hypertrophy after hemithyroidectomy in rats

OH Clark, WR Lambert, RR Cavalieri, B Rapoport, ME Hammond and SH Ingbar

Thyroid enlargement occurs in association with a variety of circumstances characterized by an impaired capacity of the gland to secrete adequate amounts of hormone. To elucidate the factors responsible for such compensatory thyroid growth, particularly the role of TSH, we have observed the response of the serum TSH, T3 and T4 concentrations following hemithyroidectomy in the rat, and have attempted to correlate changes in these functions with changes in the weight and histology of the thyroid remnant. Hemithyroidectomy was performed in male Sprague-Dawley rats weighing 150 to 370 g, sham- operated animals serving as controls. As compared to findings in sham- operated animals, serum T4 concentrations declined promptly after hemithyroidectomy. In Experiment I serum T4 concentrations remained low for about 10 days and then returned to initial values. In Experiment II serum T4 concentrations remained lower than initial T4 values or values found in sham-operated animals until 34 days after hemithyroidectomy. Serum T3 concentrations were not significantly altered after hemithyroidectomy in either group but tended to be lower in the hemithyroidectomized animals. Serum TSH concentrations increased within 3 days after hemithyroidectomy and, for as long as 21 weeks, remained at values higher than those present preoperatively or those seen in sham-operated animals. Thyroid lobe weight increased following removal of the contralateral lobe and this increase was also sustained throughout the duration of the experiments. Biochemical and histological observations indicated that enlargement of the residual lobe was due to hypertrophy rather than hyperplasia.


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S. M. McLachlan, H. Braley-Mullen, C.-R. Chen, H. Aliesky, P. N. Pichurin, and B. Rapoport
Dissociation between Iodide-Induced Thyroiditis and Antibody-Mediated Hyperthyroidism in NOD.H-2h4 Mice
Endocrinology, January 1, 2005; 146(1): 294 - 300.
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