ArticleBone2008
Iodothyronine deiodinase enzyme activities in bone.
Article in Bone, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- American Thyroid Association Guide to investigating thyroid hormone economy and action in rodent and cell models.Thyroid : official journal of the American Thyroid Association · 2014Guideline
- Spectrum and functions of ion channels and transporters in osteoclasts.Bone research · 2026Review
- The influence of hormonal changes during pregnancy on bone metabolism - a mini review.Frontiers in endocrinology · 2026Review
- Correlation between thyroid sensitivity indices and bone metabolism in newly diagnosed middle aged and elderly patients with type 2 diabetes mellitus with normal thyroid function.BMC endocrine disorders · 2025Article
- Hyperthyroidism-driven bone loss depends on BMP receptor Bmpr1a expression in osteoblasts.Communications biology · 2024Article
- How does Hashimoto's thyroiditis affect bone metabolism?Reviews in endocrine & metabolic disorders · 2023Review
- Optimizing Growth: The Case for Iodine.Nutrients · 2023Review
- Endocrine Regulation on Bone by Thyroid.Frontiers in endocrinology · 2022Review
- T4 rather than TSH correlates with BMD among euthyroid adults.Frontiers in endocrinology · 2022Article
- Cochlear Fibrocyte and Osteoblast Lineages Expressing Type 2 Deiodinase Identified with a Dio2CreERt2 Allele.Endocrinology · 2021Article
- Thyroid Hormone Deiodinases: Dynamic Switches in Developmental Transitions.Endocrinology · 2021Review
- Influence of Low Total Triiodothyronine Levels on Bone Turnover Markers in Type 2 Diabetes Mellitus.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Role of thyroid hormones in craniofacial development.Nature reviews. Endocrinology · 2020Review
- Skeletal Effects of Early-Life Exposure to Soy Isoflavones-A Review of Evidence From Rodent Models.Frontiers in pediatrics · 2020Review
- Association between dietary selenium intake and the prevalence of osteoporosis: a cross-sectional study.BMC musculoskeletal disorders · 2019Article
- Paradigms of Dynamic Control of Thyroid Hormone Signaling.Endocrine reviews · 2019Review
- Thyroid Mediation of the Isoflavone Effects on Osteoporotic Bone: The Endocrine Interference With a Beneficial Outcome.Frontiers in endocrinology · 2019Article
- Abnormal Thyroid Hormone Status Differentially Affects Bone Mass Accrual and Bone Strength in C3H/HeJ Mice: A Mouse Model of Type I Deiodinase Deficiency.Frontiers in endocrinology · 2019Article
- Review
- Thyroid Hormone Signaling in the Development of the Endochondral Skeleton.Vitamins and hormones · 2018Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Euthyroid status is essential for normal skeletal development and maintenance of the adult skeleton, but the mechanisms which control supply of thyroid hormone to bone cells are poorly understood. Thyroid hormones enter target cells via monocarboxylate transporter-8 (MCT8), which provides a functional link between thyroid hormone uptake and metabolism in the regulation of T3-action but has not been investigated in bone. Most circulating active thyroid hormone (T3) is derived from outer ring deiodination of thyroxine (T4) mediated by the type 1 deiodinase enzyme (D1). The D2 isozyme regulates intra-cellular T3 supply and determines saturation of the nuclear T3-receptor (TR), whereas a third enzyme (D3) inactivates T4 and T3 to prevent hormone availability and reduce TR-saturation. The aim of this study was to determine whether MCT8 is expressed in the skeleton and whether chondrocytes, osteoblasts and osteoclasts express functional deiodinases. Gene expression was analyzed by RT-PCR and D1, D2 and D3 function by sensitive and highly specific determination of enzyme activities. MCT8 mRNA was expressed in chondrocytes, osteoblasts and osteoclasts at all stages of cell differentiation. D1 activity was undetectable in all cell types, D2 activity was only present in mature osteoblasts whereas D3 activity was evident throughout chondrocyte, osteoblast and osteoclast differentiation in primary cell cultures. These data suggest that T3 availability especially during skeletal development may be limited by D3-mediated catabolism rather than by MCT8 mediated cellular uptake or D2-dependent T3 production.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.