TY - JOUR AU - Werneck, de Castro JP AU - Fonseca, TL AU - Ueta, CB AU - McAninch, EA AU - Abdalla, S AU - Wittmann, Gábor AU - Lechan, RM AU - Gereben, Balázs AU - Bianco, AC TI - Differences in hypothalamic type 2 deiodinase ubiquitination explain localized sensitivity to thyroxine. JF - JOURNAL OF CLINICAL INVESTIGATION J2 - J CLIN INVEST VL - 125 PY - 2015 IS - 2 SP - 769 EP - 781 PG - 13 SN - 0021-9738 DO - 10.1172/JCI77588 UR - https://m2.mtmt.hu/api/publication/2922923 ID - 2922923 N1 - Division of Endocrinology, Diabetes and Metabolism, University of Miami, School of Medicine, Miami, FL, United States Division of Endocrinology and Metabolism, Rush University, Medical Center, 1653 W. Congress Parkway, 301 Jones, Chicago, IL 60612, United States Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, Tufts Medical Center, Boston, MA, United States Department of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary Cited By :111 Export Date: 2 June 2023 CODEN: JCINA Correspondence Address: Bianco, A.C.; Division of Endocrinology and Metabolism, 1653 W. Congress Parkway, 301 Jones, United States Chemicals/CAS: liothyronine, 6138-47-2, 6893-02-3; thyroxine, 7488-70-2; thyroxine deiodinase, 70712-46-8; tissue extract, 1390-94-9, 8001-49-8, 9007-32-3; iodide peroxidase, 9031-28-1; thyrotropin, 9002-71-5; ubiquitin protein ligase, 134549-57-8; Iodide Peroxidase; iodothyronine deiodinase type II; Thyrotropin; Thyroxine; Ubiquitin-Protein Ligases; Wsb1 protein, mouse Funding details: National Institute of Diabetes and Digestive and Kidney Diseases, NIDDK, R01DK058538, R01DK077148 AB - The current treatment for patients with hypothyroidism is levothyroxine (L-T4) along with normalization of serum thyroid-stimulating hormone (TSH). However, normalization of serum TSH with L-T4 monotherapy results in relatively low serum 3,5,3'-triiodothyronine (T3) and high serum thyroxine/T3 (T4/T3) ratio. In the hypothalamus-pituitary dyad as well as the rest of the brain, the majority of T3 present is generated locally by T4 deiodination via the type 2 deiodinase (D2); this pathway is self-limited by ubiquitination of D2 by the ubiquitin ligase WSB-1. Here, we determined that tissue-specific differences in D2 ubiquitination account for the high T4/T3 serum ratio in adult thyroidectomized (Tx) rats chronically implanted with subcutaneous L-T4 pellets. While L-T4 administration decreased whole-body D2-dependent T4 conversion to T3, D2 activity in the hypothalamus was only minimally affected by L-T4. In vivo studies in mice harboring an astrocyte-specific Wsb1 deletion as well as in vitro analysis of D2 ubiquitination driven by different tissue extracts indicated that D2 ubiquitination in the hypothalamus is relatively less. As a result, in contrast to other D2-expressing tissues, the hypothalamus is wired to have increased sensitivity to T4. These studies reveal that tissue-specific differences in D2 ubiquitination are an inherent property of the TRH/TSH feedback mechanism and indicate that only constant delivery of L-T4 and L-T3 fully normalizes T3-dependent metabolic markers and gene expression profiles in Tx rats. LA - English DB - MTMT ER - TY - JOUR AU - Fonseca, TL AU - Medina, MC AU - Campos, MPO AU - Wittmann, Gábor AU - Werneck-de-Castro, JP AU - Arrojo, e Drigo Rafael AU - Mora-Garzon, ME AU - Ueta, CB AU - Caicedo, A AU - Fekete, Csaba AU - Gereben, Balázs AU - Lechan, RM AU - Bianco, AC TI - Coordination of hypothalamic and pituitary T3 production regulates TSH expression JF - JOURNAL OF CLINICAL INVESTIGATION J2 - J CLIN INVEST VL - 123 PY - 2013 IS - 4 SP - 1492 EP - 1500 PG - 9 SN - 0021-9738 DO - 10.1172/JCI61231 UR - https://m2.mtmt.hu/api/publication/2194586 ID - 2194586 LA - English DB - MTMT ER - TY - JOUR AU - Gereben, Balázs AU - Zavacki, AM AU - Ribich, S AU - Kim, BW AU - Huang, SA AU - Simonides, WS AU - Zeöld, Anikó AU - Bianco, AC TI - Cellular and Molecular Basis of Deiodinase-Regulated Thyroid Hormone Signaling JF - ENDOCRINE REVIEWS J2 - ENDOCR REV VL - 29 PY - 2008 IS - 7 SP - 898 EP - 938 PG - 41 SN - 0163-769X DO - 10.1210/er.2008-0019 UR - https://m2.mtmt.hu/api/publication/109956 ID - 109956 N1 - Laboratory of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, H-1083, Hungary Division of Endocrinology, Diabetes and Hypertension, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, United States Laboratory for Physiology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, Netherlands Division of Endocrinology and Metabolism, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115, United States Division of Endocrinology, Diabetes and Metabolism, University of Miami, Miller School of Medicine, Miami, FL 33136, United States Division of Endocrinology, Diabetes and Metabolism, Dominion Towers, 1400 NW 10th Avenue, Miami, FL 33136, United States Cited By :562 Export Date: 4 February 2022 CODEN: ERVID Correspondence Address: Bianco, A. C.; Division of Endocrinology, Diabetes and Metabolism, 1400 NW 10th Avenue, Miami, FL 33136, United States; email: abianco@deiodinase.org Chemicals/CAS: alanine, 56-41-7, 6898-94-8; iodide peroxidase, 9031-28-1; iodothyronine, 29354-16-3; liothyronine, 6138-47-2, 6893-02-3; protirelin, 24305-27-9; selenocysteine, 3614-08-2; thioredoxin, 52500-60-4; threonine, 36676-50-3, 72-19-5; thyrotropin, 9002-71-5; thyroxine deiodinase, 70712-46-8; Iodide Peroxidase, EC 1.11.1.8; Thyroxine, 7488-70-2; Triiodothyronine, 6893-02-3 Funding details: National Institute of Diabetes and Digestive and Kidney Diseases, NIDDK, F32DK078476, K08DK064643, R01DK058538, R01DK065055, R01DK076099, R01DK076117 AB - The iodothyronine deiodinases initiate or terminate thyroid hormone action, and therefore are critical for the biological effects mediated by thyroid hormone. Over the years research has focused on their role in preserving serum levels of the biologically active molecule triiodothyronine (T3) during iodine deficiency. More recently, a fascinating new role of these enzymes has been unveiled. The activating deiodinase (D2) and the inactivating deiodinase (D3) can locally increase or decrease thyroid hormone signaling in a tissue- and temporal-specific fashion, independently of changes in thyroid hormone serum concentrations. This mechanism is particularly relevant as deiodinase expression can be modulated by a wide variety of endogenous signaling molecules such as sonic hedgehog, NF-kappaB, growth factors, bile acids, HIF-1alpha, as well as a growing number of xenobiotic substances. In light of these findings, it seems clear that deiodinases play a much broader role than once thought, with great ramifications for the control of thyroid hormone signaling during vertebrate development and metamorphosis, as well as injury response, tissue repair, hypothalamic function, and energy homeostasis in adults. LA - English DB - MTMT ER - TY - JOUR AU - Zeöld, Anikó AU - Pormuller, L AU - Dentice, M AU - Harney, JW AU - Curcio, Morelli C AU - Tente, SM AU - Bianco, AC AU - Gereben, Balázs TI - Metabolic instability of type 2 deiodinase is transferable to stable proteins independently of subcellular localization JF - JOURNAL OF BIOLOGICAL CHEMISTRY J2 - J BIOL CHEM VL - 281 PY - 2006 SP - 31538 EP - 31543 PG - 6 SN - 0021-9258 DO - 10.1074/jbc.M604728200 UR - https://m2.mtmt.hu/api/publication/109768 ID - 109768 N1 - Laboratory of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony Street 43, Budapest H-1083, Hungary Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital, Harvard University Medical School, Boston, MA 02115, United States Cited By :37 Export Date: 27 March 2020 CODEN: JBCHA Correspondence Address: Gereben, B.; Laboratory of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony Street 43, Budapest H-1083, Hungary; email: gereben@koki.hu Chemicals/CAS: thyroxine deiodinase, 70712-46-8; Iodide Peroxidase, 1.11.1.8; Membrane Transport Proteins; Symporters; iodothyronine deiodinase type II, 1.11.1.-; sodium-iodide symporter Laboratory of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony Street 43, Budapest H-1083, Hungary Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital, Harvard University Medical School, Boston, MA 02115, United States Cited By :37 Export Date: 28 March 2020 CODEN: JBCHA Correspondence Address: Gereben, B.; Laboratory of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony Street 43, Budapest H-1083, Hungary; email: gereben@koki.hu Chemicals/CAS: thyroxine deiodinase, 70712-46-8; Iodide Peroxidase, 1.11.1.8; Membrane Transport Proteins; Symporters; iodothyronine deiodinase type II, 1.11.1.-; sodium-iodide symporter LA - English DB - MTMT ER - TY - JOUR AU - Dentice, M AU - Bandyopadhyay, A AU - Gereben, Balázs AU - Callebaut, I AU - Christoffolete, MA AU - Kim, BW AU - Nissim, S AU - Mornon, JP AU - Zavacki, AM AU - Zeöld, Anikó AU - Capelo, LP AU - Curcio, Morelli C AU - Ribeiro, R AU - Harney, JW AU - Tabin, CJ AU - Bianco, AC TI - The Hedgehog-inducible ubiquitin ligase subunit WSB-1 modulates thyroid hormone activation and PTHrP secretion in the developing growth plate JF - NATURE CELL BIOLOGY J2 - NAT CELL BIOL VL - 7 PY - 2005 SP - 698 EP - 705 PG - 8 SN - 1465-7392 DO - 10.1038/ncb1272 UR - https://m2.mtmt.hu/api/publication/109594 ID - 109594 N1 - Thyroid Section, Divison of Endocrinology, Diabetes and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, United States Department of Genetics, Harvard Medical School, Boston, MA 02115, United States Laboratory of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083, Hungary Département de Biologie Structurale, LMCP, University Paris 6, Paris 75252 Cedex 05, France Cited By :182 Export Date: 2 June 2023 CODEN: NCBIF Correspondence Address: Bianco, A.C.; Thyroid Section, , Boston, MA 02115, United States; email: abianco@partners.org Chemicals/CAS: thyroxine deiodinase, 70712-46-8; beta-Transducin Repeat-Containing Proteins; elongin; Hedgehog Proteins; Iodide Peroxidase, EC 1.11.1.8; iodothyronine deiodinase type II, EC 1.11.1.-; Parathyroid Hormone-Related Protein; Protein Subunits; Proteins; Thyroid Hormones; Trans-Activators; Transcription Factors; Ubiquitin; Ubiquitin-Protein Ligases, EC 6.3.2.19; WSB1 protein, human; Wsb1 protein, mouse, EC 6.3.2.19 Funding details: National Institutes of Health, NIH Funding details: Fogarty International Center, FIC, R03TW006467 Funding details: National Institute of Diabetes and Digestive and Kidney Diseases, NIDDK, P01DK056246, R01DK058538 Funding text 1: We thank P. R. Larsen, H. Kronenberg and D. Salvatore for helpful insights and comments on the manuscript. This work was supported by DK058538, DK56246 and TW006467 NIH grants. LA - English DB - MTMT ER - TY - JOUR AU - Carvalho, Bianco SD AU - Kim, BW AU - Zhang, JX AU - Harney, JW AU - Ribeiro, RS AU - Gereben, Balázs AU - Bianco, AC AU - Mende, U AU - Larsen, PR TI - Chronic cardiac-specific thyrotoxicosis increases myocardial β adrenergic