Role of iodine in thyroid physiology

Abstract

Adequate levels of iodine, a trace element variably distributed on the earth, are required for the synthesis of the thyroid hormones thyroxine (T₄) and triiodothyronine (T₃). The iodide cycle consists of a series of transport, oxidation and coupling steps in thyroid follicular cells to produce thyroid hormone. The sodium/iodide symporter (NIS) transports iodide into the thyrocyte. Competitive inhibitors of NIS, such as perchlorate and thiocyanate, can decrease the entrance of iodide into the follicular cell. Pendrin is the primary protein that is responsible for iodide efflux out of the thyrocyte and into the follicular lumen. T₄ is deiodinated in target tissues to produce the active form of thyroid hormone, T₃, and other metabolites. Exposure to excessive iodine or chronic iodine deficiency may result in various clinical disorders. The Wolff–Chaikoff effect and Jöd-Basedow phenomenon describe mechanisms of thyroid autoregulation and dysregulation, respectively, during iodine excess. Population studies have determined that iodine deficiency exists in approximately 38% of the world’s population, is the leading cause of preventable mental retardation, and is of particular concern to women and their infants. Finally, the unique role of iodine utilization in thyroid physiology has applications in many important clinical areas.

Keywords::

• deiodinase
• iodide
• iodine
• Jöd-Basedow phenomenon
• pendrin physiology
• selenium
• sodium/iodide symporter
• thyroid
• Wolff–Chaikoff effect

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.