Iodine
Iodine was one of the first miconutrients to be recognized as vital to nutrition, and it is still considered one of the most important.
Metabolism and function of iodine and thyroid activity
Before surveys were made of the iodine content of soil, it had been noted that the disease of common goiter was unevenly distributed over the United States and that it seemed to be most prevalent in the regions where there was the least iodine. This early suspicion was confirmed, and we now recognize that common goiter is primarily an iodine deficiency disease.
An essential constituent of the thyroid gland in humans and in animals, iodine in sufficient quantity must be suppliect if that gland is to synthesize enough of the hormones thyroxine (T4) and triiodothyronine (T3) to function normally.
Dietary iodine is absorbed from the gastrointestinal tract as iodide 0) and is rapidly distributed throughout the extracellular fluid. Approximately one-third of the absorbed iodide is removed by the thyroid gland, and the remaindrr is excreted in the urine. There is no renal conservation of iodine in response to low intake, but the thyroid gland can recycle some of its iodine supply and, if needed, the iodide released from other tissues from degradation of the thyroid hormones. Of the estimated 25 mg of iodine in an adult, 10 mg to 15 mg is found in the thyroid in thyroglobulin, an iodinated glycoprotein, which serves as a reserve of the thyroid hormones.
Iodide is taken up by an energy-dependent process into the epithelial cells that surround the colloid-filled follicles of the gland where it immediately enters the pathway of thyroid hormone synthesis. After undergoing an oxidative activation, iodide is incorporated into tyrosine residues of thyroglobulin to form mono- and diiodotprosille, then these compounds are coupled to complete the synthesis of thyroxine and triiodothyronine. The iodinated thyroglobulin is stored in the follicular colloid and, when needed, the hormones are released through proteolytic degradation of thyroglobulin by lysosomal enzymes of the follicular cells. The remaining iodinated tyrosine residues undergo enzymatic deiodination, and e liberated iodide is reused for hormone synthesis. Thyroid activity is controlled by the thyroid-stimulating horne (TSH) of the anterior pituitary. When the level of lating thyroid hormones declines, a hypothalamic ,Totropin-releasing factor (TRF) stimulates the release of (TSH), which, in turn, signals the thyroid gland to inease its activity. When iodine supply is not adequate to maintain normal synthesis of thyroid hormones, continuous thyrotropic stimulation to both hypertrophy and hyperplasia ofthe follicular - in an attempt to produce more hormone. The resulting enlargement of the thyroid gland is known as simple goiter.
T4 and T3 are transported in plasma by two specific port proteins, thyroxine-binding globulin and thyroxine-binding prealbumin. This protein-bound iodine (PEI) appears to serve as a plasma reserve for the much er fractions of active T4 and T3, which circulate freely. The level of T3 is small compared to that ofT4, but the: latter is deiodinated by tissues to form both active T3 d its inactive isomer, known as reverse T3. Triiodothyronine thyronine is the more potent of the two hormones and may be the major functioning thyroid hormone in the tissues.
Iodine itself has no known metabolic function, but effects of the thyroid hormones are many, although not well characterized. The thyroid hormones regulate metabolic rate of the body through their effect on the oxidative reactions; hyper- and hypothyroidism are reed in high or low basal metabolic rates, respectively. At high concentrations, the overall effects of thyroid hormones are catabolic, whereas in moderate tration they are anabolic. They are essential for normal tissue growth and differentiation. Protein synthesis is facilitated both at the nuclear level by increased synthesis of RNA and at the ribosomal level by stimulation of the translation process. Administration of thyroxine stimulates the intestinal absorption of glucose and the level of cholesterol in the blood.
Severe thyroid hormone deficiency in adults can lead myxedema, which is associated with distinct bodily and facial changes. Thyroid insufficiency during fetal development may cause cretinism, which is characterized by retarded physical and mental development.
