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Effects of Maternal Thyroid Status on Thyroid Hormones and Growth in Congenitally Hypothyroid Goat Fetuses during the Second Half of Gestation¹

Departments of Neurology (P.A.P., M.v.G., F.B.) and Pediatrics (J.J.M.d.V.), Academic Medical Center, University of Amsterdam, Amsterdam; and the Department of Endocrinology, Wilhelmina Children’s Hospital (J.v.D.), Utrecht, The Netherlands

Address all correspondence and requests for reprints to: Dr. F. Baas, Department of Neurology, Academic Medical Center, University of Amsterdam, P.O. Box 22700, 1100 DE Amsterdam, The Netherlands.

Congenital hypothyroidism in Dutch goats is due to a thyroglobulin (TG) synthesis defect that is inherited in an autosomal recessive manner. Minute amounts of mutated TG messenger RNA are translated into glycosylated TG fragments that contain the N-terminal hormonogenic site and are able to form T₄, albeit less efficiently. We analyzed the effects of maternal thyroid status on fetal plasma thyroid hormones and growth during the second half of gestation (E90–E150).

Maternal hypothyroidism, present from midgestation, resulted in decreased brain and cerebellum weights of affected goitrous fetuses, most evident at term gestation (E150). Brain and cerebellum weights of affected fetuses from unaffected mothers were not decreased. T₄ and FT₄ levels in affected fetuses were dependent on the maternal phenotype, as was the degree of enlargement of the goiter at E150. Newborn unaffected lambs from affected mothers had plasma T₄ levels within the normal range.

The present data show that in late gestation, fetal goats have to rely on their own thyroidal T₄ production. The results suggest that affected fetuses are able to maintain sufficiently high T₄ and T₃ levels to prevent severe adverse effects of thyroid hormone deficiency on the brain if maternal iodide supply is adequate, although a possible increased transfer of maternal T₄ to affected fetuses cannot be excluded. Under normal conditions, sufficient amounts of iodine are provided by the efficient iodine metabolism in euthyroid mothers. In affected mothers, much iodine is wasted because the thyroid also iodinates proteins other than the aberrant TG, resulting in insufficient iodine provision of the fetus and, consequently, in severe hypothyroidism.

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