Impaired base excision repair is related to the pathogenesis of non-alcoholic fatty liver disease

Authors

DOI:

https://doi.org/10.18778/1730-2366.16.01

Keywords:

DNA repair, non-alcoholic fatty liver, base excision repair

Abstract

Non-alcoholic fatty disease (NAFLD) is a liver disorder that affects up to 30% of the population, mainly in Western countries. It is estimated that up to 75% of NAFLD patients will develop a more aggressive form of the disease, non-alcoholic steatohepatitis (NASH). NAFLD can lead to fibrosis and liver failure; however, it is difficult to diagnose NAFLD due to its non-specific symptoms. Unfortunately, there is no treatment available for this disease. The risk factors of NAFLD are obesity and insulin resistance (IR). The molecular factors that seem to play an important role in the pathogenesis of NAFLD are oxidative stress as well as impaired DNA damage repair processes; a great body of evidence confirms an association with the base excision repair (BER) pathway. The activity of BER is decreased in patients with NAFLD and in animal models of this disease. In order to better understand the underlying basis of the disease, knowledge should be broadened in the area of DNA repair in NAFLD.

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References

Abd El-Kader, S.M., El-Den Ashmawy, E.M.S. 2015. Non-Alcoholic fatty liver disease: The diagnosis and management. World Journal of Hepatology, 7(6): 846–858. DOI: https://doi.org/10.4254/wjh.v7.i6.846

Alexeyev, M., Shokolenko, I., Wilson, G., LeDoux, S. 2013. The maintenance of mitochondrial DNA integrity-critical analysis and update. Cold Spring Harbor Perspectives in Biology, 5(5): a012641–a012641. DOI: https://doi.org/10.1101/cshperspect.a012641

Boden, G. 1997. Role of fatty acids in the pathogenesis of insulin resistance and NIDDM. Diabetes, 46(1): 3–10. DOI: https://doi.org/10.2337/diabetes.46.1.3

Bril, F., Kalavalapalli, S., Clark, V.C., Lomonaco, R., Soldevila-Pico, C., Liu, I.-C., Orsak, B., Tio, F., Cusi, K. 2018. Response to pioglitazone in patients with non-alcoholic steatohepatitis with vs without type 2 diabetes. Clinical Gastroenterology and Hepatology, 16(4): 558–566.e2. DOI: https://doi.org/10.1016/j.cgh.2017.12.001

Caballero, F., Fernández, A., De Lacy, A.M., Fernández-Checa, J.C., Caballería, J., García-Ruiz, C. 2009. Enhanced free cholesterol, SREBP-2 and StAR expression in human NASH. Journal of Hepatology, 50(4): 789–796. DOI: https://doi.org/10.1016/j.jhep.2008.12.016

Caligiuri, A., Gentilini, A., Marra, F. 2016. Molecular pathogenesis of NASH. International Journal of Molecular Sciences, 17(9): 1575. DOI: https://doi.org/10.3390/ijms17091575

Chatterjee, N., Walker, G.C. 2017. Mechanisms of DNA damage, repair, and mutagenesis. Environmental and Molecular Mutagenesis, 58(5): 235–263. DOI: https://doi.org/10.1002/em.22087

Chitturi, S., Wong, V.W.-S., Chan, W.-K., Wong G.L.-H., Wong, S.K.-H., Sollano, J., Ni, Y.-H., Liu, C.-J., Lin, Y.-C., Lesmana, L.A., Kim, S.U., Hashimoto, E., Hamaguchi, M., Goh, K.-L., Fan, J., Duseja, A., Dan, Y.Y., Chawla, Y., Farrell, G., Chan H.L.-Y. 2018. The Asia-Pacific working party on non-alcoholic fatty liver disease guidelines 2017-Part 2: Management and special groups. Journal of Gastroenterology and Hepatology, 33(1): 86 –98. DOI: https://doi.org/10.1111/jgh.13856

Cioffi, F., Senese, R., Lasala, P., Ziello, A., Mazzoli, A., Crescenzo, R., Liverini, G., Lanni, A., Goglia, F., Iossa, S. 2017. Fructose-rich diet affects mitochondrial DNA damage and repair in rats. Nutrients, 9(4): 323. DOI: https://doi.org/10.3390/nu9040323

Cohen, J.C., Horton, J.D., Hobbs, H.H. 2011. Human fatty liver disease: old questions and new insights. Science, 332(6037): 1519–1523. DOI: https://doi.org/10.1126/science.1204265

