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Department of Human and Animal Physiology, Agricultural University, Wageningen, The Netherlands.
During pregnancy maternal thyroid hormones are of great importance for normal development of the central nervous system of the fetus. Iodine deficiency of the mother carl result in an impaired development of the fetal brain. In large areas of the world iodine intake is moderately low. To study the effects of marginal iodine deficiency (MID) on the production, distribution, and transport of thyroxine (T4) and 3,5,3'-tri-iodothyronine (T3) in nonpregnant and near-term pregnant rats we performed kinetic experiments (three-compartment analysis). Despite unchanged plasma T4 and T3 during MID, the production and plasma clearance rates of T4 decreased 30% (P = 0.01) in MID nonpregnant (MID-C) rats. For T3, the plasma clearance rate was increased 70% (P = 0.046), while the T3 production was more than doubled (P = 0.042) in MID-C rats. In MID near-term pregnant rats T3 production was decreased 20% (P = 0.04). Hepatic deiodinase type I activity increased during MID in both nonpregnant and pregnant rats. It appears that during MID, rats are able to maintain their euthyroid status. The pronounced increase in transport of T4 from plasma to the fast pool observed in pregnant rats on a normal iodine diet did not occur during MID. In conclusion, in rats MID affects maternal thyroid hormone metabolism, thus influencing the availability of maternal T4 for the fetus.
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