responsiveness JF - MOLECULAR ENDOCRINOLOGY J2 - MOL ENDOCRINOL VL - 18 PY - 2004 IS - 7 SP - 1840 EP - 1849 PG - 10 SN - 0888-8809 DO - 10.1210/me.2003-0125 UR - https://m2.mtmt.hu/api/publication/109451 ID - 109451 N1 - WoS:hiba:000222259000022 2019-03-09 21:24 első szerző nem egyezik LA - English DB - MTMT ER - TY - JOUR AU - Bianco, AC AU - Salvatore, D AU - Gereben, Balázs AU - Berry, MJ AU - Larsen, PR TI - Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases JF - ENDOCRINE REVIEWS J2 - ENDOCR REV VL - 23 PY - 2002 IS - 1 SP - 38 EP - 89 PG - 52 SN - 0163-769X DO - 10.1210/er.23.1.38 UR - https://m2.mtmt.hu/api/publication/109174 ID - 109174 LA - English DB - MTMT ER - TY - JOUR AU - Lakatos, Péter AU - Földes, János AU - Horváth, Csaba AU - Kiss, L AU - Tatrai, A AU - Takács, István AU - Tarjan, G AU - Stern, P H TI - Serum interleukin-6 and bone metabolism in patients with thyroid function disorders JF - JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM J2 - J CLIN ENDOCR METAB VL - 82 PY - 1997 IS - 1 SP - 78 EP - 81 PG - 4 SN - 0021-972X DO - 10.1210/jcem.82.1.3641 UR - https://m2.mtmt.hu/api/publication/1802122 ID - 1802122 N1 - Összes idézések száma a WoS-ban: 0 1st Department of Medicine, Semmelweis University Medical School, Budapest, H-1083, Hungary Hetenyi Geza County Hospital, Szolnok, H-5000, Hungary Dept. Molec. Pharmacol. Biol. Chem., NW University Medical School, Chicago, IL 60611, United States 1st Department of Medicine, Semmelweis University Medical School, Koranyi 2/A, Budapest, H-1083, Hungary Cited By :72 Export Date: 13 March 2020 CODEN: JCEMA Correspondence Address: Lakatos, P.; 1st Department of Medicine, Semmelweis University Medical School, Koranyi 2/A, Budapest H-1083, Hungary Chemicals/CAS: Amino Acids; deoxypyridinoline, 90032-33-0; Interleukin-6; Osteocalcin, 104982-03-8 AB - To determine the possible involvement of interleukin-6(IL-6) in the bone loss of hyperthyroidism, relationships between thyroid status, biochemical and densitometric parameters of bone metabolism, and IL-6 were studied in female subjects. Patients with hyperthyroidism caused by either toxic nodular goiter or Graves' disease had significantly higher serum IL-6 concentrations than normal controls. Within the control group, serum IL-6 was higher in postmenopausal than in premenopausal women, but this influence of menopausal status was not seen in the hyperthyroid patients. The production of IL-6 by blood mononuclear cells was higher in cells from the hyperthyroid women. Bone turnover was increased in the hyperthyroid patients based on serum osteocalcin and urinary deoxypyridinoline excretion, and the hyperthyroid group also had reduced radius bone mineral content (BMC). A subgroup of hyperthyroid patients who had the lowest BMC (values more than 1 SD below normal age-matched controls) also had serum IL-6 concentrations significantly greater than those of hyperthyroid patients showing less reduction of BMC. The correlations observed in this study support the possibility that IL-6 plays a role in mediating the bone loss that results from excess thyroid hormone. LA - English DB - MTMT ER - TY - JOUR AU - Lakatos, Péter AU - Caplice, M D AU - Khanna, V AU - Stern, P H TI - Thyroid hormones increase insulin-like growth factor I content in the medium of rat bone tissue JF - JOURNAL OF BONE AND MINERAL RESEARCH J2 - J BONE MINER RES VL - 8 PY - 1993 IS - 12 SP - 1475 EP - 1481 PG - 7 SN - 0884-0431 DO - 10.1002/jbmr.5650081210 UR - https://m2.mtmt.hu/api/publication/1802374 ID - 1802374 N1 - Összes idézések száma a WoS-ban: 0 Cited By :44 Export Date: 14 March 2020 Correspondence Address: