Effect of Eight Weeks of High-Intensity Interval Swimming on Visceral Adipose Tissue Asprosin and Serum Adiponectin in Rats with High-Fat Diet-Induced Non-Alcoholic Steatohepatitis

Abstract

Background and purpose: Non-alcoholic fatty liver disease (NAFLD) is one of the most common metabolic diseases worldwide. Asprosin has been identified as a novel adipokine closely associated with hepatic glucose metabolism, but limited information is available regarding its role and the effect of exercise on it. Insulin resistance is a key factor in the pathogenesis of NAFLD, particularly in non-alcoholic steatohepatitis (NASH). Adiponectin, the most abundant fat-specific adipokine, plays a crucial role in reducing hepatic and systemic insulin resistance, as well as liver inflammation and fibrosis. Adiponectin levels are predictive of the degree of steatosis and the severity of NASH. While there is no proven pharmacological treatment for NASH, recent therapeutic strategies have focused on indirectly regulating adiponectin through the administration of various therapeutic agents and/or lifestyle modifications. Therefore, the aim of the present study was to examine the effect of eight weeks of high-intensity intermittent swimming training on visceral adipose tissue asprosin protein and serum adiponectin in rats with NASH induced by a high-fat diet. Materials and methods: Forty male Sprague-Dawley rats were divided into two groups: diseased (high-fat diet) (N=20) and healthy (N=20). For eight weeks, the diseased group received a high-fat diet in the form of a daily emulsion (10 ml/kg) via gavage, while the healthy group received an equivalent amount of saline solution. After eight weeks, and confirmation of the disease, the rats were further divided into four subgroups: healthy-control (N=9), healthy-swimming (N=9), diseased-control (N=9), and diseased-swimming (N=9). The swimming groups performed a high-intensity swimming interval training protocol three times per week for eight weeks, while the high-fat diet continued for the diseased groups throughout the training period. At the end of the study, serum adiponectin levels were measured using the ELISA method, and asprosin protein levels in visceral adipose tissue were measured using western blotting. The Shapiro-Wilk test was used to confirm the normality of the data distribution, and one-way ANOVA was used to compare group differences. If significant, Bonferroni's post hoc test was applied to identify pairwise differences. All statistical analyses were performed using SPSS version 26, with a significance level of P<0.05. Results: The findings showed a significant increase in serum adiponectin levels in the diseased-swimming group compared to the diseased-control group (P= 0.022). A significant increase in serum adiponectin was also observed in the healthy-swimming group compared to the healthy-control group (P= 0.008). In terms of asprosin protein levels in visceral adipose tissue, a significant decrease was found in the healthy-swimming group compared to the diseased-control group (P= 0.001). In the diseased-swimming group, asprosin protein levels decreased compared to the diseased-control group, but this reduction was not statistically significant (P= 0.946). Conclusion: In conclusion, despite the continuous consumption of a high-fat diet in the diseased group, high-intensity interval swimming exercises were able to improve two key markers of NASH: increasing adiponectin levels and decreasing asprosin levels. These changes suggest that such exercises could potentially reduce inflammation and insulin resistance in NASH. However, as this research is among the first to examine the effects of high-intensity interval swimming on these two variables in a progressive NASH model, further research is required to draw definitive conclusions.

Keywords

• non-alcoholic steatohepatitis
• exercise
• adiponectin
• asprosin
• insulin resistance