Endogenous Liver Protections Against Lipotoxicity and Oxidative Stress to Avoid the Progression of Non-alcoholic Fatty Liver to more Serious Disease

Page: [401 - 420] Pages: 20

  • * (Excluding Mailing and Handling)

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a metabolic disorder characterized by an ectopic accumulation of lipids in at least 5% of hepatocytes. The first phase of the disease, called hepatic steatosis, progresses over time to chronic conditions, such as steatohepatitis, cirrhosis, and finally, hepatic insufficiency and cancer. The accumulation of free fatty acids in hepatocytes, particularly saturated fatty acids, is a key process in the development and progression of NAFLD. Furthermore, the accumulation of oxidative stress markers in NAFLD is closely linked to lipotoxicity due to impaired lipid metabolism and increased generation of reactive oxygen species (ROS). However, endogenous mechanisms are activated early in the liver to protect against lipotoxicity and oxidative stress, thus preventing liver mass loss and disease progression. Thus, in order to develop appropriate therapies, the purpose of this review is to discuss recent data from the literature regarding the importance of intrinsic mechanisms deployed by the liver in protecting itself against the adverse effects related to chronic lipid accumulation and ROS generation.

Keywords: Antioxidant enzymes, Free fatty acids, Lipotoxicity, NAFLD, Oxidative stress, metabolic disorder.

[1]
Patell R, Dosi R, Joshi H, Sheth S, Shah P, Jasdanwala S. Non-alcoholic fatty liver disease (NAFLD) in obesity. J Clin Diagn Res 2014; 8(1): 62-6.
[PMID: 24596725]
[2]
Marchesini G, Day CP, Dufour J-F, et al. EASL-EASD-EASO clinical practice guidelines for the management of non-alcoholic fatty liver disease. J Hepatol 2016; 64(6): 1388-402.
[http://dx.doi.org/10.1016/j.jhep.2015.11.004] [PMID: 27062661]
[3]
Estep JM, Birerdinc A, Younossi Z. Non-invasive diagnostic tests for non-alcoholic fatty liver disease. Curr Mol Med 2010; 10(2): 166-72.
[http://dx.doi.org/10.2174/156652410790963321] [PMID: 20196730]
[4]
Polyzos SA, Kountouras J, Mantzoros CS. Obesity and nonalcoholic fatty liver disease: From pathophysiology to therapeutics. Metabolism 2019; 92: 82-97.
[http://dx.doi.org/10.1016/j.metabol.2018.11.014] [PMID: 30502373]
[5]
Motamed N, Rabiee B, Poustchi H, et al. Non-alcoholic fatty liver disease (NAFLD) and 10-year risk of cardiovascular diseases. Clin Res Hepatol Gastroenterol 2017; 41(1): 31-8.
[http://dx.doi.org/10.1016/j.clinre.2016.07.005] [PMID: 27597641]
[6]
Le MH, Devaki P, Ha NB, et al. Prevalence of non-alcoholic fatty liver disease and risk factors for advanced fibrosis and mortality in the United States. PLoS One 2017; 12(3): e0173499.
[http://dx.doi.org/10.1371/journal.pone.0173499]
[7]
Younossi ZM, Koenig AB, Abdelatif D, Fazel Y, Henry L, Wymer M. Global epidemiology of nonalcoholic fatty liver disease-Meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology 2016; 64(1): 73-84.
[http://dx.doi.org/10.1002/hep.28431] [PMID: 26707365]
[8]
Neuschwander-Tetri BA. Non-alcoholic fatty liver disease. BMC Med 2017; 15(1): 45.
[http://dx.doi.org/10.1186/s12916-017-0806-8] [PMID: 28241825]
[9]
Hess PL, Al-Khalidi HR, Friedman DJ, et al. The metabolic syndrome and risk of sudden cardiac death: The atherosclerosis risk in communities study. J Am Heart Assoc 2017; 6(8): e006103.
[10]
Hirsova P, Gores GJ. Death receptor-mediated cell death and proinflammatory signaling in nonalcoholic steatohepatitis. Cell Mol Gastroenterol Hepatol 2015; 1(1): 17-27.
[http://dx.doi.org/10.1016/j.jcmgh.2014.11.005] [PMID: 25729762]
[11]
Katsiki N, Perez-Martinez P, Anagnostis P, Mikhailidis DP, Karagiannis A. Is nonalcoholic fatty liver disease indeed the hepatic manifestation of metabolic syndrome? Curr Vasc Pharmacol 2018; 16(3): 219-27.
[http://dx.doi.org/10.2174/1570161115666170621075619] [PMID: 28669328]
[12]
Day CP, James OF. Steatohepatitis: A tale of two “hits”? Gastroenterology 1998; 114(4): 842-5.
[http://dx.doi.org/10.1016/S0016-5085(98)70599-2] [PMID: 9547102]
[13]
Pierantonelli I, Svegliati-Baroni G. Nonalcoholic fatty liver disease: Basic pathogenetic mechanisms in the progression from nafld to nash. Transplantation 2019; 103(1): e1-e13.
[http://dx.doi.org/10.1097/TP.0000000000002480] [PMID: 30300287]
[14]
Diehl AM, Day C. Cause, pathogenesis, and treatment of nonalcoholic steatohepatitis. N Engl J Med 2017; 377(21): 2063-72.
[http://dx.doi.org/10.1056/NEJMra1503519] [PMID: 29166236]
[15]
Buzzetti E, Pinzani M, Tsochatzis EA. The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). Metabolism 2016; 65(8): 1038-48.
[http://dx.doi.org/10.1016/j.metabol.2015.12.012] [PMID: 26823198]
[16]
Gastaldelli A. Insulin resistance and reduced metabolic flexibility: Cause or consequence of NAFLD? Clin Sci (Lond) 2017; 131(22): 2701-4.
[http://dx.doi.org/10.1042/CS20170987] [PMID: 29109303]
[17]
Rafiei H, Omidian K, Bandy B. Protection by different classes of dietary polyphenols against palmitic acid-induced steatosis, nitro-oxidative stress and endoplasmic reticulum stress in HepG2 hepatocytes. J Funct Foods 2018; 44: 173-82.
[http://dx.doi.org/10.1016/j.jff.2018.02.033]
[18]
McPherson S, Hardy T, Henderson E, Burt AD, Day CP, Anstee QM. Evidence of NAFLD progression from steatosis to fibrosing-steatohepatitis using paired biopsies: Implications for prognosis and clinical management. J Hepatol 2015; 62(5): 1148-55.
[http://dx.doi.org/10.1016/j.jhep.2014.11.034] [PMID: 25477264]
[19]
Listenberger LL, Han X, Lewis SE, et al. Triglyceride accumulation protects against fatty acid-induced lipotoxicity. Proc Natl Acad Sci USA 2003; 100(6): 3077-82.
[http://dx.doi.org/10.1073/pnas.0630588100] [PMID: 12629214]
[20]
Romeo S, Kozlitina J, Xing C, et al. Genetic variation in PNPLA3 confers susceptibility to nonalcoholic fatty liver disease. Nat Genet 2008; 40(12): 1461-5.
[http://dx.doi.org/10.1038/ng.257] [PMID: 18820647]
[21]
BasuRay S Smagris E, Cohen JC, Hobbs HH. The PNPLA3 variant associated with fatty liver disease (I148M) accumulates on lipid droplets by evading ubiquitylation. Hepatology 2017; 66(4): 1111-24.
[http://dx.doi.org/10.1002/hep.29273] [PMID: 28520213]
[22]
Käräjämäki AJ, Bloigu R, Kauma H, et al. Non-alcoholic fatty liver disease with and without metabolic syndrome: Different long-term outcomes. Metabolism 2017; 66: 55-63.