Stern, P.H.; Department of Pharmacology, Northwestern University Medical School, 303 East Chicago Avenue, Chicago, Illinois, 60611, United States Chemicals/CAS: 3,3',5' triiodothyronine, 5817-39-0, 70-39-3; 3,5 dibromo 3' (2,3 dihydro 3 oxo 6 pyridazinylmethyl)thyronine, 105211-23-2; diiodotyrosine, 66-02-4; liothyronine, 6138-47-2, 6893-02-3; protein, 67254-75-5; somatomedin C, 67763-96-6; thyroxine, 7488-70-2; tiratricol, 51-24-1; 3,3',5-triiodothyroacetic acid, 51-24-1; Culture Media; Insulin-Like Growth Factor I, 67763-96-6; SK&F 94901; Thyroid Hormones; Thyronines; Thyroxine, 7488-70-2; Triiodothyronine, 6893-02-3; Triiodothyronine, Reverse, 5817-39-0; Tumor Necrosis Factor Funding Agency and Grant Number: NIDDK NIH HHSUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK) [R01 DK-45269] Cited By :44 Export Date: 15 March 2020 Correspondence Address: Stern, P.H.; Department of Pharmacology, Northwestern University Medical School, 303 East Chicago Avenue, Chicago, Illinois, 60611, United States Chemicals/CAS: 3,3',5' triiodothyronine, 5817-39-0, 70-39-3; 3,5 dibromo 3' (2,3 dihydro 3 oxo 6 pyridazinylmethyl)thyronine, 105211-23-2; diiodotyrosine, 66-02-4; liothyronine, 6138-47-2, 6893-02-3; protein, 67254-75-5; somatomedin C, 67763-96-6; thyroxine, 7488-70-2; tiratricol, 51-24-1; 3,3',5-triiodothyroacetic acid, 51-24-1; Culture Media; Insulin-Like Growth Factor I, 67763-96-6; SK&F 94901; Thyroid Hormones; Thyronines; Thyroxine, 7488-70-2; Triiodothyronine, 6893-02-3; Triiodothyronine, Reverse, 5817-39-0; Tumor Necrosis Factor AB - The mechanism of action of thyroid hormones on bone is still not clear. At low concentrations, they stimulate bone formation; at high concentrations, they elicit bone resorption in vitro and in vivo. In the present study we investigated the effect of T3 and T4 as well as their active and inactive analogs (TRIAC, SKF L-94901, rT3, and DIT) on the IGF-I and TNF-α content in the medium of UMR-106 rat osteoblastic cells and fetal rat limb bones. In the dose-response studies, a biphasic increase in medium IGF-I was observed in both cells and limb bones, with peak stimulatory concentrations of 10-8 M for T3 and 10-7 M for T4 in both systems. At higher concentrations, at which thyroid hormones elicit bone resorption, the stimulatory effect diminished and finally was no longer detectable. The active analogs TRIAC and SKF L-94901 also enhanced IGF-I release in UMR-106 cells. The inactive compounds rT3 and DIT failed to increase IGF-I in these cultures. The protein content of the cell culture wells exposed to high concentrations of thyroid hormones was similar to those containing low concentrations, indicating that the decrease in IGF-I content at high doses was not due to toxic effects. This was also confirmed by trypan blue exclusion. Time course studies with UMR-106 cells revealed a significant increase in medium IGF-I after 2 days of incubation. No significant further increase was observed after this up to 5 days of culture. In contrast, the medium of limb bone cultures showed a linear increase in IGF-I content up to 7 days of culture. No TNF-α production was observed in either UMR-106 cells or fetal limb bones. Also, no increase in medium TNF-α levels was seen in response to thyroid hormones. Based on our results, we conclude that IGF-I may be responsible for some of the anabolic effects of thyroid hormones in bone tissue, but TNF-α, at least in the models we used, does not play a role in the mediation of thyroid hormone action. LA - English DB - MTMT ER - TY - JOUR AU - Lakatos, Péter AU - Stern, P H TI - Effects of cyclosporins and transforming growth factor