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IGF-DES functions through direct activation of the IGF-1 receptor (IGF-1R) tyrosine kinase, bypassing the IGFBP regulatory system that normally sequesters the majority of circulating native IGF-1

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Selenium supplementation could visibly reduce the serum levels of FT3, FT4, and TPOAb in patients with AITD, but no observable effects were detected on the levels of TSH and TGAb [65]