[http://dx.doi.org/10.1016/j.metabol.2016.06.009] [PMID: 27423871]
[23]
Martínez LA, Larrieta E, Kershenobich D, Torre A. The expression of pnpla3 polymorphism could be the key for severe liver disease in nafld in hispanic population. Ann Hepatol 2017; 16(6): 909-15.
[http://dx.doi.org/10.5604/01.3001.0010.5282] [PMID: 29055919]
[24]
Trépo E, Romeo S, Zucman-Rossi J, Nahon P. PNPLA3 gene in liver diseases. J Hepatol 2016; 65(2): 399-412.
[http://dx.doi.org/10.1016/j.jhep.2016.03.011] [PMID: 27038645]
[25]
Kozlitina J, Smagris E, Stender S, et al. Exome-wide association study identifies a TM6SF2 variant that confers susceptibility to nonalcoholic fatty liver disease. Nat Genet 2014; 46(4): 352-6.
[http://dx.doi.org/10.1038/ng.2901] [PMID: 24531328]
[26]
Mahdessian H, Taxiarchis A, Popov S, et al. TM6SF2 is a regulator of liver fat metabolism influencing triglyceride secretion and hepatic lipid droplet content. Proc Natl Acad Sci USA 2014; 111(24): 8913-8.
[http://dx.doi.org/10.1073/pnas.1323785111] [PMID: 24927523]
[27]
Ehrhardt N, Doche ME, Chen S, et al. Hepatic Tm6sf2 overexpression affects cellular ApoB-trafficking, plasma lipid levels, hepatic steatosis and atherosclerosis. Hum Mol Genet 2017; 26(14): 2719-31.
[http://dx.doi.org/10.1093/hmg/ddx159] [PMID: 28449094]
[28]
Li TT, Li TH, Peng J, et al. TM6SF2: A novel target for plasma lipid regulation. Atherosclerosis 2018; 268: 170-6.
[http://dx.doi.org/10.1016/j.atherosclerosis.2017.11.033] [PMID: 29232562]
[29]
Stephenson K, Kennedy L, Hargrove L, et al. Updates on dietary models of nonalcoholic fatty liver disease: Current studies and insights. Gene Expr 2018; 18(1): 5-17.
[http://dx.doi.org/10.3727/105221617X15093707969658] [PMID: 29096730]
[30]
Jensen T, Abdelmalek MF, Sullivan S, et al. Fructose and sugar: A major mediator of non-alcoholic fatty liver disease. J Hepatol 2018; 68(5): 1063-75.
[http://dx.doi.org/10.1016/j.jhep.2018.01.019] [PMID: 29408694]
[31]
Softic S, Cohen DE, Kahn CR. Role of dietary fructose and hepatic de novo lipogenesis in fatty liver disease. Dig Dis Sci 2016; 61(5): 1282-93.
[http://dx.doi.org/10.1007/s10620-016-4054-0] [PMID: 26856717]
[32]
Sharawy MH, El-Awady MS, Megahed N, Gameil NM. Attenuation of insulin resistance in rats by agmatine: Role of SREBP-1c, mTOR and GLUT-2. Naunyn Schmiedebergs Arch Pharmacol 2016; 389(1): 45-56.
[http://dx.doi.org/10.1007/s00210-015-1174-6] [PMID: 26449613]
[33]
Knebel B, Hartwig S, Haas J, et al. Peroxisomes compensate hepatic lipid overflow in mice with fatty liver. Biochim Biophys Acta 2015; 1851(7): 965-76.
[http://dx.doi.org/10.1016/j.bbalip.2015.03.003] [PMID: 25790917]
[34]
Kim CW, Addy C, Kusunoki J, et al. Acetyl coa carboxylase inhibition reduces hepatic steatosis but elevates plasma triglycerides in mice and humans: A bedside to bench investigation. Cell Metab 2017; 26(2): 394-406.e6.
[http://dx.doi.org/10.1016/j.cmet.2017.07.009] [PMID: 28768177]
[35]
Chen X, Li L, Liu X, et al. Oleic acid protects saturated fatty acid mediated lipotoxicity in hepatocytes and rat of non-alcoholic steatohepatitis. Life Sci 2018; 203: 291-304.
[http://dx.doi.org/10.1016/j.lfs.2018.04.022] [PMID: 29709653]
[36]
Rial SA, Ravaut G, Malaret TB, Bergeron KF, Mounier C. Hexanoic, octanoic and decanoic acids promote basal and insulin-induced phosphorylation of the akt-mtor axis and a balanced lipid metabolism in the hepg2 hepatoma cell line. Molecules 2018; 23(9): 2315.
[37]
Schwarz JM, Noworolski SM, Erkin-Cakmak A, et al. Effects of dietary fructose restriction on liver fat, de novo lipogenesis, and insulin kinetics in children with obesity. Gastroenterology 2017; 153(3): 743-52.
[http://dx.doi.org/10.1053/j.gastro.2017.05.043] [PMID: 28579536]
[38]
Lau JK, Zhang X, Yu J. Animal models of non-alcoholic fatty liver disease: Current perspectives and recent advances. J Pathol 2017; 241(1): 36-44.
[http://dx.doi.org/10.1002/path.4829] [PMID: 27757953]
[39]
Bellanti F, Villani R, Tamborra R, et al. Synergistic interaction of fatty acids and oxysterols impairs mitochondrial function and limits liver adaptation during nafld progression. Redox Biol 2018; 15: 86-96.
[http://dx.doi.org/10.1016/j.redox.2017.11.016] [PMID: 29220698]
[40]
Ruiz-Ramírez A, Chávez-Salgado M, Peñeda-Flores JA, Zapata E, Masso F, El-Hafidi M. High-sucrose diet increases ROS generation, FFA accumulation, UCP2 level, and proton leak in liver mitochondria. Am J Physiol Endocrinol Metab 2011; 301(6): E1198-207.
[http://dx.doi.org/10.1152/ajpendo.00631.2010] [PMID: 21917631]
[41]
Einer C, Hohenester S, Wimmer R, et al. Mitochondrial adaptation in steatotic mice. Mitochondrion 2018; 40: 1-12.
[http://dx.doi.org/10.1016/j.mito.2017.08.015] [PMID: 28935446]
[42]
Tsuchida T, Lee YA, Fujiwara N, et al. A simple diet- and chemical-induced murine NASH model with rapid progression of steatohepatitis, fibrosis and liver cancer. J Hepatol 2018; 69(2): 385-95.
[http://dx.doi.org/10.1016/j.jhep.2018.03.011] [PMID: 29572095]
[43]
Moon YA. The SCAP/SREBP pathway: A mediator of hepatic steatosis. Endocrinol Metab (Seoul) 2017; 32(1): 6-10.
[http://dx.doi.org/10.3803/EnM.2017.32.1.6] [PMID: 28116873]
[44]
Yoon MS. The role of mammalian target of rapamycin (mtor) in insulin signaling. Nutrients 2017; 9(11): 1176.
[45]
Lucero D, Miksztowicz V, Macri V, et al. Overproduction of altered VLDL in an insulin-resistance rat model: Influence of SREBP-1c and PPAR-α. Clin Investig Arterioscler 2015; 27(4): 167-74.
[http://dx.doi.org/10.1016/j.arteri.2014.11.002] [PMID: 25796423]
[46]
Park EJ, Lee AY, Park S, Kim JH, Cho MH. Multiple pathways are involved in palmitic acid-induced toxicity. Food Chem Toxicol 2014; 67: 26-34.
[http://dx.doi.org/10.1016/j.fct.2014.01.027] [PMID: 24486139]
[47]
Pilar Valdecantos M, Prieto-Hontoria PL, Pardo V, et al. Essential role of Nrf2 in the protective effect of lipoic acid against lipoapoptosis in hepatocytes. Free Radic Biol Med 2015; 84: 263-78.
