Thyroid hormones
Thyroid hormones are two hormones produced and released by the thyroid gland, namely triiodothyronine (T) and thyroxine (T). They are tyrosine-based hormones that are primarily responsible for regulation of metabolism. T and T are partially composed of iodine. A deficiency of iodine leads to decreased production of T and T, enlarges the thyroid tissue and will cause the disease known as simple goitre. The major form of thyroid hormone in the blood is thyroxine (T), which has a longer half-life than T. In humans, the ratio of T to T released into the blood is approximately 14:1. T is converted to the active T (three to four times more potent than T) within cells by deiodinases (5'-iodinase). These are further processed by decarboxylation and deiodination to produce iodothyronamine (Ta) and thyronamine (Ta). All three isoforms of the deiodinases are selenium-containing enzymes, thus dietary selenium is essential for T production. Edward Calvin Kendall was responsible for the isolation of thyroxine in 1915.
SOX2
There are three thyroid hormone response elements (TREs) in the region upstream of the Sox2 promoter. This region is known as the enhancer region. Studies have suggested that thyroid hormone (T3) controls Sox2 expression via the enhancer region. The expression of TRα1 (thyroid hormone receptor) is increased in proliferating and migrating neural stem cells. It has therefore been suggested that transcriptional repression of Sox2, mediated by the thyroid hormone signaling axis, allows for neural stem cell commitment and migration from the sub-ventricular zone. A deficiency of thyroid hormone, particularly during the first trimester, will lead to abnormal central nervous system development.
Further supporting this conclusion is the fact that hypothyroidism during fetal development can result in a variety of neurological deficiencies, including cretinism, characterized by stunted physical development and mental retardation.