Resistance Exercise Regulates Hepatic Lipolytic Factors as Effective as Aerobic Exercise in Obese Mice

Ju Yong Bae

doi:10.3390/ijerph17228307

Abstract

Non-alcoholic fatty liver disease (NAFLD) is associated with obesity. The effect of resistance exercise without dietary restriction on the regulation of hepatic lipolytic factors is unclear. This study aimed to analyze the effects of aerobic and resistance exercise on hepatic lipolytic factors of obese mice. High-fat diet (HFD)-induced obese mice were divided into HFD + sedentary (HF), HFD + aerobic exercise, and HFD + resistance exercise groups. Exercise group mice were subjected to treadmill or ladder climbing exercise for 8 weeks. Fat mass and liver triglycerides were significantly decreased in both aerobic and resistance training groups. In the results of protein levels related to hepatic steatosis, HFD significantly increased liver cannabinoid receptor 1 and sterol-regulatory element binding protein 1 (SREBP-1). Both aerobic and resistance training significantly (p < 0.05) increased liver carnitine palmitoyltransferase-1, phosphor-AMP-activated protein kinase (p-AMPK), and p-AMPK/AMPK and decreased liver SREBP-1. However, the type of exercise did not exert any significant effects on these protein levels. Thus, resistance exercise, similarly to aerobic exercise, effectively regulated hepatic lipolytic factors of obese mice. Therefore, a sustainable type of exercise selected based on the fitness level, disease type, musculoskeletal disorder status, and preference of the patients is the best exercise intervention for alleviating NAFLD.

Highlights

Consumption of a chronic high-fat diet (HFD) increases body weight and fat mass, which is a well-known powerful factor of obesity
Obesity was induced in the HFD + sedentary (HF) group mice by the HFD, as shown by the significant increase in in the HF
Body weight was significantly higher in the HF group than in the CO

Summary

Introduction

Consumption of a chronic high-fat diet (HFD) increases body weight and fat mass, which is a well-known powerful factor of obesity. Excess nutrients from dietary intake are stored in the form of lipid droplets in adipose tissue, but if the storage capacity of adipose tissue is exceeded, increased fat accumulation occurs in other tissues, including the liver, muscle, and heart [1,2]. Excessive lipid accumulation in non-adipose tissues can lead to cellular dysfunction, lipotoxicity, and cell death [3]. Non-alcoholic fatty liver disease (NAFLD) is closely associated with obesity [4] and has currently emerged as the most common chronic liver disease [5]. Even though hepatocellular carcinoma and end-stage liver disease, which are secondary to NAFLD, rarely occur, NAFLD has shown a rising trend in prevalence [7] and an increase in mortality [8]

Objectives

Methods

Results

Conclusion