[http://dx.doi.org/10.1016/j.freeradbiomed.2015.03.019] [PMID: 25841776]
[48]
Koliaki C, Szendroedi J, Kaul K, et al. Adaptation of hepatic mitochondrial function in humans with non-alcoholic fatty liver is lost in steatohepatitis. Cell Metab 2015; 21(5): 739-46.
[http://dx.doi.org/10.1016/j.cmet.2015.04.004] [PMID: 25955209]
[49]
Ruiz-Ramírez A, Barrios-Maya MA, López-Acosta O, Molina-Ortiz D, El-Hafidi M. Cytochrome c release from rat liver mitochondria is compromised by increased saturated cardiolipin species induced by sucrose feeding. Am J Physiol Endocrinol Metab 2015; 309(9): E777-86.
[http://dx.doi.org/10.1152/ajpendo.00617.2014] [PMID: 26353385]
[50]
Domínguez-Pérez M, Simoni-Nieves A, Rosales P, et al. Cholesterol burden in the liver induces mitochondrial dynamic changes and resistance to apoptosis. J Cell Physiol 2019; 234(5): 7213-23.
[http://dx.doi.org/10.1002/jcp.27474] [PMID: 30239004]
[51]
Marra F, Svegliati-Baroni G. Lipotoxicity and the gut-liver axis in NASH pathogenesis. J Hepatol 2018; 68(2): 280-95.
[http://dx.doi.org/10.1016/j.jhep.2017.11.014] [PMID: 29154964]
[52]
Geng Y, Hernández Villanueva A, Oun A, et al. Protective effect of metformin against palmitate-induced hepatic cell death. Biochim Biophys Acta Mol Basis Dis 2020; 1866(3): 165621.
[http://dx.doi.org/10.1016/j.bbadis.2019.165621] [PMID: 31786336]
[53]
Paton CM, Ntambi JM. Biochemical and physiological function of stearoyl-CoA desaturase. Am J Physiol Endocrinol Metab 2009; 297(1): E28-37.
[http://dx.doi.org/10.1152/ajpendo.90897.2008] [PMID: 19066317]
[54]
Igal RA. Stearoyl-CoA desaturase-1: A novel key player in the mechanisms of cell proliferation, programmed cell death and transformation to cancer. Carcinogenesis 2010; 31(9): 1509-15.
[http://dx.doi.org/10.1093/carcin/bgq131] [PMID: 20595235]
[55]
ALJohani AM Syed DN, Ntambi JM. Insights into stearoyl-coa desaturase-1 regulation of systemic metabolism. Trends Endocrinol Metab 2017; 28(12): 831-42.
[http://dx.doi.org/10.1016/j.tem.2017.10.003] [PMID: 29089222]
[56]
Liao X, Song L, Zhang L, et al. LAMP3 regulates hepatic lipid metabolism through activating PI3K/Akt pathway. Mol Cell Endocrinol 2018; 470: 160-7.
[http://dx.doi.org/10.1016/j.mce.2017.10.010] [PMID: 29056532]
[57]
Stamatikos AD, Paton CM. Role of stearoyl-CoA desaturase-1 in skeletal muscle function and metabolism. Am J Physiol Endocrinol Metab 2013; 305(7): E767-75.
[http://dx.doi.org/10.1152/ajpendo.00268.2013] [PMID: 23941875]
[58]
Scaglia N, Igal RA. Stearoyl-CoA desaturase is involved in the control of proliferation, anchorage-independent growth, and survival in human transformed cells. J Biol Chem 2005; 280(27): 25339-49.
[http://dx.doi.org/10.1074/jbc.M501159200] [PMID: 15851470]
[59]
Li ZZ, Berk M, McIntyre TM, Feldstein AE. Hepatic lipid partitioning and liver damage in nonalcoholic fatty liver disease: Role of stearoyl-CoA desaturase. J Biol Chem 2009; 284(9): 5637-44.
[http://dx.doi.org/10.1074/jbc.M807616200] [PMID: 19119140]
[60]
Dalla Valle A, Vertongen P, Spruyt D, et al. Induction of stearoyl-coa 9-desaturase 1 protects human mesenchymal stromal cells against palmitic acid-induced lipotoxicity and inflammation. Front Endocrinol (Lausanne) 2019; 10(726): 1-14.
[61]
Dobosz AM, Janikiewicz J, Borkowska AM, et al. Stearoyl-coa desaturase 1 activity determines the maintenance of dnmt1-mediated dna methylation patterns in pancreatic β-cells. Int J Mol Sci 2020; 21(18): 6844.
[62]
Allard JP, Aghdassi E, Mohammed S, et al. Nutritional assessment and hepatic fatty acid composition in non-alcoholic fatty liver disease (NAFLD): A cross-sectional study. J Hepatol 2008; 48(2): 300-7.
[http://dx.doi.org/10.1016/j.jhep.2007.09.009] [PMID: 18086506]
[63]
Puri P, Wiest MM, Cheung O, et al. The plasma lipidomic signature of nonalcoholic steatohepatitis. Hepatology 2009; 50(6): 1827-38.
[http://dx.doi.org/10.1002/hep.23229] [PMID: 19937697]
[64]
Chong MF, Hodson L, Bickerton AS, et al. Parallel activation of de novo lipogenesis and stearoyl-CoA desaturase activity after 3 d of high-carbohydrate feeding. Am J Clin Nutr 2008; 87(4): 817-23.
[http://dx.doi.org/10.1093/ajcn/87.4.817] [PMID: 18400702]
[65]
Chiappini F, Coilly A, Kadar H, et al. Metabolism dysregu-lation induces a specific lipid signature of nonalcoholic steatohepatitis in patients. Sci Rep 2017; 7(46658): 46658.
[http://dx.doi.org/10.1038/srep46658] [PMID: 28436449]
[66]
Souza CO, Teixeira AAS, Biondo LA, et al. Palmitoleic acid reduces high fat diet-induced liver inflammation by promoting PPAR-γ-independent M2a polarization of myeloid cells. Biochim Biophys Acta Mol Cell Biol Lipids 2020; 1865(10): 158776.
[http://dx.doi.org/10.1016/j.bbalip.2020.158776] [PMID: 32738301]
[67]
Bril F, Barb D, Portillo-Sanchez P, et al. Metabolic and histological implications of intrahepatic triglyceride content in nonalcoholic fatty liver disease. Hepatology 2017; 65(4): 1132-44.
[http://dx.doi.org/10.1002/hep.28985] [PMID: 27981615]
[68]
Ogino N, Miyagawa K, Kusanaga M, et al. Involvement of sarco/endoplasmic reticulum calcium ATPase-mediated calcium flux in the protective effect of oleic acid against lipotoxicity in hepatocytes. Exp Cell Res 2019; 385(1): 111651.
[http://dx.doi.org/10.1016/j.yexcr.2019.111651] [PMID: 31568762]
[69]
Liu J, Chang F, Li F, et al. Palmitate promotes autophagy and apoptosis through ROS-dependent JNK and p38 MAPK. Biochem Biophys Res Commun 2015; 463(3): 262-7.
[http://dx.doi.org/10.1016/j.bbrc.2015.05.042] [PMID: 26002468]
[70]
Tomizawa M, Kawanabe Y, Shinozaki F, et al. Triglyceride is strongly associated with nonalcoholic fatty liver disease among markers of hyperlipidemia and diabetes. Biomed Rep 2014; 2(5): 633-6.
[http://dx.doi.org/10.3892/br.2014.309] [PMID: 25054002]
[71]
Stone SJ, Levin MC, Zhou P, Han J, Walther TC, Farese RV Jr. The endoplasmic reticulum enzyme DGAT2 is found in mitochondria-associated membranes and has a mitochondrial targeting signal that promotes its association with mitochondria. J Biol Chem 2009; 284(8): 5352-61.
