Aerobic exercise promotes the expression of ATGL and attenuates inflammation to improve hepatic steatosis via lncRNA SRA

Abstract

The role of aerobic exercise in preventing and improving non-alcoholic fatty liver has been widely established. SRA is a long non-coding RNA, which has received increasing attention due to its important role in lipid metabolism. However, it is unclear whether aerobic exercise can prevent and treat hepatic lipid accumulation via SRA. The mice were randomly divided into four groups as follows, normal control group, normal aerobic exercise group, high-fat diet group (HFD), and high-fat diet plus aerobic exercise (8 weeks, 6 days/week, 18 m/min for 50 min, 6% slope) group (HAE). After 8 weeks, the mice in the HAE group showed significant improvement in hepatic steatosis. Body weight as well as blood TC, LDL-C, and liver TG levels were significantly lower in the HAE group than in the HFD group. Compared with the HFD group, the expression of SRA was markedly suppressed and the expression of ATGL was significantly increased in the HAE group. Additionally, the JNK/P38 signaling was inhibited, the pro-inflammatory factors were down-regulated, and the anti-inflammatory factor was increased. In addition to this, the same results were shown in experiments with overexpression of SRA. The results of this study provided new support for aerobic exercise to improve hepatic lipid metabolism via lncRNA.

Comparison of the Effect of 8- and 12-Week Aerobic Exercise with Calorie Restriction on the Bax and Bcl-2 Expression in Rats with Non-alcoholic Fatty Liver Disease

“…Also, no significant differences were observed between AE and CR and CR+AE groups. Similarly, the findings did not show a considerable difference between the AE12, CR12, CR+AE12 and AE8, CR8, CR+AE8 groups, which was in line with the study results of Fredrickson et al (24), van der Windt et al (25), and Wu et al (26).…”

Physical Activity Protocols in Non-Alcoholic Fatty Liver Disease Management: A Systematic Review of Randomized Clinical Trials and Animal Models

“…A large number of experimental model studies suggest that exercise intervention may reduce the pathological markers of NAFLD, such as lipid droplet size, fibrosis, vesicular steatosis, hepatocellular ballooning, as well as triglycerides, cholesterol, and glycogen content. In addition, physical activity improves insulin signaling, glucose tolerance, LDL-c, and hepatic β-oxidation [23][24][25][26][27]38,47,66]. The best available evidence of exercise-treated mice showed amendment of NAFLD onset and change in lipogenic gene expression.…”

“…An aerobic exercise protocol increased the phosphorylation of AMP-activated protein kinase (AMPK), which plays a major role in the regulation of cellular energy balance and increase in the rate of catabolic pathways [67]. Evidence has shown that increase in lipogenic factors, starting with AMPK, could upregulate hepatic carnitine palmitoyl-CoA transferase 1 (CPT1) and adipose triglyceride lipase (ATGL) [23,26,27]. CPT1 modulates the mitochondrial fatty acid β-oxidation pathway [68] [23,66].…”

“…In addition, hepatocytes also suffer from high lipid deposition by the transferring of free fatty acids from the adipose tissue, which is usually associated with an inflammatory state [27,47]. Furthermore, the deposition of free fatty acids in the mitochondria may induce the production of reactive oxygen species (ROS), tumor necrosis factor-alpha (TNF-α), as well as other pro-inflammatory cytokines associated with hepatic endoplasmic reticulum (ER) stress [69,70].…”