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Reversal of high-fat diet-induced hepatic steatosis by n-3 LCPUFA: role of PPAR-α and SREBP-1c.
J Nutr Biochem. 2014 Sep; 25(9):977-84.JN

Abstract

Nonalcoholic fatty liver disease is characterized by an abnormal accumulation of triacylglycerides in the liver in absence of significant alcohol consumption. Under these conditions, it has been observed an impaired bioavailability of hepatic n-3 long-chain polyunsaturated fatty acids (LCPUFAs). The aim of this study was to test the reversion of the prosteatotic and proinflammatory effects of high-fat diet (HFD) in the mouse liver by changing to normocaloric diet and n-3 LCPUFA supplementation. Male C57BL/6J mice were given either control diet (CD) or HFD for 12 weeks. Control and HFD groups were divided into subgroups that continue with CD or subjected to CD plus n-3 LCPUFA for 8 additional weeks. After this time, blood and liver samples were taken and metabolic, morphologic, oxidative stress, inflammatory and signaling parameters were analyzed. The dietary change from HFD to a normocaloric diet with n-3 LCPUFA supplementation significantly reduced insulin resistance and liver steatosis when compared to switching HFD to normocaloric diet alone. In addition, HFD-induced increases in adiposity, adipocyte enlargement and liver oxidative stress and inflammatory cytokine expression were suppressed by n-3 LCPUFA to control values. Importantly, n-3 LCPUFA supplementation abolish HFD-induced enhancement in hepatic SREBP-1c/PPAR-α ratios, suggesting a change in the metabolic status of the liver from a lipogenic condition to one favoring fatty acid oxidation and steatosis attenuation. These findings may provide the rational basis for the use of normocaloric diets supplemented with n-3 LCPUFA in patients with liver steatosis.

Authors+Show Affiliations

Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile.Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile.Department of Medical Technology, Faculty of Medicine, University of Chile, Santiago, Chile.Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile.Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile. Electronic address: adespessailles@ug.uchile.cl.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24993917

Citation

Dossi, Camila G., et al. "Reversal of High-fat Diet-induced Hepatic Steatosis By N-3 LCPUFA: Role of PPAR-α and SREBP-1c." The Journal of Nutritional Biochemistry, vol. 25, no. 9, 2014, pp. 977-84.
Dossi CG, Tapia GS, Espinosa A, et al. Reversal of high-fat diet-induced hepatic steatosis by n-3 LCPUFA: role of PPAR-α and SREBP-1c. J Nutr Biochem. 2014;25(9):977-84.
Dossi, C. G., Tapia, G. S., Espinosa, A., Videla, L. A., & D'Espessailles, A. (2014). Reversal of high-fat diet-induced hepatic steatosis by n-3 LCPUFA: role of PPAR-α and SREBP-1c. The Journal of Nutritional Biochemistry, 25(9), 977-84. https://doi.org/10.1016/j.jnutbio.2014.04.011
Dossi CG, et al. Reversal of High-fat Diet-induced Hepatic Steatosis By N-3 LCPUFA: Role of PPAR-α and SREBP-1c. J Nutr Biochem. 2014;25(9):977-84. PubMed PMID: 24993917.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reversal of high-fat diet-induced hepatic steatosis by n-3 LCPUFA: role of PPAR-α and SREBP-1c. AU - Dossi,Camila G, AU - Tapia,Gladys S, AU - Espinosa,Alejandra, AU - Videla,Luis A, AU - D'Espessailles,Amanda, Y1 - 2014/06/02/ PY - 2013/12/16/received PY - 2014/04/10/revised PY - 2014/04/24/accepted PY - 2014/7/5/entrez PY - 2014/7/6/pubmed PY - 2015/4/1/medline KW - High fat diet KW - Liver steatosis KW - PPAR-α KW - SREBP-1c KW - n-3 Long-chain polyunsaturated fatty acid SP - 977 EP - 84 JF - The Journal of nutritional biochemistry JO - J. Nutr. Biochem. VL - 25 IS - 9 N2 - Nonalcoholic fatty liver disease is characterized by an abnormal accumulation of triacylglycerides in the liver in absence of significant alcohol consumption. Under these conditions, it has been observed an impaired bioavailability of hepatic n-3 long-chain polyunsaturated fatty acids (LCPUFAs). The aim of this study was to test the reversion of the prosteatotic and proinflammatory effects of high-fat diet (HFD) in the mouse liver by changing to normocaloric diet and n-3 LCPUFA supplementation. Male C57BL/6J mice were given either control diet (CD) or HFD for 12 weeks. Control and HFD groups were divided into subgroups that continue with CD or subjected to CD plus n-3 LCPUFA for 8 additional weeks. After this time, blood and liver samples were taken and metabolic, morphologic, oxidative stress, inflammatory and signaling parameters were analyzed. The dietary change from HFD to a normocaloric diet with n-3 LCPUFA supplementation significantly reduced insulin resistance and liver steatosis when compared to switching HFD to normocaloric diet alone. In addition, HFD-induced increases in adiposity, adipocyte enlargement and liver oxidative stress and inflammatory cytokine expression were suppressed by n-3 LCPUFA to control values. Importantly, n-3 LCPUFA supplementation abolish HFD-induced enhancement in hepatic SREBP-1c/PPAR-α ratios, suggesting a change in the metabolic status of the liver from a lipogenic condition to one favoring fatty acid oxidation and steatosis attenuation. These findings may provide the rational basis for the use of normocaloric diets supplemented with n-3 LCPUFA in patients with liver steatosis. SN - 1873-4847 UR - https://www.unboundmedicine.com/medline/citation/24993917/Reversal_of_high_fat_diet_induced_hepatic_steatosis_by_n_3_LCPUFA:_role_of_PPAR_α_and_SREBP_1c_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0955-2863(14)00109-0 DB - PRIME DP - Unbound Medicine ER -