[http://dx.doi.org/10.1074/jbc.M805768200] [PMID: 19049983]
[72]
Villanueva CJ, Monetti M, Shih M, et al. Specific role for acyl CoA:Diacylglycerol acyltransferase 1 (Dgat1) in hepatic steatosis due to exogenous fatty acids. Hepatology 2009; 50(2): 434-42.
[http://dx.doi.org/10.1002/hep.22980] [PMID: 19472314]
[73]
Gluchowski NL, Gabriel KR, Chitraju C, et al. Hepatocyte deletion of triglyceride-synthesis enzyme acyl coa: Diacylglycerol acyltransferase 2 reduces steatosis without increasing inflammation or fibrosis in mice. Hepatology 2019; 70(6): 1972-85.
[http://dx.doi.org/10.1002/hep.30765] [PMID: 31081165]
[74]
Nakajima S, Gotoh M, Fukasawa K, Murakami-Murofushi K, Kunugi H. Oleic acid is a potent inducer for lipid droplet accumulation through its esterification to glycerol by diacylglycerol acyltransferase in primary cortical astrocytes. Brain Res 2019; 1725: 146484.
[http://dx.doi.org/10.1016/j.brainres.2019.146484] [PMID: 31562840]
[75]
Nguyen TB, Louie SM, Daniele JR, et al. DGAT1-dependent lipid droplet biogenesis protects mitochondrial function during starvation-induced autophagy. Dev Cell 2017; 42(1): 9-21.e5.
[http://dx.doi.org/10.1016/j.devcel.2017.06.003] [PMID: 28697336]
[76]
Chitraju C, Mejhert N, Haas JT, et al. Triglyceride synthesis by dgat1 protects adipocytes from lipid-induced er stress during lipolysis. Cell Metab 2017; 26(2): 407-418.e3.
[http://dx.doi.org/10.1016/j.cmet.2017.07.012] [PMID: 28768178]
[77]
Dircks L, Sul HS. Acyltransferases of de novo glycerophospholipid biosynthesis. Prog Lipid Res 1999; 38(5-6): 461-79.
[http://dx.doi.org/10.1016/S0163-7827(99)00012-0] [PMID: 10793891]
[78]
Magtanong L, Ko PJ, To M, et al. Exogenous monounsaturated fatty acids promote a ferroptosis-resistant cell state. Cell Chem Biol 2019; 26(3): 420-432.e9.
[http://dx.doi.org/10.1016/j.chembiol.2018.11.016] [PMID: 30686757]
[79]
Li N, Sancak Y, Frasor J, Atilla-Gokcumen GE. A protective role for triacylglycerols during apoptosis. Biochemistry 2018; 57(1): 72-80.
[http://dx.doi.org/10.1021/acs.biochem.7b00975] [PMID: 29188717]
[80]
Shih LM, Tang HY, Lynn KS, Huang CY, Ho HY, Cheng ML. Stable isotope-labeled lipidomics to unravel the heterogeneous development lipotoxicity. Molecules 2018; 23(11): 2862.
[http://dx.doi.org/10.3390/molecules23112862]
[81]
Okada LSDRR, Oliveira CP, Stefano JT, et al. Omega-3 PUFA modulate lipogenesis, ER stress, and mitochondrial dysfunction markers in NASH - proteomic and lipidomic insight. Clin Nutr 2018; 37(5): 1474-84.
[http://dx.doi.org/10.1016/j.clnu.2017.08.031] [PMID: 29249532]
[82]
Musso G, Cassader M, Paschetta E, Gambino R. Bioactive lipid species and metabolic pathways in progression and resolution of nonalcoholic steatohepatitis. Gastroenterology 2018; 155(2): 282-302.e8.
[http://dx.doi.org/10.1053/j.gastro.2018.06.031] [PMID: 29906416]
[83]
Khadge S, Sharp JG, Thiele GM, et al. Dietary omega-3 and omega-6 polyunsaturated fatty acids modulate hepatic pathology. J Nutr Biochem 2018; 52: 92-102.
[http://dx.doi.org/10.1016/j.jnutbio.2017.09.017] [PMID: 29175671]
[84]
Hong L, Zahradka P, Cordero-Monroy L, Wright B, Taylor CG. Dietary docosahexaenoic acid (dha) and eicosapentaenoic acid (epa) operate by different mechanisms to modulate hepatic steatosis and hyperinsulemia in fa/fa zucker rats. Nutrients 2019; 11(4): 917.
[85]
Lamaziere A, Wolf C, Barbe U, Bausero P, Visioli F. Lipidomics of hepatic lipogenesis inhibition by omega 3 fatty acids. Prostaglandins Leukot Essent Fatty Acids 2013; 88(2): 149-54.
[http://dx.doi.org/10.1016/j.plefa.2012.12.001] [PMID: 23313470]
[86]
Yang J, Fernández-Galilea M, Martínez-Fernández L, et al. Oxidative stress and non-alcoholic fatty liver disease: Effects of omega-3 fatty acid supplementation. Nutrients 2019; 11(4): 872.
[http://dx.doi.org/10.3390/nu11040872] [PMID: 31003450]
[87]
Scorletti E, Byrne CD. Omega-3 fatty acids and non-alcoholic fatty liver disease: Evidence of efficacy and mechanism of action. Mol Aspects Med 2018; 64: 135-46.
[http://dx.doi.org/10.1016/j.mam.2018.03.001] [PMID: 29544992]
[88]
Chang M, Zhang T, Han X, et al. Comparative analysis of epa/dha-pl forage and liposomes in orotic acid-induced nonalcoholic fatty liver rats and their related mechanisms. J Agric Food Chem 2018; 66(6): 1408-18.
[http://dx.doi.org/10.1021/acs.jafc.7b05173] [PMID: 29345914]
[89]
Guo XF, Yang B, Tang J, Li D. Fatty acid and non-alcoholic fatty liver disease: Meta-analyses of case-control and randomized controlled trials. Clin Nutr 2018; 37(1): 113-22.
[http://dx.doi.org/10.1016/j.clnu.2017.01.003] [PMID: 28161092]
[90]
Miotto PM, Horbatuk M, Proudfoot R, et al. α-Linolenic acid supplementation and exercise training reveal independent and additive responses on hepatic lipid accumulation in obese rats. Am J Physiol Endocrinol Metab 2017; 312(6): E461-70.
[http://dx.doi.org/10.1152/ajpendo.00438.2016] [PMID: 28270444]
[91]
Chen ZY, Liu M, Jing LP, et al. Erythrocyte membrane n-3 polyunsaturated fatty acids are inversely associated with the presence and progression of nonalcoholic fatty liver disease in Chinese adults: A prospective study. Eur J Nutr 2020; 59(3): 941-51.
[http://dx.doi.org/10.1007/s00394-019-01953-2] [PMID: 30937580]
[92]
Wang Y, Nakajima T, Gonzalez FJ, Tanaka N. PPARs as metabolic regulators in the liver: Lessons from liver-specific ppar-null mice. Int J Mol Sci 2020; 21(6): 2061.
[93]
Serviddio G, Bellanti F, Vendemiale G. Free radical biology for medicine: Learning from nonalcoholic fatty liver disease. Free Radic Biol Med 2013; 65: 952-68.
[http://dx.doi.org/10.1016/j.freeradbiomed.2013.08.174] [PMID: 23994574]
[94]
Cariello M, Piccinin E, Moschetta A. Transcriptional regulation of metabolic pathways via lipid-sensing nuclear receptors ppars, fxr, and lxr in nash. Cell Mol Gastroenterol Hepatol 2021; 11(5): 1519-39.
[http://dx.doi.org/10.1016/j.jcmgh.2021.01.012] [PMID: 33545430]
[95]
Cheng HS, Tan WR, Low ZS, Marvalim C, Lee JYH, Tan NS. Exploration and development of ppar modulators in health and disease: An update of clinical evidence. Int J Mol Sci 2019; 20(20): 5055.
