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  • Title: Endocrine studies of the untreated progeny of thyroidectomized rats.
    Author: Bakke JL, Lawrence NL, Robinson S, Bennett J.
    Journal: Pediatr Res; 1975 Sep; 9(9):742-8. PubMed ID: 812049.
    Abstract:
    Experiments were conducted to assess late and persistent endocrine changes in the progeny of rats born and/or nursed by thyroidectomized (Tx) dams. Forty-five female rats were radiothyroidectomized several weeks before mating with normal males, and compared with the progeny of 26 control females. In all, 248 progeny were studied when adult. Tx dams had significantly reduced fertility (87% of controls), increased pup (11% versus 0) and maternal mortality (27% versus 0), and smaller litters (6.5 versus 11.8 pups/litter). It was shown that the offspring of thyroidectomized female rats had delayed eye opening (15.3 versus 14.3 days), smaller weaning (40.4 versus 54.4 g) and adult body weight (230 versus 260 g), smaller pituitary glands (12.2 versus 14.0 mg), and enlarged thyroid gland (14.2 versus 12.4 mg). Ovarian and testicular weight were decreased (73.9 versus 83.7 mg and 3.2 versus 3.6 g, respectively). The serum thyroid stimulating hormone (TSH) concentrations were increased from 53.8 to 84.4 muU/ml in the males. The pituitary TSH contents were not significantly altered, and the serum TSH response to thyrotropin releasing hormone (TRH) was normal. These persistent effects differed from the late effects of both fetal and neonatal hypothyroidism and neonatal underfeeding. Cross-fostering experiments showed that the diminished weaning weights were the result of the pups being nursed by the hypothyroid dams. The increased nursing mortality and the pituitary and thyroidal changes were the result of prenatal influences produced by the hypothyroid dams, since being nursed by a normal foster dam did not prevent them. The persistently enlarged thyroid glands and the elevated serum TSH in the male offspring of thyroidectomized dams suggested a permanent alteration in the set point of pituitary-thyroid regulation as the consequence of maternal hypothyroidism.
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