Risk Factors of Non-Alcoholic Fatty Liver Disease

Authors

  • Yiyang Shen

DOI:

https://doi.org/10.61173/612v5y33

Keywords:

Non-alcoholic fatty liver disease, risk factors, pathogenesis, treatment

Abstract

An increasing number of people worldwide are suffering from non-alcoholic fatty liver disease (NAFLD), a condition characterized by fat buildup in the liver. Numerous categories can be used to group the risk factors for non-alcoholic fatty liver disease (NAFLD), including metabolic, genetic, epigenetic, demographic, and environmental factors. First, metabolic variables—obesity and insulin resistance in particular—are among the main risk factors for non-alcoholic fatty liver disease (NAFLD). The accumulation of fat in the liver is largely caused by obesity, and the disruption of normal fat metabolism caused by insulin resistance adds to the burden on the liver. Furthermore, there is a strong correlation between the onset of NAFLD and the existence of metabolic syndrome. Second, how susceptible a person is to NAFLD depends largely on hereditary factors. The start of the disease is also significantly influenced by epigenetic variables. Age, gender, and other demographic traits are linked to an increased risk of developing nonalcoholic fatty liver disease (NAFLD). In addition, smoking, leading a poor lifestyle, and being around pollutants can all increase the risk of developing the condition. In order to lower the incidence of NAFLD, effective prevention and intervention methods will be devised with the help of a thorough analysis of the interactions among these factors.

References

[1] anyal AJ, Brunt EM, Kleiner DE, Kowdley KV, Chalasani N, Lavine JE, Ratziu V, McCullough A. Endpoints and clinical trial design for nonalcoholic steatohepatitis. Hepatology. 2011 Jul;54(1):344-53.

[2] Eslam M, Valenti L, Romeo S. Genetics and epigenetics of NAFLD and NASH: Clinical impact. J Hepatol. 2018 Feb;68(2):268-279.

[3] Huang Y, Cohen JC, Hobbs HH. Expression and characterization of a PNPLA3 protein isoform (I148M) associated with nonalcoholic fatty liver disease. J Biol Chem. 2011 Oct 28;286(43):37085-93.

[4] Kozlitina J, Smagris E, Stender S, Nordestgaard BG, Zhou HH, Tybjærg-Hansen A, Vogt TF, Hobbs HH, Cohen JC. Exomewide association study identifies a TM6SF2 variant that confers susceptibility to nonalcoholic fatty liver disease. Nat Genet. 2014 Apr;46(4):352-6.

[5] Luukkonen PK, Zhou Y, Nidhina Haridas PA, Dwivedi OP, Hyötyläinen T, Ali A, Juuti A, Leivonen M, Tukiainen T, Ahonen L, Scott E, Palmer JM, Arola J, Orho-Melander M, Vikman P, Anstee QM, Olkkonen VM, Orešič M, Groop L, Yki-Järvinen H. Impaired hepatic lipid synthesis from polyunsaturated fatty acids in TM6SF2 E167K variant carriers with NAFLD. J Hepatol. 2017 Jul;67(1):128-136.

[6] Beer NL, Tribble ND, McCulloch LJ, Roos C, Johnson PR, Orho-Melander M, Gloyn AL. The P446L variant in GCKR associated with fasting plasma glucose and triglyceride levels exerts its effect through increased glucokinase activity in liver. Hum Mol Genet. 2009 Nov 1;18(21):4081-8.

[7] Valenti L, Alisi A, Nobili V. Unraveling the genetics of fatty liver in obese children: additive effect of P446L GCKR and I148M PNPLA3 polymorphisms. Hepatology. 2012 Mar;55(3):661-3.

[8] Eslam M, Valenti L, Romeo S. Genetics and epigenetics of NAFLD and NASH: Clinical impact. J Hepatol. 2018 Feb;68(2):268-279.

[9] Ahrens M, Ammerpohl O, von Schönfels W, Kolarova J, Bens S, Itzel T, Teufel A, Herrmann A, Brosch M, Hinrichsen H, Erhart W, Egberts J, Sipos B, Schreiber S, Häsler R, Stickel F, Becker T, Krawczak M, Röcken C, Siebert R, Schafmayer C, Hampe J. DNA methylation analysis in nonalcoholic fatty liver disease suggests distinct disease-specific and remodeling signatures after bariatric surgery. Cell Metab. 2013 Aug 6;18(2):296-302.

[10] Szabo G, Csak T. Role of MicroRNAs in NAFLD/NASH. Dig Dis Sci. 2016 May;61(5):1314-24.

[11] Anderson EL, Howe LD, Jones HE, Higgins JP, Lawlor DA, Fraser A. The Prevalence of Non-Alcoholic Fatty Liver Disease in Children and Adolescents: A Systematic Review and Meta- Dean&Francis Yiyang Shen Analysis. PLoS One. 2015 Oct 29;10(10):e0140908.

[12] Ballestri S, Nascimbeni F, Baldelli E, Marrazzo A, Romagnoli D, Lonardo A. NAFLD as a Sexual Dimorphic Disease: Role of Gender and Reproductive Status in the Development and Progression of Nonalcoholic Fatty Liver Disease and Inherent Cardiovascular Risk. Adv Ther. 2017 Jun;34(6):1291-1326.

[13] Kim NH, Jung YS, Hong HP, Park JH, Kim HJ, Park DI, Cho YK, Sohn CI, Jeon WK, Kim BI. Association between cotinine-verified smoking status and risk of nonalcoholic fatty liver disease. Liver Int. 2018 Aug;38(8):1487-1494.

[14] Arciello M, Gori M, Maggio R, Barbaro B, Tarocchi M, Galli A, Balsano C. Environmental pollution: a tangible risk for NAFLD pathogenesis. Int J Mol Sci. 2013 Nov 7;14(11):22052- 66.

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Published

2024-12-31