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Spared bone mass in rats treated with thyroid hormone receptor TR beta-selective compound GC-1
Fatima R S Freitas1, Anselmo S Moriscot, Vanda Jorgetti
1Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, 05508-900, Brazil.
American Journal of Physiology. Endocrinology and Metabolism
|September 11, 2003
Summary
Thyroid hormone receptor-beta (TR beta) selective activation does not cause bone loss. This suggests TR beta is not critical for triiodothyronine (T3)-induced osteopenia, offering hope for bone-sparing therapies.
Area of Science:
- Endocrinology
- Bone Biology
- Pharmacology
Background:
- Thyrotoxicosis is linked to increased bone turnover and reduced bone mass.
- Thyroid hormone receptor-beta (TR beta) is a potential mediator of these effects.
Purpose of the Study:
- To investigate the role of TR beta in mediating triiodothyronine (T3)-induced bone loss.
- To evaluate the effects of a TR beta-selective thyromimetic compound on bone mass.
Main Methods:
- Adult female rats were treated with GC-1 (TR beta-selective), T3, or a control.
- Bone mineral density (BMD) was assessed using dual-energy X-ray absorptiometry.
- Histomorphometry of the distal femur was performed.
Main Results:
- T3 treatment significantly reduced BMD (10-15%) and trabecular bone in the femur.
- GC-1 treatment did not affect BMD or trabecular bone.
- GC-1 effectively reduced TSH and cholesterol levels, confirming its thyromimetic efficacy.
Conclusions:
- Selective TR beta activation does not induce the bone loss associated with thyrotoxicosis.
- TR beta is not critical for T3-induced osteopenia.
- TR-selective T3 analogs may offer improved long-term TSH-suppressive therapy with bone preservation.