作者: INDER J. CHOPRA , DAVID H. SOLOMON , USHA CHOPRA , SING YUNG WU , DELBERT A. FISHER
DOI: 10.1016/B978-0-12-571134-0.50018-1
关键词: Triiodothyronine 、 Biochemistry 、 Metabolism 、 Homeostasis 、 Catabolism 、 Metabolic pathway 、 Internal medicine 、 In vitro 、 Hormone 、 Endocrinology 、 Chemistry 、 Thyroid
摘要: Publisher Summary This chapter explores the metabolic pathways of thyroid hormones. In vitro studies have been employed to study nature this peripheral regulatory mechanism and factors that influence its activity. Apart from thyroxine (T4) 3,5,3'-triiodothyronine (T3), several other iodothyronines, including 3,3',5'-triiodothyronine (reverse T3, rT3), 3,3'-diiodothyronine (3,3'-T2), 3',5'-diiodothyronine (3',5'-T2), tetraiodothyroacetic acid (3'-T19 Tetrac), Triac are also present in biological fluids. Conversion T4 T3 rT3 is not a result random monodeiodination but probably two parallel independent processes. most potent catabolic hormone, suggesting inhibition conversion may be defense reaction body various situations where catabolism overactive homeostasis requires contrary force. enzymic nature, tissue sulfhydryl groups essential for The state fetal deficiency caused by relative unavailability rather than outer ring monodeiodinase. Monodeiodination 3,3'-T2 rT3. Iodothyronines metabolized via well-organized sequence or cascade monodeiodinations resulting formation T0. These sequences altered considerably pharmacological agents. This knowledge lead significant improvements treatment hyperthyroidism.