Czarny, P., Wigner, P., Galecki, P., Sliwinski, T. 2018. The interplay between inflammation, oxidative stress, DNA damage, DNA repair and mitochondrial dysfunction in depression. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 80: 309–321. DOI: https://doi.org/10.1016/j.pnpbp.2017.06.036

Day, C.P., James, O.F.W. 1998. Steatohepatitis: A tale of two “hits”? Gastroenterology, 114(4): 842–845. DOI: https://doi.org/10.1016/S0016-5085(98)70599-2

Gao, D., Wei, C., Chen, L., Huang, J., Yang, S., Diehl, A.M. 2004. Oxidative DNA damage and DNA repair enzyme expression are inversely related in murine models of fatty liver disease. American Journal of Physiology. Gastrointestinal and Liver Physiology, 287(5): G1070–1077. DOI: https://doi.org/10.1152/ajpgi.00228.2004

Hsiao, P.-J., Hsieh, T.-J., Kuo, K.-K., Hung, W.-W., Tsai, K.-B., Yang, C.-H., Yu, M.-L., Shin, S.-J. 2008. Pioglitazone retrieves hepatic antioxidant DNA repair in a mice model of high fat diet. BMC Molecular Biology, 9: 82. DOI: https://doi.org/10.1186/1471-2199-9-82

Ibarrola-Villava, M., Peña-Chilet, M., Fernandez, L.P., Aviles, J.A., Mayor, M., Martin-Gonzalez, M., Gomez-Fernandez, C., Casado, B., Lazaro, P., Lluch, A., Benitez, J., Lozoya, R., Boldo, E., Pizarro, A., Martinez-Cadenas, C., Ribas, G. 2011. Genetic polymorphisms in DNA repair and oxidative stress pathways associated with malignant melanoma susceptibility. European Journal of Cancer (Oxford, England, 1990) 47(17): 2618–2625. DOI: https://doi.org/10.1016/j.ejca.2011.05.011

Kershaw, E.E., Flier, J.S. 2004. Adipose tissue as an endocrine organ. The Journal of Clinical Endocrinology and Metabolism, 89(6): 2548–2556. DOI: https://doi.org/10.1210/jc.2004-0395

Kim, D., Touros, A., Kim, W.R. 2018. Non-alcoholic fatty liver disease and metabolic syndrome. Clinics in Liver Disease, 22(1): 133–140. DOI: https://doi.org/10.1016/j.cld.2017.08.010

Kim, Y.-J., Wilson 3rd, D.M. 2012. Overview of base excision repair biochemistry. Current Molecular Pharmacology, 5(1): 3–13. DOI: https://doi.org/10.2174/1874467211205010003

Koek, G.H., Liedorp, P.R., Bast, A. 2011. The role of oxidative stress in non-alcoholic steato-hepatitis. Clinica Chimica Acta, 412(15–16): 1297–1305. DOI: https://doi.org/10.1016/j.cca.2011.04.013

Koo, S.-H. 2013. Non-alcoholic fatty liver disease: molecular mechanisms for the hepatic steatosis. Clinical and Molecular Hepatology, 19(3): 210–215. DOI: https://doi.org/10.3350/cmh.2013.19.3.210

Lee, Y., Hirose, H., Ohneda, M., Johnson, J.H., McGarry, J.D., Unger, R.H. 1994. Beta-cell lipotoxicity in the pathogenesis of non-insulin-dependent diabetes mellitus of obese rats: impairment in adipocyte-beta-cell relation-ships. Proceedings of the National Academy of Sciences of the United States of America, 91(23): 10878–10882. DOI: https://doi.org/10.1073/pnas.91.23.10878

Liao, W., Hui, T.Y., Young, S.G., Davis, R.A. 2003. Blocking microsomal triglyceride transfer protein interferes with ApoB secretion without causing retention or stress in the ER. Journal of Lipid Research, 44(5): 978–985. DOI: https://doi.org/10.1194/jlr.M300020-JLR200

Lillenes, M.S., Støen, M., Günther, C.-C., Selnes, P., Stenset, V.T. V, Espeseth, T., Reinvang, I., Fladby, T., Tønjum, T. 2017. Mitochondrial transcription factor A (TFAM) Rs1937 and AP endonuclease 1 (APE1) Rs1130409 alleles are associated with reduced cognitive performance. Neuroscience Letters 645: 46–52. DOI: https://doi.org/10.1016/j.neulet.2017.02.062

