Abstract

Non-alcoholic fatty liver disease (NAFLD) is a common metabolic disorder that causes excess lipid accumulation in the liver and is the leading cause of end-stage liver disease. Liriope platyphylla is a medicinal herb that has long been used to treat cough, obesity, and diabetes. However, the effect of Liriope platyphylla on NAFLD has not been studied. The aim of this study was to investigate the effect of Liriope platyphylla root ethanolic extract (LPE) on hepatic lipid accumulation in high-fat diet (HFD)-induced obese mice. Six-week-old C57BL/6 male mice were fed a HFD for 8 weeks and then treated with LPE (100 or 250 mg/kg/day) by oral gavage for another 8 weeks. Body weight gain and liver weight were significantly lower in the 250 mg/kg LPE-treated HFD group than in the vehicle-treated HFD group. Histological analysis of liver sections demonstrated that LPE treatment reduced lipid accumulation compared to the vehicle treatment. The serum total cholesterol, AST, and ALT levels significantly decreased in the LPE-treated HFD group compared to those in the vehicle-treated HFD group. The LPE significantly decreases the protein expression levels of SREBP1, ACC, p-ACC, FAS, and SCD1, which are involved in lipogenesis, and PPARγ, CD36/FAT, and FATP5, which are involved in fatty acid uptake, both in vivo and in vitro. Thus, LPE may attenuate HFD-induced NAFLD by decreasing lipid accumulation by inhibiting lipogenesis and fatty acid uptake.

Highlights

  • The increase in obesity and type 2 diabetes worldwide has led to a corresponding increase in the incidence of non-alcoholic fatty liver disease (NAFLD) [1]

  • NAFLD is characterized by excessive lipid accumulation in the liver, which can progress from simple steatosis to non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma [2]

  • We focused on the effect of L. platyphylla root ethanol extract (LPE) on hepatic lipid accumulation in high-fat diet (HFD)-induced obese mice to determine whether Liriope platyphylla root ethanolic extract (LPE) could potentially be used to therapeutically treat NAFLD

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Summary

Introduction

The increase in obesity and type 2 diabetes worldwide has led to a corresponding increase in the incidence of non-alcoholic fatty liver disease (NAFLD) [1]. NAFLD is characterized by excessive lipid accumulation in the liver, which can progress from simple steatosis to non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma [2]. It is known that hepatic dyslipidemia is a key contributor to the development of NAFLD. It is induced by obesity, type 2 diabetes, insulin resistance, inflammation, and oxidative stress [7,8]. Hepatic lipid accumulation is affected by de novo lipogenesis (DNL), uptake of circulating lipids, and fatty acid oxidation [9,10]. DNL contributes to hepatic steatosis and steatohepatitis by synthesizing saturated fatty acids, such as palmitate, which can induce inflammation and apoptosis [13]. Fatty acid oxidation occurs mainly in the mitochondria, peroxisomes, and cytochromes, and is regulated by several genes, such as carnitine palmitoyltransferase 1 (CPT1) and peroxisomal acyl-coenzyme A oxidase 1 (ACOX1) [11]

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