Pituitary Resistance to Thyroxine Action Due to a Defect in the Type 2 Deiodinase
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The first evidence that thyroid function is controlled by a hormone secreted by the pituitary gland was obtained in tadpoles in 1922, when Smith and Smith demonstrated that the atrophic thyroid gland of hypophysectomized tadpoles underwent hypertrophy following administration of bovine anterior pituitary extract (1). Comparable findings in rats were reported in 1926 (2). Five years later, despite the severe limitations posed by the absence of sensitive hormone assays, Aron et al. obtained evidence that the secretion of thyroid-stimulating hormone (TSH) was increased by lack of thyroid hormone and inhibited when thyroid hormone levels were raised (3). These findings strongly suggested that the level of each hormone influenced the rate of secretion of the other. Over the next decade a plethora of studies related to this phenomenon were reported leading Hoskins in 1949 to propose the feed-back hypothesis (4). He emphasized that the system was a homeostatic one which functioned to maintain plasma thyroid hormone levels constant, and he referred to the system as a `hormostae . He also suggested that the level at which thyroid hormone was maintained depended on the ‘setting’ of the pituitary gland, a function which itself may be influenced by environmental factors (4).
KeywordsThyroid Hormone Brown Adipose Tissue D2KO Mouse Iodothyronine Deiodinase Anterior Pituitary Tissue
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