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Toxicol Appl Pharmacol. 2017 Aug 1;328:1-9. doi: 10.1016/j.taap.2017.05.001. Epub 2017 May 2.

Curcumin improves alcoholic fatty liver by inhibiting fatty acid biosynthesis.

Author information

1
School of Life Sciences, Longyan University, Longyan 364012, People's Republic of China; Fujian Provincial Key Laboratory for the Prevention and Control of Animal Infectious Diseases and Biotechnology, Longyan 364012, People's Republic of China; Key Laboratory of Preventive Veterinary Medicine and Biotechnology (Longyan University), Fujian Province University, Longyan 364012, People's Republic of China.
2
School of Life Sciences, Longyan University, Longyan 364012, People's Republic of China.
3
School of Life Sciences, Longyan University, Longyan 364012, People's Republic of China; Fujian Provincial Key Laboratory for the Prevention and Control of Animal Infectious Diseases and Biotechnology, Longyan 364012, People's Republic of China; Key Laboratory of Preventive Veterinary Medicine and Biotechnology (Longyan University), Fujian Province University, Longyan 364012, People's Republic of China. Electronic address: qlongxin@tom.com.
4
School of Life Sciences, Longyan University, Longyan 364012, People's Republic of China; School of Life Sciences, University of Science and Technology of China, Hefei 230027, People's Republic of China. Electronic address: lpwen@ustc.edu.cn.

Abstract

Alcoholic fatty liver is a threat to human health. It has been long known that abstinence from alcohol is the most effective therapy, other effective therapies are not available for the treatment in humans. Curcumin has a great potential for anti-oxidation and anti-inflammation, but the effect on metabolic reconstruction remains little known. Here we performed metabolomic analysis by gas chromatography/mass spectrometry and explored ethanol pathogenic insight as well as curcumin action pattern. We identified seventy-one metabolites in mouse liver. Carbohydrates and lipids were characteristic categories. Pathway analysis results revealed that ethanol-induced pathways including biosynthesis of unsaturated fatty acids, fatty acid biosynthesis and pentose and glucuronate interconversions were suppressed by curcumin. Additionally, ethanol enhanced galactose metabolism and pentose phosphate pathway. Glyoxylate and dicarboxylate metabolism and pyruvate metabolism were inhibited in mice fed ethanol diet plus curcumin. Stearic acid, oleic acid and linoleic acid were disease biomarkers and therapical biomarkers. These results reflect the landscape of hepatic metabolism regulation. Our findings illustrate ethanol pathological pathway and metabolic mechanism of curcumin therapy.

KEYWORDS:

Alcoholic fatty liver; Curcumin; Fatty acid biosynthesis; Metabolomics

PMID:
28476407
DOI:
10.1016/j.taap.2017.05.001
[Indexed for MEDLINE]

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