IGF-1 receptor deficiency in thyrocytes impairs thyroid hormone secretion and completely inhibits TSH-stimulated goiter
- Authors
- Ock, Sangmi; Ahn, Jihyun; Lee, Seok Hong; Kang, Hyun; Offermanns, Stefan; Ahn, Hwa Young; Jo, Young Suk; Shong, Minho; Cho, Bo Youn; Jo, Daewoong; Abel, E. Dale; Lee, Tae Jin; Park, Woo Jin; Lee, In-Kyu; Kim, Jaetaek
- Issue Date
- Dec-2013
- Publisher
- FEDERATION AMER SOC EXP BIOL
- Keywords
- MCT8; T-4; hypertrophy; proliferation
- Citation
- FASEB JOURNAL, v.27, no.12, pp 4899 - 4908
- Pages
- 10
- Journal Title
- FASEB JOURNAL
- Volume
- 27
- Number
- 12
- Start Page
- 4899
- End Page
- 4908
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/14110
- DOI
- 10.1096/fj.13-231381
- ISSN
- 0892-6638
1530-6860
- Abstract
- 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 (T-4) concentrations were decreased by 30% in concert with a 43% down-regulation of the monocarboxylate transporter 8 (MCT8), which is involved in T-4 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.
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