[96]
Francque S, Szabo G, Abdelmalek MF, et al. Nonalcoholic steatohepatitis: The role of peroxisome proliferator-activated receptors. Nat Rev Gastroenterol Hepatol 2021; 18(1): 24-39.
[http://dx.doi.org/10.1038/s41575-020-00366-5] [PMID: 33093663]
[97]
Chen J, Chen J, Fu H, et al. Hypoxia exacerbates nonalcoholic fatty liver disease via the HIF-2α/PPARα pathway. Am J Physiol Endocrinol Metab 2019; 317(4): E710-22.
[http://dx.doi.org/10.1152/ajpendo.00052.2019] [PMID: 31430204]
[98]
Liang N, Damdimopoulos A, Goñi S, et al. Hepatocyte-specific loss of GPS2 in mice reduces non-alcoholic steatohepatitis via activation of PPARα. Nat Commun 1684; 10(1): 1684.
[99]
Ju J, Huang Q, Sun J, et al. Correlation between PPAR-α methylation level in peripheral blood and atherosclerosis of NAFLD patients with DM. Exp Ther Med 2018; 15(3): 2727-30.
[http://dx.doi.org/10.3892/etm.2018.5730] [PMID: 29456675]
[100]
Zarei M, Barroso E, Palomer X, et al. Pharmacological PPARβ/δ activation upregulates VLDLR in hepatocytes. Clin Investig Arterioscler 2019; 31(3): 111-8.
[PMID: 30987865]
[101]
Rogue A, Anthérieu S, Vluggens A, et al. PPAR agonists reduce steatosis in oleic acid-overloaded HepaRG cells. Toxicol Appl Pharmacol 2014; 276(1): 73-81.
[http://dx.doi.org/10.1016/j.taap.2014.02.001] [PMID: 24534255]
[102]
Boeckmans J, Natale A, Rombaut M, et al. Anti-NASH drug development hitches a lift on ppar agonism. Cells 2019; 9(1): 37.
[http://dx.doi.org/10.3390/cells9010037] [PMID: 31877771]
[103]
Shinozaki S, Tahara T, Lefor AK, Ogura M. Pemafibrate decreases markers of hepatic inflammation in patients with non-alcoholic fatty liver disease. Clin Exp Hepatol 2020; 6(3): 270-4.
[http://dx.doi.org/10.5114/ceh.2020.99528] [PMID: 33145434]
[104]
Liang N, Jakobsson T, Fan R, Treuter E. The nuclear receptor-co-repressor complex in control of liver metabolism and disease. Front Endocrinol (Lausanne) 2019; 10: 411.
[http://dx.doi.org/10.3389/fendo.2019.00411] [PMID: 31293521]
[105]
Hameed B, Terrault N. Emerging therapies for nonalcoholic fatty liver disease. Clin Liver Dis 2016; 20(2): 365-85.
[http://dx.doi.org/10.1016/j.cld.2015.10.015] [PMID: 27063275]
[106]
Kumar DP, Caffrey R, Marioneaux J, et al. The ppar α/γ agonist saroglitazar improves insulin resistance and steatohepatitis in a diet induced animal model of nonalcoholic fatty liver disease. Sci Rep 2020; 10(1): 9330.
[107]
Diniz TA, de Lima Junior E.A., Teixeira AA, et al. Aerobic training improves NAFLD markers and insulin resistance through AMPK-PPAR-α signaling in obese mice. Life Sci 2021; 266: 118868.
[http://dx.doi.org/10.1016/j.lfs.2020.118868] [PMID: 33310034]
[108]
Zheng F, Cai Y. Concurrent exercise improves insulin resistance and nonalcoholic fatty liver disease by upregulating PPAR-γ and genes involved in the beta-oxidation of fatty acids in ApoE-KO mice fed a high-fat diet. Lipids Health Dis 2019; 18(1): 6.
[http://dx.doi.org/10.1186/s12944-018-0933-z] [PMID: 30611282]
[109]
Fiorucci S, Biagioli M, Sepe V, Zampella A, Distrutti E. Bile acid modulators for the treatment of nonalcoholic steatohepatitis (NASH). Expert Opin Investig Drugs 2020; 29(6): 623-32.
[http://dx.doi.org/10.1080/13543784.2020.1763302] [PMID: 32552182]
[110]
Xi Y, Li H. Role of farnesoid X receptor in hepatic steatosis in nonalcoholic fatty liver disease. Biomed Pharmacother 2020; 121: 109609.
[http://dx.doi.org/10.1016/j.biopha.2019.109609] [PMID: 31731192]
[111]
Cave MC, Clair HB, Hardesty JE, et al. Nuclear receptors and nonalcoholic fatty liver disease. Biochim Biophys Acta 2016; 1859(9): 1083-99.
[http://dx.doi.org/10.1016/j.bbagrm.2016.03.002] [PMID: 26962021]
[112]
Goodwin B, Jones SA, Price RR, et al. A regulatory cascade of the nuclear receptors FXR, SHP-1, and LRH-1 represses bile acid biosynthesis. Mol Cell 2000; 6(3): 517-26.
[http://dx.doi.org/10.1016/S1097-2765(00)00051-4] [PMID: 11030332]
[113]
Kim TH, Kim H, Park JM, et al. Interrelationship between liver X receptor alpha, sterol regulatory element-binding protein-1c, peroxisome proliferator-activated receptor gamma, and small heterodimer partner in the transcriptional regulation of glucokinase gene expression in liver. J Biol Chem 2009; 284(22): 15071-83.
[http://dx.doi.org/10.1074/jbc.M109.006742] [PMID: 19366697]
[114]
Preidis GA, Kim KH, Moore DD. Nutrient-sensing nuclear receptors PPARα and FXR control liver energy balance. J Clin Invest 2017; 127(4): 1193-201.
[http://dx.doi.org/10.1172/JCI88893] [PMID: 28287408]
[115]
Jadhav K, Xu Y, Xu Y, et al. Reversal of metabolic disorders by pharmacological activation of bile acid receptors TGR5 and FXR. Mol Metab 2018; 9: 131-40.
[http://dx.doi.org/10.1016/j.molmet.2018.01.005] [PMID: 29361497]
[116]
Chávez-Talavera O, Tailleux A, Lefebvre P, Staels B. Bile acid control of metabolism and inflammation in obesity, type 2 diabetes, dyslipidemia, and nonalcoholic fatty liver disease. Gastroenterology 2017; 152(7): 1679-1694.e3.
[http://dx.doi.org/10.1053/j.gastro.2017.01.055] [PMID: 28214524]
[117]
Zhu Y, Liu H, Zhang M, Guo GL. Fatty liver diseases, bile acids, and FXR. Acta Pharm Sin B 2016; 6(5): 409-12.
[http://dx.doi.org/10.1016/j.apsb.2016.07.008] [PMID: 27709009]
[118]
Schoeler M, Caesar R. Dietary lipids, gut microbiota and lipid metabolism. Rev Endocr Metab Disord 2019; 20(4): 461-72.
[http://dx.doi.org/10.1007/s11154-019-09512-0] [PMID: 31707624]
[119]
Chen J, Vitetta L. Gut microbiota metabolites in nafld pathogenesis and therapeutic implications. Int J Mol Sci 2020; 21(15): 5214.
[http://dx.doi.org/10.3390/ijms21155214] [PMID: 32717871]
[120]
Khan A, Ding Z, Ishaq M, et al. Understanding the effects of gut microbiota dysbiosis on nonalcoholic fatty liver disease and the possible probiotics role: Recent updates. Int J Biol Sci 2021; 17(3): 818-33.