Mabalirajan, U., Ghosh, B. 2013. Mitochondrial dysfunction in metabolic syndrome and asthma. Journal of Allergy, 2013: 340476. DOI: https://doi.org/10.1155/2013/340476

Maloney, E., Sweet, I.R., Hockenbery, D.M., Pham, M., Rizzo, N.O., Tateya, S., Handa, P., Schwartz, M.W., Kim, F. 2009. Activation of NF-KappaB by palmitate in endothelial cells: A key role for NADPH oxidase-derived superoxide in response to TLR4 activation. Arteriosclerosis, Thrombosis, and Vascular Biology, 29(9): 1370–1375. DOI: https://doi.org/10.1161/ATVBAHA.109.188813

Masarone, M., Rosato, V., Dallio, M., Gravina, A.G., Aglitti, A., Loguercio, C., Federico, A., Persico, M. 2018. Role of oxidative stress in pathophysiology of non-alcoholic fatty liver disease. Oxidative Medicine and Cellular Longevity, 2018: 9547613. DOI: https://doi.org/10.1155/2018/9547613

Monetti, M., Levin, M.C., Watt, M.J., Sajan, M.P., Marmor, S., Hubbard, B.K., Stevens, R.D., Bain, J.R., Newgard, C.B., Farese R.V. Sr., Hevener, A.L., Farese, R.V. Jr. 2007. Dissociation of hepatic steatosis and insulin resistance in mice overexpressing DGAT in the liver. Cell Metabolism, 6(1): 69–78. DOI: https://doi.org/10.1016/j.cmet.2007.05.005

Nagahashi, M., Matsuda, Y., Moro, K., Tsuchida, J., Soma, D., Hirose, Y., Kobayashi, T., Kosugi, S.-I., Takabe, K., Komatsu, M., Wakai, T. 2016. DNA damage response and sphingolipid signaling in liver diseases. Surgery Today, 46(9): 995–1005. DOI: https://doi.org/10.1007/s00595-015-1270-8

Neuschwander-Tetri, B.A. 2010. Hepatic lipotoxi-city and the pathogenesis of non-alcoholic steatohepatitis: the central role of nontrigly-ceride fatty acid metabolites. Hepatology (Baltimore, MD), 52(2): 774–788. DOI: https://doi.org/10.1002/hep.23719

Parker, R. 2018. The role of adipose tissue in fatty liver diseases. Liver Research, 2(1): 35–42. DOI: https://doi.org/10.1016/j.livres.2018.02.002

Paschos, P., Paletas, K. 2009. Non alcoholic fatty liver disease and metabolic syndrome. Hippokratia, 13(1): 9–19.

Pinter, M., Trauner, M., Peck-Radosavljevic, M., Sieghart, W. 2016. Cancer and liver cirrhosis: implications on prognosis and management. ESMO Open, 1(2): e000042. DOI: https://doi.org/10.1136/esmoopen-2016-000042

Popanda, O., Seibold, P., Nikolov, I., Oakes, C.C., Burwinkel, B., Hausmann, S., Flesch-Janys, D., Plass, C., Chang-Claude, J., Schmezer, P. 2013. Germline variants of base excision repair genes and breast cancer: a polymorphism in DNA polymerase gamma modifies gene expression and breast cancer risk. International Journal of Cancer 132(1): 55–62. DOI: https://doi.org/10.1002/ijc.27665

Rotter, V., Nagaev, I., Smith, U. 2003. Interleukin-6 (IL-6) induces insulin resistance in 3T3-L1 adipocytes and Is, like IL-8 and tumor necrosis factor-alpha, overexpressed in human fat cells from insulin-resistant subjects. Journal of Biological Chemistry, 278(46): 45777–45784. DOI: https://doi.org/10.1074/jbc.M301977200

Sampath, H., Vartanian, V., Rollins, M.R., Sakumi, K., Nakabeppu, Y., Lloyd, R.S. 2012. 8-Oxoguanine DNA glycosylase (OGG1) deficiency increases susceptibility to obesity and metabolic dysfunction. PLoS One, 7(12): e51697. DOI: https://doi.org/10.1371/journal.pone.0051697

Schults, M.A., Nagle, P.W., Rensen, S.S., Godschalk, R.W., Munnia, A., Peluso, M., Claessen, S.M., Greve, J.W., Driessen, A., Verdam, F.J., Buurman, W.A., van Schooten, F.J., Chiu, R.K. 2012. Decreased nucleotide excision repair in steatotic livers associates with myeloperoxidase-immunoreactivity. Mutation Research, 736(1-2): 75–81. DOI: https://doi.org/10.1016/j.mrfmmm.2011.11.001

