Aerobic Exercise Increases Meteorin-Like Protein in Muscle and Adipose Tissue of Chronic High-Fat Diet-Induced Obese Mice.

Ju Yong Bae

doi:10.1155/2018/6283932

Abstract

Upregulated meteorin-like (Metrnl) protein in peripheral tissues because of exercise-induced increases in intramuscular Metrnl may effectively alleviate obesity by improving metabolism in whole-body tissues. The objective was to analyse the effects of regular treadmill exercise on Metrnl levels in muscle and peripheral tissues of chronic high-fat diet- (HFD-) induced obese mice. Forty-eight-week-old male C57BL/6 mice were first divided equally into normal-diet (CO) and high-fat diet (HF) groups. Following 16 weeks of a HFD, each group was again split equally into control (CO, HF) and training groups (COT, HFT). The HFT group expressed significantly higher phospho-AMP-activated protein kinase (AMPK), AMPK activity, and peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) in muscle tissue than the HF group (p < 0.05). Similar to muscle energy sensing network protein levels, the HFT group also expressed significantly higher muscle, plasma, and adipose tissue Metrnl (p < 0.05). Moreover, regular exercise increased acyl-CoA oxidase 1 (ACOX-1) and monoglyceride lipase (MGL) expression in adipose tissue (p < 0.05) and significantly decreased abdominal fat mass (p < 0.05). This study suggests that exercise-induced muscle Metrnl effectively reduces fat accumulation through the increase of Metrnl in adipose tissue, which may be a therapeutic target for chronic obesity.

Highlights

The risks of a continuous high-fat diet (HFD) and obesity are well established
Thereafter, the CO group was divided into a CO group (푛 = 10) or a normal-diet + training group (COT, 푛 = 10) and the HF group was divided into a HF group (푛 = 10) or a HFD + training group (HFT, 푛 = 10)
In the absence of ATP, for example, during fasting and after exercise, energy metabolism is regulated by increasing the level of muscle energy sensing network proteins that lead to AMPK, Sirtuin 1 (SIRT1), and PGC1훼 expression [15, 16]

Summary

Introduction

The risks of a continuous high-fat diet (HFD) and obesity are well established. the prevalence of obesity is increasing globally [1]. Obesity resulting from a HFD is associated with significant metabolic disturbance and may induce pathology in various organs [4,5,6]. Exercise is one of the most effective treatments to alleviate obesity. Exercise through repeated muscle contraction and relaxation promotes the release of metabolism-related proteins in skeletal muscle. Both aerobic and resistance exercises improve insulin sensitivity [7] by improving insulin action and glucose uptake [8, 9]. Regular exercise may be an effective preventive and therapeutic treatment for metabolic disturbance in HFD-induced obesity through upregulation of metabolism-related proteins, in muscle, and in peripheral tissues

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Conclusion