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          Institute: MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut)     Collection: Yearbook_2014     Display Documents



ID: 682170.0, MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut) / Yearbook_2014
IGF-1 receptor deficiency in thyrocytes impairs thyroid hormone secretion and completely inhibits TSH-stimulated goiter
Authors:Ock, S.; Ahn, J.; Lee, S. H.; Kang, H.; Offermanns, S.; Ahn, H. Y.; Jo, Y. S.; Shong, M.; Cho, B. Y.; Jo, D.; Abel, E. D.; Lee, T. J.; Park, W. J.; Lee, I. K.; Kim, J.
Date of Publication (YYYY-MM-DD):2013-12
Journal Abbrev.:FASEB J
Volume:27
Issue / Number:12
Start Page:4899
End Page:4908
Audience:Not Specified
Abstract / Description:Although thyroid-stimulating hormone (TSH) is known to be a major regulator of thyroid hormone biosynthesis and thyroid growth, insulin-like growth factor 1 (IGF-1) is required for mediating thyrocyte growth in concert with TSH in vitro. We generated mice with thyrocyte-selective ablation of IGF-1 receptor (TIGF1RKO) to explore the role of IGF-1 receptor signaling on thyroid function and growth. In 5-wk-old TIGF1RKO mice, serum thyroxine (T4) concentrations were decreased by 30% in concert with a 43% down-regulation of the monocarboxylate transporter 8 (MCT8), which is involved in T4 secretion. Despite a 3.5-fold increase in circulating concentrations of TSH, thyroid architecture and size were normal. Furthermore, thyrocyte area was increased by 40% in WT thyroids after 10 d TSH injection, but this effect was absent in TSH-injected TIGF1RKO mice. WT mice treated with methimazole and sodium perchlorate for 2 or 6 wk exhibited pronounced goiter development (2.0 and 5.4-fold, respectively), but in TIGF1RKO mice, goiter development was completely abrogated. These data reveal an essential role for IGF-1 receptor signaling in the regulation of thyroid function and TSH-stimulated goitrogenesis.
Free Keywords:Animals; Antithyroid Agents/pharmacology; Down-Regulation; Goiter/chemically induced/*metabolism; Membrane Transport Proteins/genetics/metabolism; Methimazole/pharmacology; Mice; Mice, Knockout; Perchlorates/toxicity; Receptor, IGF Type 1/deficiency/*genetics; Sodium Compounds/toxicity; Thyroid Gland/drug effects/metabolism/pathology; Thyrotropin/*metabolism; Thyroxine/*secretion
External Publication Status:published
Document Type:Article
Communicated by:Svea Hümmer
Affiliations:MPI für physiologische und klinische Forschung
Identifiers:ISSN:1530-6860 (Electronic) 0892-6638 (Linking) %R 10.1096/fj.13-231381
URL:http://www.ncbi.nlm.nih.gov/pubmed/23982142
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