Abstract

We investigated the therapeutic potential of polymerized anthocyanin (PA) on a nonalcoholic fatty liver disease (NAFLD) model in mice. C57BL/6 mice were fed a high-fat diet (HFD) for 8 weeks to establish the NAFLD mouse model and randomly divided into four groups: control diet (con), NAFLD mice treated with saline (NAFLD), NAFLD mice treated with PA (PA), and NAFLD mice treated with orlistat (Orlistat) for four weeks. Mice were euthanized at the end of the four weeks. Total cholesterol (TC) and triglyceride (TG) levels were estimated, and pathological changes in the liver, white adipose tissue, and signaling pathways related to lipid metabolism were evaluated. Results revealed that the body, liver, and white fat weight of the NAFLD group was significantly increased compared to that of the con group, while that of the PA group showed significant reduction. NAFLD led to an increase in blood lipids in mice (except for HDL). Conversely, PA effectively reduced TC and LDL-C. Compared to the control group, the degree of steatosis in the mice of PA group was decreased. Moreover, PA also regulated the NAFLD signaling pathway. In agreement with improved lipid deposition, PA supplementation inhibited the activation of inflammatory pathways, depressing oxidative stress through increased antioxidant levels, and increasing β-oxidation to inhibit mitochondrial dysfunction. Taken together, our results demonstrate that PA can improve the liver function of NAFLD mice, regulating blood lipids, reducing liver-fat accumulation, and regulating lipid metabolism.

Highlights

  • Accumulating evidence indicates that excessive intake of fat is associated with the risk of developing nonalcoholic fatty liver disease (NAFLD) in humans and animals [1]

  • Our results demonstrate that polymerized anthocyanin (PA) can improve the liver function of NAFLD mice, regulating blood lipids, reducing liver-fat accumulation, and regulating lipid metabolism

  • The impact of PA on body weight and fat composition was evaluated in mice under a high-fat-diet regimen

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Summary

Introduction

Accumulating evidence indicates that excessive intake of fat is associated with the risk of developing nonalcoholic fatty liver disease (NAFLD) in humans and animals [1]. NAFLD is a stress-related liver injury and metabolic disorder characterized by diffuse hepatic steatosis and triglyceride accumulation [2,3], resulting in simple fatty liver, steatohepatitis, and cirrhosis [4]. The global prevalence of NAFLD is approximately 30% [5]. NAFLD causes hepatic-cell steatosis and affects the liver’s metabolic function, it further progresses into cirrhosis and leads to metabolic diseases such as diabetes [7,8]. The occurrence and development of NAFLD can be related to several factors, such as lipid accumulation, inflammatory factors, abnormal expression of adipokines, gut microbiota, genetic

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