[http://dx.doi.org/10.7150/ijbs.56214] [PMID: 33767591]
[121]
Tan X, Liu Y, Long J, et al. Trimethylamine n-oxide aggravates liver steatosis through modulation of bile acid metabolism and inhibition of farnesoid x receptor signaling in nonalcoholic fatty liver disease. Mol Nutr Food Res 2019; 63(17): e1900257.
[http://dx.doi.org/10.1002/mnfr.201900257] [PMID: 31095863]
[122]
Jiang C, Xie C, Li F, et al. Intestinal farnesoid X receptor signaling promotes nonalcoholic fatty liver disease. J Clin Invest 2015; 125(1): 386-402.
[http://dx.doi.org/10.1172/JCI76738] [PMID: 25500885]
[123]
Gonzalez FJ, Jiang C, Patterson AD. An intestinal microbiota-farnesoid x receptor axis modulates metabolic disease. Gastroenterology 2016; 151(5): 845-59.
[http://dx.doi.org/10.1053/j.gastro.2016.08.057] [PMID: 27639801]
[124]
Jiang C, Xie C, Lv Y, et al. Intestine-selective farnesoid X receptor inhibition improves obesity-related metabolic dysfunction. Nat Commun 2015; 6: 10166.
[http://dx.doi.org/10.1038/ncomms10166] [PMID: 26670557]
[125]
Younossi ZM, Ratziu V, Loomba R, et al. Regenerate study investigators Obeticholic acid for the treatment of non-alcoholic steatohepatitis: Interim analysis from a multicentre, randomised, placebo-controlled phase 3 trial. Lancet (London) 2019; 394(10215): 2184-96.
[http://dx.doi.org/10.1016/S0140-6736(19)33041-7]
[126]
Bowlus CL. Obeticholic acid for the treatment of primary biliary cholangitis in adult patients: Clinical utility and patient selection. Hepat Med 2016; 8: 89-95.
[http://dx.doi.org/10.2147/HMER.S91709] [PMID: 27621676]
[127]
Li J, Liu M, Li Y, et al. Discovery and optimization of non-bile acid fxr agonists as preclinical candidates for the treatment of nonalcoholic steatohepatitis. J Med Chem 2020; 63(21): 12748-72.
[http://dx.doi.org/10.1021/acs.jmedchem.0c01065] [PMID: 32991173]
[128]
Li H, Xi Y, Xin X, Tian H, Hu Y. Salidroside improves high-fat diet-induced non-alcoholic steatohepatitis by regulating the gut microbiota-bile acid-farnesoid X receptor axis. Biomed Pharmacother 2020; 124: 109915.
[http://dx.doi.org/10.1016/j.biopha.2020.109915] [PMID: 31986416]
[129]
Hsu WH, Chen TH, Lee BH, Hsu YW, Pan TM. Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice. Food Chem Toxicol 2014; 64: 94-103.
[http://dx.doi.org/10.1016/j.fct.2013.11.015] [PMID: 24275089]
[130]
Vakifahmetoglu-Norberg H, Ouchida AT, Norberg E. The role of mitochondria in metabolism and cell death. Biochem Biophys Res Commun 2017; 482(3): 426-31.
[http://dx.doi.org/10.1016/j.bbrc.2016.11.088] [PMID: 28212726]
[131]
Papazyan R, Sun Z, Kim YH, et al. Physiological suppression of lipotoxic liver damage by complementary actions of hdac3 and scap/srebp. Cell Metab 2016; 24(6): 863-74.
[http://dx.doi.org/10.1016/j.cmet.2016.10.012] [PMID: 27866836]
[132]
Rector RS, Thyfault JP, Uptergrove GM, et al. Mitochondrial dysfunction precedes insulin resistance and hepatic steatosis and contributes to the natural history of non-alcoholic fatty liver disease in an obese rodent model. J Hepatol 2010; 52(5): 727-36.
[http://dx.doi.org/10.1016/j.jhep.2009.11.030] [PMID: 20347174]
[133]
Speijer D, Manjeri GR, Szklarczyk R. How to deal with oxygen radicals stemming from mitochondrial fatty acid oxidation. Philos Trans R Soc Lond B Biol Sci 2014; 369(1646): 20130446.
[http://dx.doi.org/10.1098/rstb.2013.0446]
[134]
Woyda-Ploszczyca AM, Jarmuszkiewicz W. The conserved regulation of mitochondrial uncoupling proteins: From unicellular eukaryotes to mammals. Biochim Biophys Acta Bioenerg 2017; 1858(1): 21-33.
[http://dx.doi.org/10.1016/j.bbabio.2016.10.003] [PMID: 27751905]
[135]
Busiello RA, Savarese S, Lombardi A. Mitochondrial uncoupling proteins and energy metabolism. Front Physiol 2015; 6: 36.
[http://dx.doi.org/10.3389/fphys.2015.00036]
[136]
Cheng J, Nanayakkara G, Shao Y, et al. Mitochondrial proton leak plays a critical role in pathogenesis of cardiovascular diseases. Adv Exp Med Biol 2017; 982: 359-70.
[http://dx.doi.org/10.1007/978-3-319-55330-6_20] [PMID: 28551798]
[137]
Kelly LJ, Vicario PP, Thompson GM, et al. Peroxisome proliferator-activated receptors gamma and alpha mediate in vivo regulation of uncoupling protein (UCP-1, UCP-2, UCP-3) gene expression. Endocrinology 1998; 139(12): 4920-7.
[http://dx.doi.org/10.1210/endo.139.12.6384] [PMID: 9832429]
[138]
Rius-Pérez S, Torres-Cuevas I, Millán I, Ortega ÁL, Pérez S. PGC-1α, inflammation, and oxidative stress: An integrative view in metabolism. Oxid Med Cell Longev 2020.
[139]
Coelho MS, de Lima CL, Royer C, et al. GQ-16, a tzd-derived partial pparγ agonist, induces the expression of thermogenesis-related genes in brown fat and visceral white fat and decreases visceral adiposity in obese and hyperglycemic mice. PLoS One 2016; 11(5): e0154310.
[140]
Bond LM, Ntambi JM. UCP1 deficiency increases adipose tissue monounsaturated fatty acid synthesis and trafficking to the liver. J Lipid Res 2018; 59(2): 224-36.
[http://dx.doi.org/10.1194/jlr.M078469] [PMID: 29203476]
[141]
Tutunchi H, Ostadrahimi A, Saghafi-Asl M, et al. Oleoylethanolamide supplementation in obese patients newly diagnosed with non-alcoholic fatty liver disease: Effects on metabolic parameters, anthropometric indices, and expression of PPAR-α, UCP1, and UCP2 genes. Pharmacol Res 2020; 156: 104770.
[142]
Li L, Chen J, Ni Y, et al. TRPV1 activation prevents nonalcoholic fatty liver through UCP2 upregulation in mice. Pflugers Arch 2012; 463(5): 727-32.
[http://dx.doi.org/10.1007/s00424-012-1078-y] [PMID: 22395410]
[143]
Almanza-Perez JC, Alarcon-Aguilar FJ, Blancas-Flores G, et al. Glycine regulates inflammatory markers modifying the energetic balance through PPAR and UCP-2. Biomed Pharmacother 2010; 64(8): 534-40.
[http://dx.doi.org/10.1016/j.biopha.2009.04.047] [PMID: 19864106]
[144]
Berardi MJ, Chou JJ. Fatty acid flippase activity of UCP2 is essential for its proton transport in mitochondria. Cell Metab 2014; 20(3): 541-52.
[http://dx.doi.org/10.1016/j.cmet.2014.07.004] [PMID: 25127353]
[145]
Camara Y, Mampel T, Armengol J, Villarroya F, Dejean L. UCP3 expression in liver modulates gene expression and oxidative metabolism in response to fatty acids, and sensitizes mitochondria to permeability transition. Cell Physiol Biochem 2009; 24(3-4): 243-52.