β1 on thyroid hormone action in cultured fetal rat limb bones JF - CALCIFIED TISSUE INTERNATIONAL J2 - CALCIFIED TISSUE INT VL - 50 PY - 1992 IS - 2 SP - 123 EP - 128 PG - 6 SN - 0171-967X DO - 10.1007/BF00298788 UR - https://m2.mtmt.hu/api/publication/1802377 ID - 1802377 N1 - Manufacturers: sandoz, United States; sigma, United States; smith kline beecham, United States AB - To study the mechanism of action of thyroid hormones on bone, we examined the effects of immunosuppressive and nonimmunosuppressive cyclosporins, as well as of transforming growth factor β1 (TGFβ1), 17β-estradiol (E2), and dihydroxytestosterone (DHT) on thyroxine (T4)- and triiodothyronine (T3)-stimulated bone resorption in fetal rat limb bones. The immunosuppressive cyclosporins A (CsA) and G (CsG) inhibited thyroid hormone (T4 + T3)-stimulated resorption and β-glucuronidase release into the culture medium, whereas the weak or nonimmunosuppressive cyclosporins D (CsD) and H (CsH) did not show this effect. Increasing the medium calcium concentration reduced the ability of T4 to stimulate 45Ca release, while not significantly affecting the response to CsA. TGFβ1 elicited a biphasic effect when administered together with T4. During the first 3 days of culture, TGFβ1 elicited a small, nonsignificant decrease in released 45Ca; during a subsequent 3 days of culture, it enhanced T4-stimulated bone resorption significantly. These effects differed from those of TGFβ1 on parathormone-stimulated resorption. E2 and DHT did not influence the action of T4 on bone tissue. These results suggest that the mechanism of action of thyroid hormones on bone may involve immune factors, as well. LA - English DB - MTMT ER - TY - JOUR AU - Lakatos, Péter AU - Stern, P H TI - Evidence for direct non-genomic effects of triiodothyronine on bone rudiments in rats: Stimulation of the inositol phosphate second messenger system JF - ACTA ENDOCRINOLOGICA J2 - ACTA ENDOCRINOL VL - 125 PY - 1991 IS - 5 SP - 603 EP - 608 PG - 6 SN - 0001-5598 DO - 10.1530/acta.0.1250603 UR - https://m2.mtmt.hu/api/publication/1802379 ID - 1802379 AB - Thyroid hormones increase cytosolic free calcium by binding to plasma membrane receptors in several tissues. This calcium increase appears to initiate extranuclear effects in these tissues. Increases in cytosolic calcium are often a consequence of stimulation of inositol phosphate second messenger pathway. Several calcemic hormones act via this signal transduction route. Therefore we investigated the effects of the metabolically active T3 and the inactive analogues 3,5-diiodotyrosine and rT3 on the inositol phosphate pathway in fetal rat limb bone cultures prelabeled with [3H]myoinositol. Labelled inositol and inositol phosphates were separated by HPLC. There was a significant increase in the radioactivity in inositol bis- and trisphosphates after 1 min of exposure to 10-7 mol/l T3. Stimulation was also observed at 10-6 mol/l T3, but not at 10-5 mol/l. Time course studies demonstrated a rapid effect of T3 on inositol phosphates within 30 seconds that lasted through 5 min. After 20 min incubation with T3, no increase was observed in inositol mono- and bisphoshates, and a decrease was seen in inositol trisphosphate. Pretreatment with indomethacin prevented these effects of T3. 3,5-diiodothyrosine and rT3 did not affect inositol phosphate metabolism. These results suggest the existence of plasma membrane-associated receptors for T3 in bone, in addition to the nuclear receptors demonstrated previously. The role of these receptors in the effects of thyroid hormones on bone remains to be established. LA - English DB - MTMT ER -