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Targeting n-3 polyunsaturated fatty acids in non-alcoholic fatty liver disease
dc.contributor.author | Valenzuela, Rodrigo | |
dc.contributor.author | Ortiz, Macarena | |
dc.contributor.author | Hernández-Rodas, María Catalina | |
dc.contributor.author | Echeverría, Francisca | |
dc.contributor.author | Videla, Luis A. | |
dc.date.accessioned | 2023-04-18T14:49:07Z | |
dc.date.available | 2023-04-18T14:49:07Z | |
dc.date.issued | 2020 | |
dc.identifier.uri | http://repositorio.ucm.cl/handle/ucm/4675 | |
dc.description.abstract | Background: Non-Alcoholic Fatty Liver Disease (NAFLD) is characterized by abnormal hepatic accumulation of triacylglycerides in the absence of alcohol consumption, in association with Oxidative Stress (OS), a pro-inflammatory state and Insulin Resistance (IR), which are attenuated by n-3 long-chain polyunsaturated Fatty Acids (FAs) C20-C22 (LCPUFAs) supplementation. Main causes of NAFLD comprise high caloric intake and a sedentary lifestyle, with high intakes of saturated FAs. Methods: The review includes several searches considering the effects of n-3 LCPUFAs in NAFLD in vivo and in vitro models, using the PubMed database from the National Library of Medicine- National Institutes of Health. Result: The LCPUFAs eicosapentaenoic acid (C20:5 n-3, EPA) and docosahexaenoic acid (C22:6 n- 3, DHA) have a positive effect in diminishing liver steatosis, OS, and the levels of aspartate aminotransferase, alanine aminotransferase and pro-inflammatory cytokines, with improvement of insulin sensitivity and adiponectin levels. The molecular pathways described for n-3 LCPUFAs in cellular and animal models and humans include peroxisome proliferator–activated receptor-α activation favouring FA oxidation, diminution of lipogenesis due to sterol responsive element binding protein-1c downregulation and inflammation resolution. Besides, nuclear factor erythroid-2-related factor-2 activation is elicited by n-3 LCPUFA-derived oxidation products producing direct and indirect antioxidant responses, with concomitant anti-fibrogenic action. Conclusion: The discussed effects of n-3 LCPUFA supplementation support its use in NAFLD, although having a limited value in NASH, a contention that may involve n-3 LCPUFA oxygenated derivatives. Clinical trials establishing optimal dosages, intervention times, type of patients and possible synergies with other natural products are needed in future studies. | es_CL |
dc.language.iso | en | es_CL |
dc.rights | Atribución-NoComercial-SinDerivadas 3.0 Chile | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/cl/ | * |
dc.source | Current Medicinal Chemistry, 27(31), 5250-5272 | es_CL |
dc.subject | Liver steatosis | es_CL |
dc.subject | N-3 polyunsaturated fatty acids | es_CL |
dc.subject | α-linolenic acid | es_CL |
dc.subject | Eicosapentaenoic acid | es_CL |
dc.subject | Docosahexaenoic acid | es_CL |
dc.subject | Anti-lipogenic mechanism | es_CL |
dc.title | Targeting n-3 polyunsaturated fatty acids in non-alcoholic fatty liver disease | es_CL |
dc.type | Article | es_CL |
dc.ucm.facultad | Facultad de Ciencias de la Salud | es_CL |
dc.ucm.indexacion | Scopus | es_CL |
dc.ucm.indexacion | Isi | es_CL |
dc.ucm.uri | www.eurekaselect.com/article/97974 | es_CL |
dc.ucm.doi | doi.org/10.2174/0929867326666190410121716 | es_CL |
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