Abstract

Our aim was to investigate whether hot water extract (CLW) of Curcuma longa L. could prevent non-alcoholic fatty liver disease (NAFLD). HepG2 cells were treated with free fatty acid (FFA) mixture (oleic acid: palmitic acid, 2:1) for 24 h to stimulate in vitro fatty liver. In addition, C57BL/6 mice were fed 60 kcal% high-fat (HF) diet for eight weeks to induce fatty liver in vivo. Intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) productions were increased by FFA and HF-diet, but supplementation with CLW significantly decreased these levels. CLW treatment ameliorated antioxidant activities that were suppressed by exposure to the FFA and HF-diet. Cluster of differentiation 36 (CD36) and fatty acid transport proteins (FATP2 and FATP5) were increased in HF-diet groups, while CLW suppressed their expression levels. Moreover, sterol regulatory element-binding protein-1c (SREBP-1c), acetyl-coenzyme A carboxylase (ACC), and fatty acid synthase (FAS) expression levels were down-regulated in the CLW groups compared to HF-diet groups. On the other hand, 5′ adenosine monophosphate-activated protein kinase (AMPK), Peroxisome proliferator-activated receptor alpha (PPAR-α), and carnitine palmitoyltransferase 1 (CPT-1) expressions were up-regulated in the CLW groups. HF-diet fed mice showed high hepatic triglycerides (TG) content compared to the normal diet mice. However, the administration of CLW restored the hepatic TG level, indicating an inhibitory effect against lipid accumulation by CLW. These results suggest that CLW could be a potentially useful agent for the prevention of NAFLD through modulating fatty acid uptake.

Highlights

  • The liver is the central organ of lipid metabolism

  • free fatty acid (FFA)-treated group was reactive oxygen species (ROS) formation was When suppressed in were a dose-dependent compared to that in the only significantly increased

  • These results indicated that fatty acid indicated that fatty acid uptake was blocked down-regulated fatty acid levels, which wereby comparable to those of the SILY group

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Summary

Introduction

The liver is the central organ of lipid metabolism. Dietary fatty acids are transported to the liver and oxidized to produce as much energy as the hepatocyte needs. The excess fatty acids are converted to triglycerides (TG) and stored in the hepatocyte [1]. When the amount of TG accounts for more than 5% of the liver weight, the organ function is impaired, and this condition is known as fatty liver disease. Chronic alcohol intake has long been considered the major cause of alcoholic fatty liver, while non-alcoholic fatty liver has been shown to be unrelated to alcohol intake [2]. The causes of non-alcoholic fatty liver are Nutrients 2019, 11, 2536; doi:10.3390/nu11102536 www.mdpi.com/journal/nutrients

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