[http://dx.doi.org/10.1159/000233249] [PMID: 19710539]
[146]
Lombardi A, Busiello RA, De Matteis R, et al. Absence of uncoupling protein-3 at thermoneutrality impacts lipid handling and energy homeostasis in mice. Cells 2019; 8(8): 916.
[http://dx.doi.org/10.3390/cells8080916]
[147]
Song Q, Guo R, Wei W, et al. Histidine-alleviated hepatocellular death in response to 4-hydroxynonenal contributes to the protection against high-fat diet-induced liver injury. J Funct Foods 2017; 39: 74-83.
[http://dx.doi.org/10.1016/j.jff.2017.09.056]
[148]
Ore A, Akinloye OA. Oxidative stress and antioxidant biomarkers in clinical and experimental models of non-alcoholic fatty liver disease. Medicina (Kaunas) 2019; 55(2): 26.
[http://dx.doi.org/10.3390/medicina55020026]
[149]
Masarone M, Rosato V, Dallio M, et al. Role of oxidative stress in pathophysiology of nonalcoholic fatty liver disease. Oxid Med Cell Longev 2018; •••: 9547613.
[http://dx.doi.org/10.1155/2018/9547613]
[150]
Berdichevsky A, Guarente L, Bose A. Acute oxidative stress can reverse insulin resistance by inactivation of cytoplasmic JNK. J Biol Chem 2010; 285(28): 21581-9.
[http://dx.doi.org/10.1074/jbc.M109.093633] [PMID: 20430894]
[151]
Han CY. Roles of reactive oxygen species on insulin resistance in adipose tissue. Diabetes Metab J 2016; 40(4): 272-9.
[http://dx.doi.org/10.4093/dmj.2016.40.4.272] [PMID: 27352152]
[152]
Xu D, Xu M, Jeong S, et al. The role of nrf2 in liver disease: Novel molecular mechanisms and therapeutic approaches. Front Pharmacol 2019; 9: 1428.
[153]
Feng X, Yu W, Li X, et al. Apigenin, a modulator of PPARγ, attenuates HFD-induced NAFLD by regulating hepatocyte lipid metabolism and oxidative stress via Nrf2 activation. Biochem Pharmacol 2017; 136: 136-49.
[http://dx.doi.org/10.1016/j.bcp.2017.04.014] [PMID: 28414138]
[154]
Sharma RS, Harrison DJ, Kisielewski D, et al. Experimental nonalcoholic steatohepatitis and liver fibrosis are ameliorated by pharmacologic activation of nrf2 (nf-e2 p45-related factor 2). Cell Mol Gastroenterol Hepatol 2017; 5(3): 367-98.
[http://dx.doi.org/10.1016/j.jcmgh.2017.11.016] [PMID: 29552625]
[155]
Jung BJ, Yoo HS, Shin S, Park YJ, Jeon SM. Dysregulation of NRF2 in cancer: From molecular mechanisms to therapeutic opportunities. Biomol Ther (Seoul) 2018; 26(1): 57-68.
[http://dx.doi.org/10.4062/biomolther.2017.195] [PMID: 29212307]
[156]
Fukai T, Ushio-Fukai M. Superoxide dismutases: Role in redox signaling, vascular function, and diseases. Antioxid Redox Signal 2011; 15(6): 1583-606.
[http://dx.doi.org/10.1089/ars.2011.3999] [PMID: 21473702]
[157]
Wang Y, Branicky R, Noë A, Hekimi S. Superoxide dismutases: Dual roles in controlling ROS damage and regulating ROS signaling. J Cell Biol 2018; 217(6): 1915-28.
[http://dx.doi.org/10.1083/jcb.201708007] [PMID: 29669742]
[158]
Boden MJ, Brandon AE, Tid-Ang JD, et al. Overexpression of manganese superoxide dismutase ameliorates high-fat diet-induced insulin resistance in rat skeletal muscle. Am J Physiol Endocrinol Metab 2012; 303(6): E798-805.
[http://dx.doi.org/10.1152/ajpendo.00577.2011] [PMID: 22829583]
[159]
Kwak HB, Lee Y, Kim JH, Van Remmen H, Richardson AG, Lawler JM. MnSOD overexpression reduces fibrosis and pro-apoptotic signaling in the aging mouse heart. J Gerontol A Biol Sci Med Sci 2015; 70(5): 533-44.
[http://dx.doi.org/10.1093/gerona/glu090] [PMID: 25016531]
[160]
Cui R, Gao M, Qu S, Liu D. Overexpression of superoxide dismutase 3 gene blocks high-fat diet-induced obesity, fatty liver and insulin resistance. Gene Ther 2014; 21(9): 840-8.
[http://dx.doi.org/10.1038/gt.2014.64] [PMID: 25030609]
[161]
Li S, Dou X, Ning H, et al. Sirtuin 3 acts as a negative regulator of autophagy dictating hepatocyte susceptibility to lipotoxicity. Hepatology 2017; 66(3): 936-52.
[http://dx.doi.org/10.1002/hep.29229] [PMID: 28437863]
[162]
Arya A, Azarmehr N, Mansourian M, Doustimotlagh AH. Inactivation of the superoxide dismutase by malondialdehyde in the nonalcoholic fatty liver disease: A combined molecular docking approach to clinical studies. Arch Physiol Biochem 2019; •••: 1-8.
[http://dx.doi.org/10.1080/13813455.2019.1659827] [PMID: 31475569]
[163]
Perriotte-Olson C, Adi N, Manickam DS, et al. Nanoformulated copper/zinc superoxide dismutase reduces adipose inflammation in obesity. Obesity (Silver Spring) 2016; 24(1): 148-56.
[http://dx.doi.org/10.1002/oby.21348] [PMID: 26612356]
[164]
Coudriet GM, Delmastro-Greenwood MM, Previte DM, et al. Treatment with a catalytic superoxide dismutase (sod) mimetic improves liver steatosis, insulin sensitivity, and inflammation in obesity-induced type 2 diabetes. Antioxidants (Basel) 2017; 6(4): 85.
[165]
Natarajan G, Perriotte-Olson C, Casey CA, et al. Effect of nanoformulated copper/zinc superoxide dismutase on chronic ethanol-induced alterations in liver and adipose tissue. Alcohol 2019; 79(79): 71-9.
[http://dx.doi.org/10.1016/j.alcohol.2018.12.005] [PMID: 30611703]
[166]
Qiu Y, Cao X, Liu L, et al. Modulation of mnsod and foxm1 is involved in invasion and emt suppression by isovitexin in hepatocellular carcinoma cells. Cancer Manag Res 2020; 12: 5759-71.
[http://dx.doi.org/10.2147/CMAR.S245283] [PMID: 32765079]
[167]
Ma X, Deng D, Chen W. Inhibitors and activators of sod, gsh‐px, and catEnzyme inhibitors and activators. IntechOpen 2017; pp. 207-24.
[168]
Kumar A, Sharma A, Duseja A, et al. Patients with nonalcoholic fatty liver disease (nafld) have higher oxidative stress in comparison to chronic viral hepatitis. J Clin Exp Hepatol 2013; 3(1): 12-8.
[http://dx.doi.org/10.1016/j.jceh.2012.10.009] [PMID: 25755466]
[169]
Heit C, Marshall S, Singh S, et al. Catalase deletion promotes prediabetic phenotype in mice. Free Radic Biol Med 2017; 103: 48-56.
[http://dx.doi.org/10.1016/j.freeradbiomed.2016.12.011] [PMID: 27939935]
[170]
Piao L, Choi J, Kwon G, Ha H. Endogenous catalase delays high-fat diet-induced liver injury in mice. Korean J Physiol Pharmacol 2017; 21(3): 317-25.
