Exercise alters myostatin protein expression in sedentary and exercised streptozotocin-diabetic rats.

Daniela Bassi,Angela Merice De Oliveira Leal,Keico Okino Nonaka,Patricia De Godoy Bueno,Heloisa Sobreiro Selistre-Araujo

doi:10.1590/2359-3997000000028

Daniela Bassi, Angela Merice De Oliveira Leal + Show 3 more

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https://doi.org/10.1590/2359-3997000000028

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Abstract

The aim of this study was to analyze the effect of exercise on the pattern of muscle myostatin (MSTN) protein expression in two important metabolic disorders, i.e., obesity and diabetes mellitus. MSTN, is a negative regulator of skeletal muscle mass. We evaluated the effect of exercise on MSTN protein expression in diabetes mellitus and high fat diet-induced obesity. MSTN protein expression in gastrocnemius muscle was analyzed by Western Blot. P < 0.05 was assumed. Exercise induced a significant decrease in glycemia in both diabetic and obese animals. The expression of precursor and processed protein forms of MSTN and the weight of gastrocnemius muscle did not vary in sedentary or exercised obese animals. Diabetes reduced gastrocnemius muscle weight in sedentary animals. However, gastrocnemius muscle weight increased in diabetic exercised animals. Both the precursor and processed forms of muscle MSTN protein were significantly higher in sedentary diabetic rats than in control rats. The precursor form was significantly lower in diabetic exercised animals than in diabetic sedentary animals. However, the processed form did not change. These results demonstrate that exercise can modulate the muscle expression of MSTN protein in diabetic rats and suggest that MSTN may be involved in energy homeostasis.

Highlights

Myostatin (MSTN) or growth and differentiation factor 8 (GDF8) is a member of the transforming growth factor-β (TGFβ) superfamily and has been characterized as a negative regulator of skeletal muscle mass in different [1]
The present results show that the expression of MSTN protein varies in muscle of both sedentary and exercised rats with streptozotocin-induced diabetes, but not in animals with high fat diet-induced obesity
There is evidence suggesting that exercise increases insulin secretion and has a protective effect in STZ-induced diabetes by decreasing oxidative stress and preserving pancreatic beta cell integrity [21,22,23] observed was increasing muscle mass by myostatin inhibition elevates basal metabolic rate dystrophic muscle by myostatin blockade

Summary

Introduction

Myostatin (MSTN) or growth and differentiation factor 8 (GDF8) is a member of the transforming growth factor-β (TGFβ) superfamily and has been characterized as a negative regulator of skeletal muscle mass in different [1]. It is expressed mainly in muscle and in adipose tissue [2]. Following synthesis as a precursor protein, MSTN is processed by proteolysis by the furin family enzymes, with removal of the 24-amino acid signal peptide and generation of an N-terminal propeptide domain and a C-terminal domain These peptides dimerize through disulfide bonds (latent MSTN) and are cleaved again by members of the BMP-1/tolloid family of metalloproteinases. The mature MSTN binds to its cell surface receptors, activin receptor type II or IIb, and activates intracellular members of the SMAD family of signaling proteins, which translocate to the nucleus and regulate transcription of specific genes in association with diverse transcription factors [3,4]

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