Abstract |
Non-alcoholic fatty liver disease ( NAFLD) is the most important cause of chronic liver disease that is characterized by hepatocyte triacylglycerol accumulation (steatosis), which can progress to inflammation, fibrosis, and cirrhosis ( steatohepatitis). Overnutrition triggers the onset of oxidative stress in the liver due to higher availability and oxidation of fatty acids (FA), with development of hyperinsulinemia and insulin resistance (IR), and n-3 long-chain polyunsaturated FA (n-3 LCPUFA) depletion, with enhancement in the n-6/n-3 LCPUFA ratio favouring a pro-inflammatory state. These changes may lead to hepatic steatosis by different mechanisms, namely, (i) IR-dependent higher peripheral lipolysis and FA flux to the liver, (ii) n-3 LCPUFA depletion-induced changes in DNA binding activity of sterol regulatory element-binding protein 1c (SREBP-1c) and peroxisome proliferator-activated receptor α ( PPAR-α) favouring lipogenesis over FA oxidation, and (iii) hyperinsulinemia-induced activation of lipogenic factor PPAR-γ. Supplementation with n-3 LCPUFA appears to reduce nutritional hepatic steatosis in adults, however, other histopathologic features of NAFLD remain to be studied.
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Authors | Rodrigo Valenzuela, Luis A Videla |
Journal | Food & function
(Food Funct)
Vol. 2
Issue 11
Pg. 644-8
(Nov 2011)
ISSN: 2042-650X [Electronic] England |
PMID | 22008843
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
- Fatty Acids, Omega-3
- Fatty Acids, Omega-6
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Topics |
- Animals
- Fatty Acids, Omega-3
(metabolism)
- Fatty Acids, Omega-6
(metabolism)
- Fatty Liver
(metabolism)
- Humans
- Lipolysis
- Non-alcoholic Fatty Liver Disease
- Obesity
(metabolism, pathology)
- Oxidative Stress
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