Seki, E., De Minicis, S., Österreicher, C.H., Kluwe, J., Osawa, Y., Brenner, D.A., Schwabe, R.F. 2007. TLR4 enhances TGF-β signaling and hepatic fibrosis. Nature Medicine, 13(11): 1324–1332. DOI: https://doi.org/10.1038/nm1663

Sharma, M., Mitnala, S., Vishnubhotla, R.K., Mukherjee, R., Reddy, D.N., Rao, P.N. 2015. The riddle of non-alcoholic fatty liver disease: progression from non-alcoholic fatty liver to non-alcoholic steatohepatitis. Journal of Clinical and Experimental Hepatology, 5(2): 147–158. DOI: https://doi.org/10.1016/j.jceh.2015.02.002

Shi, H., Kokoeva, M. V, Inouye, K., Tzameli, I., Yin, H., Flier, J.S. 2006. TLR4 links innate immunity and fatty acid-induced insulin resistance. Journal of Clinical Investigation, 116(11): 3015–3025. DOI: https://doi.org/10.1172/JCI28898

Skurk, T., Alberti-Huber, C., Herder, C., Hauner, H. 2007. Relationship between adipocyte size and adipokine expression and secretion. Journal of Clinical Endocrinology and Metabolism, 92(3): 1023–1033. DOI: https://doi.org/10.1210/jc.2006-1055

Stienstra, R., Saudale, F., Duval, C., Keshtkar, S., Groener, J.E.M., van Rooijen, N., Staels, B., Kersten, S., Muller, M. 2010. Kupffer cells promote hepatic steatosis via interleukin-1beta-dependent suppression of peroxisome proliferator-activated receptor alpha activity. Hepatology (Baltimore, MD), 51(2): 511–522. DOI: https://doi.org/10.1002/hep.23337

Takumi, S., Okamura, K., Yanagisawa, H., Sano, T., Kobayashi, Y., Nohara, K. 2015. The effect of a methyl-deficient diet on the global DNA methylation and the DNA methylation regulatory pathways. Journal of Applied Toxicology, 35(12): 1550–1556. DOI: https://doi.org/10.1002/jat.3117

Tanaka, N., Takahashi, S., Hu, X., Lu, Y., Fujimori, N., Golla, S., Fang, Z.-Z., Aoyama, T., Krausz, K.W., Gonzalez, F.J. 2017. Growth arrest and DNA damage-inducible 45α protects against non-alcoholic steatohepatitis induced by methionine- and choline-deficient diet. Biochimica et Biophysica Acta. Molecular Basis of Disease, 1863(12): 3170–3182. DOI: https://doi.org/10.1016/j.bbadis.2017.08.017

Tomita, K., Teratani, T., Suzuki, T., Shimizu, M., Sato, H., Narimatsu, K., Okada, Y., Kurihara, C., Irie, R., Yokoyama, H., Shimamura, K., Usui, S., Ebinuma, H., Saito., H., Watanabe, C., Komoto, S., Kawaguchi, A., Nagao, S., Sugiyama, K., Hokari, R., Kanai, T., Miura, S., Hibi, T. 2014. Free cholesterol accumulation in hepatic stellate cells: mechanism of liver fibrosis aggravation in non-alcoholic steatohepatitis in mice. Hepatology (Baltimore, MD), 59(1): 154–169. DOI: https://doi.org/10.1002/hep.26604

Wong, V.W.-S., Singal, A.K. 2019. Emerging medical therapies for non-alcoholic fatty liver disease and for alcoholic hepatitis. Translational Gastroenterology and Hepato-logy, 4: 53. DOI: https://doi.org/10.21037/tgh.2019.06.06

Yang, J., Fernández-Galilea, M., Martínez-Fernández, L., González-Muniesa, P., Pérez-Chávez, A., Martínez, J.A., Moreno-Aliaga, M.J. 2019. Oxidative stress and non-alcoholic fatty liver disease: effects of omega-3 fatty acid supplementation. Nutrients, 11(4): 872. DOI: https://doi.org/10.3390/nu11040872

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2020-12-30

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Ziółkowska, Sylwia, Piotr Czarny, and Janusz Szemraj. 2020. “Impaired Base Excision Repair Is Related to the Pathogenesis of Non-Alcoholic Fatty Liver Disease”. Acta Universitatis Lodziensis. Folia Biologica Et Oecologica 16 (December): 5-11. https://doi.org/10.18778/1730-2366.16.01.