Oyster Hydrolysates Attenuate Muscle Atrophy via Regulating Protein Turnover and Mitochondria Biogenesis in C2C12 Cell and Immobilized Mice.

So-Hyun Jeon,Se-Young Choung

doi:10.3390/nu13124385

Abstract

Sarcopenia, also known as skeletal muscle atrophy, is characterized by significant loss of muscle mass and strength. Oyster (Crassostrea gigas) hydrolysates have anti-cancer, antioxidant, and anti-inflammation properties. However, the anti-sarcopenic effect of oyster hydrolysates remains uninvestigated. Therefore, we prepared two different oyster hydrolysates, namely TGPN and PNY. This study aimed to determine the anti-muscle atrophy efficacy and molecular mechanisms of TGPN and PNY on both C2C12 cell lines and mice. In vitro, the TGPN and PNY recovered the dexamethasone-induced reduction in the myotube diameters. In vivo, TGPN and PNY administration not only improved grip strength and exercise endurance, but also attenuated the loss of muscle mass and muscle fiber cross-sectional area. Mechanistically, TGPN and PNY increased the expression of protein synthesis-related protein levels via phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of the rapamycin pathway, and reduced the expression of protein degradation-related protein levels via the PI3K/Akt/forkhead box O pathway. Also, TGPN and PNY stimulated NAD-dependent deacetylase sirtuin-1(SIRT1), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α), nuclear respiratory factor 1,2, mitochondrial transcription factor A, along with mitochondrial DNA content via SIRT1/PGC-1α signaling. These findings suggest oyster hydrolysates could be used as a valuable natural material that inhibits skeletal muscle atrophy via regulating protein turnover and mitochondrial biogenesis.

Highlights

The skeletal muscles, the largest metabolic tissue in the body, significantly contribute to the body’s overall energy balance, and the mitochondria’s oxidative function [1]
TGPN and PNY Protected against Dexamethasone-Induced Muscle Atrophy in C2C12
Two types of oyster hydrolysates (TGPN and PNY) enhanced C2C12 myotube diameter reduced by dexamethasone treatment

Summary

Introduction

The skeletal muscles, the largest metabolic tissue in the body, significantly contribute to the body’s overall energy balance, and the mitochondria’s oxidative function [1]. Sarcopenia, known as skeletal muscle atrophy, is an age-associated condition characterized by the significant loss of muscle mass and function [2,3], and muscle fiber cross-sectional area (CSA), thereby restricting physical activities of affected patients, and reducing their quality of life [4]. Skeletal muscle mass mainly depends on muscle fiber size and protein turnover. Slow-twitch muscle fibers contract slowly, have a high content of mitochondria, and primarily rely on oxidative metabolism as an energy source. Fast-twitch muscle fibers rapidly contract, have a low content of mitochondria [15], and mainly depend on glycolysis metabolism as a source of energy. Atrophic slow-twitch fibers are reduced compared to fast-twitch fibers [19]. The fiber type shifts from slow- to fast-twitching [12]

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