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Hypoglycemia and glycogen deficits in fetuses of hypothyroid pregnant rats
Maternal hypothyroidism, when induced by surgical thyroidectomy with parathyroid hormone replacement, results in fewer live fetuses and smaller fetuses at the 22nd day of gestation. The hypothyroid mother shows the ability to mobilize adequate amounts of glucose even at the expense of her own reserves but the supply of glucose to the fetus appears to be impaired. These fetuses have subnormal skeletal muscle and liver glycogen and are severely hypoglycemic. The impaired development of these fetuses may result from alterations of either transplacental carbohydrate transport or placentofetal carbohydrate metabolism.
Maternal hypothyroidism, when induced by surgical thyroidectomy with parathyroid hormone replacement, results in fewer live fetuses and smaller fetuses at the 22nd day of gestation. The hypothyroid mother shows the ability to mobilize adequate amounts of glucose even at the expense of her own reserves but the supply of glucose to the fetus appears to be impaired. These fetuses have subnormal skeletal muscle and liver glycogen and are severely hypoglycemic. The impaired development of these fetuses may result from alterations of either transplacental carbohydrate transport or placentofetal carbohydrate metabolism.
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