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Nutrients 2014, 6(7), 2552-2571; doi:10.3390/nu6072552

The Effects of Choline on Hepatic Lipid Metabolism, Mitochondrial Function and Antioxidative Status in Human Hepatic C3A Cells Exposed to Excessive Energy Substrates

1,2,3,* , 4
,
1
,
4
and
1,2,3
1
Department of Clinical Nutrition, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China
2
Key Laboratory of Pediatric Gastroenterology and Nutrition, Shanghai Institute for Pediatric Research, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China
3
Department of Nutrition, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
4
Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, China
*
Author to whom correspondence should be addressed.
Received: 23 April 2014 / Revised: 12 June 2014 / Accepted: 18 June 2014 / Published: 9 July 2014
(This article belongs to the Special Issue Nutrition and Liver Disease)
View Full-Text   |   Download PDF [1157 KB, uploaded 9 July 2014]   |  

Abstract

Choline plays a lipotropic role in lipid metabolism as an essential nutrient. In this study, we investigated the effects of choline (5, 35 and 70 μM) on DNA methylation modifications, mRNA expression of the critical genes and their enzyme activities involved in hepatic lipid metabolism, mitochondrial membrane potential (Δψm) and glutathione peroxidase (GSH-Px) in C3A cells exposed to excessive energy substrates (lactate, 10 mM; octanoate, 2 mM and pyruvate, 1 mM; lactate, octanoate and pyruvate-supplemented medium (LOP)). Thirty five micromole or 70 μM choline alone, instead of a low dose (5 μM), reduced hepatocellular triglyceride (TG) accumulation, protected Δψm from decrement and increased GSH-Px activity in C3A cells. The increment of TG accumulation, reactive oxygen species (ROS) production and Δψm disruption were observed under LOP treatment in C3A cells after 72 h of culture, which were counteracted by concomitant treatment of choline (35 μM or 70 μM) partially via reversing the methylation status of the peroxisomal proliferator-activated receptor alpha (PPARα) gene promoter, upregulating PPARα, carnitine palmitoyl transferase-I (CPT-I) and downregulating fatty acid synthase (FAS) gene expression, as well as decreasing FAS activity and increasing CPT-I and GSH-Px activities. These findings provided a novel insight into the lipotropic role of choline as a vital methyl-donor in the intervention of chronic metabolic diseases. View Full-Text
Keywords: choline; hepatic lipid metabolism; mitochondria; proliferator-activated receptor alpha; methylation choline; hepatic lipid metabolism; mitochondria; proliferator-activated receptor alpha; methylation
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Zhu, J.; Wu, Y.; Tang, Q.; Leng, Y.; Cai, W. The Effects of Choline on Hepatic Lipid Metabolism, Mitochondrial Function and Antioxidative Status in Human Hepatic C3A Cells Exposed to Excessive Energy Substrates. Nutrients 2014, 6, 2552-2571.

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