Key result
Hypothyroidism induced in young rats resulted in the persistence of neonatal and embryonic myosin in developing fast and slow muscles up to at least 28 days after birth.
Hypothyroidism in developing rats delays the transition of myosin isozymes, causing persistence of neonatal and embryonic forms and inhibiting adult fast myosin appearance.
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Hypothyroidism may delay myosin maturation in neonates; leaves open relevance to human cardiac development.
Hypothyroidism was induced in young rats by methylthiouracil treatment of pregnant mothers from 18 days of gestation to 4 weeks after birth. Electrophoretic analysis of native myosin isozymes revealed a persistence of neonatal and embryonic myosin in developing fast and slow muscles up to at least 28 days after birth. The appearance of adult fast myosin was inhibited in 28-day old animals, however adult slow myosin was found in the soleus muscle. Immunocytochemical results on the soleus demonstrate a cellular heterogeneity in the response to hypothyroidism. About half fibers have a normal complement of slow myosin and do not contain neonatal myosin. Only the remaining fibers contain the large amounts of neonatal myosin demonstrated by electrophoresis.
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Butler‐Browne et al. (1984) studied Hypothyroidism. Hypothyroidism (induced by methylthiouracil) was evaluated on Myosin isozyme transitions in developing fast and slow muscles. Hypothyroidism induced in young rats resulted in the persistence of neonatal and embryonic myosin in developing fast and slow muscles up to at least 28 days after birth.
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