http://orcid.org/0000-0002-6750-2617
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Abstract
Excess alcohol exposure leads to alcoholic liver disease (ALD), a predominant cause of liver-related morbidity and mortality worldwide. In the past decade, increasing attention has been paid to understand the association between n-3 polyunsaturated fatty acids (n-3 PUFAs) and ALD. In this review, we summarize the metabolism of n-3 PUFAs, animal model of ALD, and the findings from recent studies determining the role of n-3 PUFAs in ALD as a possible treatment. The animal models of acute ethanol exposure, chronic ethanol exposure and chronic-plus-single binge ethanol feeding have been widely used to explore the impact of n-3 PUFAs. Although the results of studies regarding the role of n-3 PUFAs in ALD have been inconsistent or controversial, increasing evidence has demonstrated that n-3 PUFAs may be useful in alleviating alcoholic steatosis and alcohol-induced liver injury through multiple mechanisms, including decreased de novo lipogenesis and lipid mobilization from adipose tissue, enhanced mitochondrial fatty acid β-oxidation, reduced hepatic inflammation and oxidative stress, and promoted intestinal homeostasis, positively suggesting that n-3 PUFAs might be promising for the management of ALD. The oxidation of n-3 PUFAs ex vivo in an experimental diet was rarely considered in most n-3 PUFA-related studies, likely contributing to the inconsistent results. Thus, the role of n-3 PUFAs in ALD deserves greater research efforts and remains to be evaluated in randomized, placebo-controlled clinic trial.
| ABBREVIATION | ||
| AA | = | arachidonic acid |
| ACC | = | acetyl-CoA carboxylase |
| ACLY | = | ATP-citrate lyase |
| ACO | = | acyl-CoA oxidase |
| ALA | = | α-linolenic acid |
| ALD | = | alcoholic liver disease |
| ALP | = | alkaline phosphatase |
| ALT | = | alanine aminotransferase |
| AMPK | = | AMP-activated protein kinase |
| AST | = | aspartate aminotransferase |
| ATGL | = | adipose triglyceride lipase |
| cAMP | = | cyclic adenosine 3’,5’-monophosphate |
| COX | = | cyclooxygenases |
| CPT1 | = | carnitine palmitoyltransferase 1 |
| CYP2E1 | = | cytochrome P450 2E1 |
| DGAT2 | = | diacylglycerol acyltransferase 2 |
| DGLA | = | dihomo-γ-linolenic acid |
| DHA | = | docosahexaenoic acid |
| DPA | = | docosapentaenoic acid |
| DTA | = | docosatetraenoic acid |
| EPA | = | eicosapentaenoic acid |
| ER | = | endoplasmic reticulum |
| ETA | = | eicosatetraenoic acid |
| FAS | = | fatty acid synthase |
| FATPs | = | fatty acid transporter proteins |
| GLA,γ | = | linolenic acid |
| GPR120 | = | G protein-coupled receptor 120 |
| GSH | = | glutathione; |
| H&E | = | haematoxylin-eosin; |
| HO-1 | = | heme oxygenase-1; |
| HSL | = | hormone-sensitive lipase; |
| IL-6 | = | interleukin-6 |
| iNOS | = | nitric oxide synthase |
| LA | = | linoleic acid |
| LBP | = | lipopolysaccharide binding protein |
| LOX | = | lipoxygenases |
| LXR | = | liver X receptor |
| LXREs | = | LXR response elements |
| MCP-1 | = | monocyte chemotactic protein-1 |
| MTP | = | microsomal triglyceride transfer protein |
| MUFA | = | monounsaturated fatty acids |
| MyD88 | = | myeloid differentiation factor 88 |
| n-3 PUFAs | = | omega-3 polyunsaturated fatty acid |
| NAFLD | = | nonalcoholic fatty liver disease |
| NASH | = | nonalcoholic steatohepatitis |
| NF-κB | = | transcription factor nuclear factor κB |
| PDE3B | = | phosphodiesterase 3B |
| PPAR | = | peroxisome proliferator-activated receptor |
| ROS | = | reactive oxygen species |
| RXR | = | retinoid X receptor |
| SCD-1 | = | stearyl CoA desaturase-1 |
| SDA | = | stearidonic acid |
| SFA | = | saturated fatty acids |
| SIRT1 | = | sirtuin 1 |
| SOD | = | superoxide dismutase |
| SREBP | = | sterol regulatory element-binding protein |
| TB | = | total bilirubin |
| TC | = | total cholesterol |
| TG | = | triacylglycerol |
| TLR4 | = | Toll-like receptor-4 |
| TNF-α | = | tumor necrosis factor-α |
| VLDLR | = | very low-density lipoprotein receptor |
| WT | = | wild type; |
| ZO-1 | = | zonula occludens-1 |
Disclosure statement
The authors report no conflicts of interest.