Regulation of neonatal heart glycogen metabolism by thyroxine.
We investigated the effect of hyperthyroidism and hypothyroidism on the myocardial glycogen metabolism by quantitating 125I-insulin binding, glycogen content, glycogen synthase and phosphorylase enzyme activities in the newborn rabbit. Although an increase in 125I-insulin binding was observed in response to hyperthyroidism (p less than 0.01), a decrease in myocardial glycogen (p less than 0.01) along with no change in the synthase and phosphorylase enzyme activity was demonstrated. On the other hand, propylthiouracil-induced hypothyroxinemia did not affect the 125I-insulin binding, glycogen content or the two enzyme systems. We conclude that the depletion of myocardial glycogen secondary to hyperthyroidism is independent of an increase in 125I-insulin binding or any change in the major glycogen enzyme activities (synthase and phosphorylase). We speculate that this decline in neonatal heart glycogen may be secondary to thyroxine-induced altered glucose uptake or modified postinsulin receptor events.
D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D003409:Congenital Hypothyroidism; D005260:Female; D005315:Fetal Diseases / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism*; D006980:Hyperthyroidism / Q000151:congenital / Q000378:metabolism; D007037:Hypothyroidism / Q000378:metabolism; D007328:Insulin / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D011247:Pregnancy; D011817:Rabbits; D013963:Thyroid Hormones / Q000097:blood; D013974:Thyroxine / Q000502:physiology*
D001786:Blood Glucose; D007328:Insulin; D013963:Thyroid Hormones; D006003:Glycogen; D013974:Thyroxine