Abstract
The different pathophysiological mechanisms which influence the formation of specific cardiac proteins are only incompletely understood. Changes in the level of specific cardiac proteins could result for example, from alterations in the hormonal milieu, changes in cardiac substrate consumption, alterations in the level of high energy phosphates and other mechanisms. Recent investigations have shown that the level of one specific group of proteins in the rat heart ventricle, the isozymes of myosin, are markedly influenced by insulin lack,1,2 and hypothyroidism. 3,4 The existence of three myosin isoenzymes in the rat ventricle (myosin V1, V2, V3) has recently been well documented.3-5 In normal rat hearts myosin V1, which has the highest Ca++-activated myosin ATPase activity, predominates, whereas in hypothyroid or diabetic rats myosin V3, which has the lowest myosin ATPase activity, becomes the predominant form.1-4 The hypothyroidism and diabetes-induced myosin V3 predominance results in a decrease in Ca++-activated myosin ATPase activity. A very close correlation between the activity of this enzyme and the maximal velocity of muscle contraction is well established.6’7 In addition a very close correlation exists between high levels of V1 isomyosin and the maximal speed of contraction of rat papillary muscle.8 Administration of physiological doses of thyroid hormone to hypothyroid rats and of insulin to diabetic rats reverts the myosin isoenzyme distribution to the normal pattern.1,2,4
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Dillmann, W.H. (1986). Diabetes Mellitus and Hypothyroidism Induce Changes in Myosin Isoenzyme Distribution in the Rat Heart — Do Alterations in Fuel Flux Mediate These Changes?. In: Brautbar, N. (eds) Myocardial and Skeletal Muscle Bioenergetics. Advances in Experimental Medicine and Biology, vol 194. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5107-8_35
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