Abstract

Modification of thyroid hormone levels has a profound effect on skeletal muscle differentiation, predominantly through direct regulation involving thyroid hormone receptors. Nevertheless, little is known about the regulation of myostatin gene expression in skeletal muscle due to altered concentrations of thyroid hormone. Thus, the goal of our study was to find out whether altered thyroid states could change the gene expression of myostatin, the most powerful inhibitor of skeletal muscle development. A hyperthyroid state was induced in rats by daily injections of L-thyroxine 20 mg/100 g body weight for 14 days, while a hypothyroid state was induced in another group of rats by administering methimazole (0.04%) in drinking water for 14 days. After a period of 14 days of L-thyroxine treatment we observed a significant increase of myostatin expression both in mRNA and protein level. However, decreased expression of myostatin mRNA and protein were observed in hypothyroid rats. Furthermore, our studies demonstrated that the upregulation of myostatin gene expression might be responsible for the loss of body weight induced by altered thyroid hormone levels. We concluded that myostatin played a role in a metabolic process in muscle that was regulated by thyroid hormone.

Highlights

  • Myostatin (MSTN), previously known as growth differentiation factor-8, is a member of the transforming growth factor superfamily, which is predominantly expressed in skeletal muscle throughout life, from the early stages of embryogenesis to late adulthood (McPherron and Lee, 1997)

  • The effectiveness of T4 treatment was determined by the concentrations of total serum T4 and body weight (BW)

  • The purpose of this study was to measure the effect of different thyroid hormone (TH) levels on the expression of myostatin in skeletal muscle

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Summary

Introduction

Myostatin (MSTN), previously known as growth differentiation factor-8, is a member of the transforming growth factor superfamily, which is predominantly expressed in skeletal muscle throughout life, from the early stages of embryogenesis to late adulthood (McPherron and Lee, 1997). The expression pattern of myostatin suggests that it might play an important role in regulating muscle development or function (McPherron and Lee, 1997). Mice completely lacking myostatin were shown to have dramatic and widespread increases in skeletal muscle mass. Increased myostatin expression has been found in certain physiological conditions in which. The precise processes by which these factors affect skeletal muscle growth or influence myostatin gene expression remain unclear

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