Iodine in milk: transport, metabolic implications, and relation to endocrine functions

Abstract

Iodine is an essential constituent of thyroid hormones thyroxine and triiodothyronine, both of which contain the element in a covalently bound form. Other than the thyroid gland which transports iodine for thyroid hormone production, the lactating mammary gland also takes up iodine and secretes it to mother's milk; the first and only source of iodine for thyroid hormone synthesis by the exclusively breastfed newborn. These hormones are crucial for development of the baby's skeleton, muscles and nervous system. In late pregnancy, colostrum contains up to 400 mu g/l of iodide (I-), which is readily available to newborns right after delivery. At postpartum, breastfeeding women excrete an average of 75-200 mu g/l of I- in milk; nearly 20 to 50 times higher than the plasma concentration. The major transporter that concentrates I- in lactating mammary glands is the Na+/I- Symporter (NIS). Functional expression of NIS in mammary alveolar cells initiates at mid-pregnancy, and significantly increases during lactation. In mammary gland cells, NIS dependent I- uptake is controlled by two types of stimuli: from mid-stages to the end of pregnancy it is subjected to developmental signals, but after delivery, breast suckling plays a decisive role in maintaining high levels of functional NIS expression, and concomitant I- secretion to milk. I- uptake in the lactating mammary gland and its excretion to milk were shown to be under control of a concerted action of steroid hormones and lactogenic hormones, such as oxytocin, prolactin, and insulin. I- ingested in milk by the newborn is then absorbed in the stomach and duodenum, and transported to thyrocytes by thyroidal NIS activity under regulatory control of thyroid stimulating hormone. In this chapter, the molecular mechanism of I- excretion to breast milk, its metabolic implications, and its relation to neonatal endocrine functions and neurodevelopment are discussed.