Abstract

Non-alcoholic fatty liver disease represents the most common liver disease and is characterized by an excess of lipid accumulation in hepatocytes, mainly stored as triglycerides. Phaeodactylum tricornutum is a marine microalga, which is rich in bioactive molecules known to be hepatoprotective, such as n-3 long-chain polyunsaturated fatty acids and fucoxanthin. The aim of this study was to investigate the effects of a carotenoid extract from P. tricornutum in a cellular model of non-alcoholic fatty liver disease induced by palmitate treatment. The combined effects of carotenoids and lipids, especially n-3 long-chain polyunsaturated fatty acids, were also investigated by using a total lipophilic extract. HepG2 cells were exposed for 24 h to 250 µM palmitate with or without the addition of carotenoid extract (6 μg/mL) or total lipophilic extract (100 μg/mL). The addition of carotenoid extract or total lipophilic extract prevented the accumulation of triglycerides, total cholesterol and cholesterol esters. The carotenoid extract and total lipophilic extract also decreased the mRNA expression levels of genes involved in lipogenesis (ACACA, FASN, SCD and DGAT1) and cholesterol esterification (ACAT1/SOAT1). In addition, the total lipophilic extract also downregulated the LXR/NR1H3 and SREBF1 genes, which are involved in lipogenesis regulation. By contrast, the carotenoid extract increased the mRNA level of CPT1A, a β-oxidation related gene, and reduced the lipid droplet accumulation. In conclusion, this study highlights the preventive effects against non-alcoholic fatty liver disease of the two microalga extracts.

Highlights

  • The changing lifestyle of our society, marked by an over-consumption of saturated fatty acids and sugars and a decrease in physical activity, is the main cause of the increase in the number of people with non-alcoholic fatty liver disease (NAFLD) [1,2]

  • The aim of this study was to investigate the impact of carotenoid extract of (CE) from P. tricornutum on NAFLD and associated metabolic pathways, in human liver HepG2 cells

  • Our analyses showed no significant change in the mRNA levels of lipogenic genes (ACACA, DGAT1, FASN and LXR/NR1H3) in our cellular model of NAFLD, the mRNA

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Summary

Introduction

The changing lifestyle of our society, marked by an over-consumption of saturated fatty acids and sugars and a decrease in physical activity, is the main cause of the increase in the number of people with non-alcoholic fatty liver disease (NAFLD) [1,2]. NAFLD is currently the most common chronic liver disease in Western countries and affects more than 30% of the general population [2,3]. NAFLD is characterized by an excessive accumulation of lipids in the parenchymal cells of the liver in the absence of excessive alcohol consumption [3]. Based on the analyses of the Dallas Heart Study cohort, NAFLD was determined by a triglyceride level above 5.5% in the liver [4]. NAFLD can progress to a more serious stage, namely non-alcoholic steatohepatitis, which can lead to hepatic fibrosis [3]

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