[http://dx.doi.org/10.4196/kjpp.2017.21.3.317] [PMID: 28461774]
[171]
Shin SK, Cho HW, Song SE, et al. Ablation of catalase promotes non-alcoholic fatty liver via oxidative stress and mitochondrial dysfunction in diet-induced obese mice. Pflugers Arch 2019; 471(6): 829-43.
[http://dx.doi.org/10.1007/s00424-018-02250-3] [PMID: 30617744]
[172]
Hwang I, Uddin MJ, Pak ES, et al. The impaired redox balance in peroxisomes of catalase knockout mice accelerates nonalcoholic fatty liver disease through endoplasmic reticulum stress. Free Radic Biol Med 2020; 148: 22-32.
[http://dx.doi.org/10.1016/j.freeradbiomed.2019.12.025] [PMID: 31877356]
[173]
El-Hafidi M, Franco M, Ramírez AR, et al. Glycine increases insulin sensitivity and glutathione biosynthesis and protects against oxidative stress in a model of sucrose-induced insulin resistance. Oxid Med Cell Longev 2018; 1-12.
[http://dx.doi.org/10.1155/2018/2101562]
[174]
Surapaneni KM, Jainu M. Comparative effect of pioglitazone, quercetin and hydroxy citric acid on the status of lipid peroxidation and antioxidants in experimental non-alcoholic steatohepatitis. J Physiol Pharmacol 2014; 65(1): 67-74.
[PMID: 24622831]
[175]
Benhar M. Roles of mammalian glutathione peroxidase and thioredoxin reductase enzymes in the cellular response to nitrosative stress. Free Radic Biol Med 2018; 127: 160-4.
[http://dx.doi.org/10.1016/j.freeradbiomed.2018.01.028] [PMID: 29378334]
[176]
Diamond AM. The subcellular location of selenoproteins and the impact on their function. Nutrients 2015; 7(5): 3938-48.
[http://dx.doi.org/10.3390/nu7053938] [PMID: 26007340]
[177]
Labunskyy VM, Hatfield DL, Gladyshev VN. Selenoproteins: Molecular pathways and physiological roles. Physiol Rev 2014; 94(3): 739-77.
[http://dx.doi.org/10.1152/physrev.00039.2013] [PMID: 24987004]
[178]
Mbemba TM, Kapepula PM, Esimo JM, Remacle J, Ngombe NK. Subcellular localization of glutathione peroxidase, subcellular localization of glutathione peroxidase, change in glutathione system during ageing and effects on cardiometabolic risks and associated diseasesGlutathione system and oxidative stress in health and disease IntechOpen 2019; 1-19.
[179]
Merry TL, Tran M, Dodd GT, et al. Hepatocyte glutathione peroxidase-1 deficiency improves hepatic glucose metabolism and decreases steatohepatitis in mice. Diabetologia 2016; 59(12): 2632-44.
[http://dx.doi.org/10.1007/s00125-016-4084-3] [PMID: 27628106]
[180]
Zhang Q, Qian ZY, Zhou PH, et al. Effects of oral selenium and magnesium co-supplementation on lipid metabolism, antioxidative status, histopathological lesions, and related gene expression in rats fed a high-fat diet. Lipids Health Dis 2018; 17(1): 165.
[http://dx.doi.org/10.1186/s12944-018-0815-4]
[181]
Yant LJ, Ran Q, Rao L, et al. The selenoprotein GPX4 is essential for mouse development and protects from radiation and oxidative damage insults. Free Radic Biol Med 2003; 34(4): 496-502.
[http://dx.doi.org/10.1016/S0891-5849(02)01360-6] [PMID: 12566075]
[182]
Imai H, Hirao F, Sakamoto T, et al. Early embryonic lethality caused by targeted disruption of the mouse PHGPx gene. Biochem Biophys Res Commun 2003; 305(2): 278-86.
[http://dx.doi.org/10.1016/S0006-291X(03)00734-4] [PMID: 12745070]
[183]
Carlson BA, Tobe R, Yefremova E, et al. Glutathione peroxidase 4 and vitamin E cooperatively prevent hepatocellular degeneration. Redox Biol 2016; 9: 22-31.
[http://dx.doi.org/10.1016/j.redox.2016.05.003] [PMID: 27262435]
[184]
Rohr-Udilova N, Bauer E, Timelthaler G, et al. Impact of glutathione peroxidase 4 on cell proliferation, angiogenesis and cytokine production in hepatocellular carcinoma. Oncotarget 2018; 9(11): 10054-68.
[http://dx.doi.org/10.18632/oncotarget.24300] [PMID: 29515790]
[185]
Zhang CX, Guo LK, Qin YM, Li GY. Association of polymorphisms of adiponectin gene promoter-11377C/G, glutathione peroxidase-1 gene C594T, and cigarette smoking in nonalcoholic fatty liver disease. J Chin Med Assoc 2016; 79(4): 195-204.
[http://dx.doi.org/10.1016/j.jcma.2015.09.003] [PMID: 26897098]
[186]
Kaser S, Ebenbichler CF, Tilg H. Pharmacological and non-pharmacological treatment of non-alcoholic fatty liver disease. Int J Clin Pract 2010; 64(7): 968-83.
[http://dx.doi.org/10.1111/j.1742-1241.2009.02327.x] [PMID: 20584230]
[187]
Vilar-Gomez E, Vuppalanchi R, Gawrieh S, et al. Vitamin e improves transplant-free survival and hepatic decom-pensation among patients with nonalcoholic steatohepatitis and advanced fibrosis. Hepatology 2020; 71(2): 495-509.
[http://dx.doi.org/10.1002/hep.30368] [PMID: 30506586]
[188]
Jakubczyk K, Skonieczna-Żydecka K, Kałduńska J, Stachowska E, Gutowska I, Janda K. Effects of resveratrol supplementation in patients with non-alcoholic fatty liver disease-a meta-analysis. Nutrients 2020; 12(8): 2435.
[http://dx.doi.org/10.3390/nu12082435] [PMID: 32823621]
[189]
Rafiee S, Mohammadi H, Ghavami A, Sadeghi E, Safari Z, Askari G. Efficacy of resveratrol supplementation in patients with nonalcoholic fatty liver disease: A systematic review and meta-analysis of clinical trials. Complement Ther Clin Pract 2021; 42: 101281.
[http://dx.doi.org/10.1016/j.ctcp.2020.101281] [PMID: 33321448]
[190]
Jalali M, Mahmoodi M, Mosallanezhad Z, Jalali R, Imanieh MH, Moosavian SP. The effects of curcumin supplementation on liver function, metabolic profile and body composition in patients with non-alcoholic fatty liver disease: A systematic review and meta-analysis of randomized controlled trials. Complement Ther Med 2020; 48: 102283.
[http://dx.doi.org/10.1016/j.ctim.2019.102283] [PMID: 31987259]
[191]
Gillessen A, Schmidt HH. Silymarin as supportive treatment in liver diseases: A narrative review. Adv Ther 2020; 37(4): 1279-301.
[http://dx.doi.org/10.1007/s12325-020-01251-y] [PMID: 32065376]
[192]
Medina-Urrutia A, Lopez-Uribe AR, El Hafidi M, et al. Chia (Salvia hispanica)-supplemented diet ameliorates non-alcoholic fatty liver disease and its metabolic abnormalities in humans. Lipids Health Dis 2020; 19(1): 96.
[http://dx.doi.org/10.1186/s12944-020-01283-x] [PMID: 32430018]
[193]
Mahmoodi M, Hosseini R, Kazemi A, Ofori-Asenso R, Mazidi M, Mazloomi SM. Effects of green tea or green tea catechin on liver enzymes in healthy individuals and people with nonalcoholic fatty liver disease: A systematic review and meta-analysis of randomized clinical trials. Phytother Res 2020; 34(7): 1587-98.
[http://dx.doi.org/10.1002/ptr.6637] [PMID: 32067271]