Abstract
Obesity is associated with nonalcoholic fatty liver disease (NAFLD), cardiovascular disease (CVD), and type 2 diabetes mellitus (T2DM). In recent years, NAFLD has emerged as the most common liver disease, affecting 25% of the global population. NAFLD is characterized by the accumulation of excessive lipids within hepatocytes, insulin resistance, abdominal fat distribution, dyslipidemia, and high blood pressure. NAFLD is highly prevalent in the United States, and represents abnormalities ranging from hepatic steatosis to more severe forms of nonalcoholic steatohepatitis, which can induce cirrhosis, fibrosis, and hepatocellular carcinoma. NAFLD involves a reprogrammed hepatic metabolic machinery that leads to excessive lipid accumulation and imbalances in lipid metabolism and lipid catabolism in the liver. Hepatic lipid homeostasis is well elucidated as a complex processes, including cellular signaling and transcriptional pathways and genes associated with fatty acid (FA) uptake and oxidation and lipogenesis. This chapter discusses the definition, risk factors, and diagnosis of NAFLD. We also describe animal models used to study the disease, i.e., dietary and genetic models. Lastly, we discuss the current therapies for NAFLD.
References
Younossi Z, et al. Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention. Nat Rev Gastroenterol Hepatol. 2018;15(1):11–20.
Kim D, et al. Changing trends in etiology-based annual mortality from chronic liver disease, from 2007 through 2016. Gastroenterology. 2018;155(4):1154–63.e3.
Fan JG, Kim SU, Wong VW. New trends on obesity and NAFLD in Asia. J Hepatol. 2017;67(4):862–73.
Estes C, et al. Modeling the epidemic of nonalcoholic fatty liver disease demonstrates an exponential increase in burden of disease. Hepatology. 2018;67(1):123–33.
Younossi Z, et al. Global perspectives on nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. Hepatology. 2019;69(6):2672–82.
Anstee QM, Targher G, Day CP. Progression of NAFLD to diabetes mellitus, cardiovascular disease or cirrhosis. Nat Rev Gastroenterol Hepatol. 2013;10(6):330–44.
Younossi ZM, et al. Global epidemiology of nonalcoholic fatty liver disease-meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology. 2016;64(1):73–84.
Feijo SG, et al. The spectrum of non alcoholic fatty liver disease in morbidly obese patients: prevalence and associate risk factors. Acta Cir Bras. 2013;28(11):788–93.
White DL, Kanwal F, El-Serag HB. Association between nonalcoholic fatty liver disease and risk for hepatocellular cancer, based on systematic review. Clin Gastroenterol Hepatol. 2012;10(12):1342.
Yang JD, et al. A global view of hepatocellular carcinoma: trends, risk, prevention and management. Nat Rev Gastroenterol Hepatol. 2019;16(10):589–604.
Yamamura S, et al. MAFLD identifies patients with significant hepatic fibrosis better than NAFLD. Liver Int. 2020;40(12):3018–30.
Eslam M, et al. A new definition for metabolic dysfunction-associated fatty liver disease: an international expert consensus statement. J Hepatol. 2020;73(1):202–9.
Chalasani N, et al. The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology. Gastroenterology. 2012;142(7):1592–609.
Rich NE, et al. Racial and ethnic disparities in nonalcoholic fatty liver disease prevalence, severity, and outcomes in the United States: a systematic review and meta-analysis. Clin Gastroenterol Hepatol. 2018;16(2):198–210 e2.
Wong RJ, Liu B, Bhuket T. Significant burden of nonalcoholic fatty liver disease with advanced fibrosis in the US: a cross-sectional analysis of 2011-2014 National Health and Nutrition Examination Survey. Aliment Pharmacol Ther. 2017;46(10):974–80.
Li J, et al. Prevalence of non-alcoholic fatty liver disease(Nafld) in Asia: a systematic review and meta-analysis of 195 studies and 1,753,168 subjects from 15 countries and areas. Gastroenterology. 2018;154(6):S1165.
Wong VW, et al. Incidence of non-alcoholic fatty liver disease in Hong Kong: a population study with paired proton-magnetic resonance spectroscopy. J Hepatol. 2015;62(1):182–9.
Lin Y, et al. Age patterns of nonalcoholic fatty liver disease incidence: heterogeneous associations with metabolic changes. Diabetol Metab Syndr. 2022;14(1):181.
Hartleb M, et al. Non-alcoholic fatty liver and advanced fibrosis in the elderly: results from a community-based polish survey. Liver Int. 2017;37(11):1706–14.
Dufour J-F, et al. The global epidemiology of nonalcoholic steatohepatitis (NASH) and associated risk factors – a targeted literature review. Endocr Metabol Sci. 2021;3:100089.
Mantovani A, et al. Complications, morbidity and mortality of nonalcoholic fatty liver disease. Metabolism. 2020;111S:154170.
Noureddin M, et al. NASH leading cause of liver transplant in women: updated analysis of indications for liver transplant and ethnic and gender variances. Am J Gastroenterol. 2018;113(11):1649–59.
Rotman Y, et al. The association of genetic variability in patatin-like phospholipase domain-containing protein 3 (PNPLA3) with histological severity of nonalcoholic fatty liver disease. Hepatology. 2010;52(3):894–903.
Smagris E, et al. Inactivation of Tm6sf2, a gene defective in fatty liver disease, impairs lipidation but not secretion of very low density lipoproteins. J Biol Chem. 2016;291(20):10659–76.
Kozlitina J, 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.
Holmen OL, et al. Systematic evaluation of coding variation identifies a candidate causal variant in TM6SF2 influencing total cholesterol and myocardial infarction risk. Nat Genet. 2014;46(4):345–51.
Sookoian S, Pirola CJ. PNPLA3, the triacylglycerol synthesis/hydrolysis/storage dilemma, and nonalcoholic fatty liver disease. World J Gastroenterol. 2012;18(42):6018–26.
BasuRay S, et al. The PNPLA3 variant associated with fatty liver disease (I148M) accumulates on lipid droplets by evading ubiquitylation. Hepatology. 2017;66(4):1111–24.
Yang A, et al. Dynamic interactions of ABHD5 with PNPLA3 regulate triacylglycerol metabolism in brown adipocytes. Nat Metab. 2019;1(5):560–9.
Teo K, et al. rs641738C>T near MBOAT7 is associated with liver fat, ALT and fibrosis in NAFLD: a meta-analysis. J Hepatol. 2021;74(1):20–30.
Thangapandi VR, et al. Loss of hepatic Mboat7 leads to liver fibrosis. Gut. 2021;70(5):940–50.
Meroni M, et al. Mboat7 down-regulation by hyper-insulinemia induces fat accumulation in hepatocytes. EBioMedicine. 2020;52:102658.
Stancakova A, et al. Effects of 34 risk loci for type 2 diabetes or hyperglycemia on lipoprotein subclasses and their composition in 6,580 nondiabetic Finnish men. Diabetes. 2011;60(5):1608–16.
Petta S, et al. Glucokinase regulatory protein gene polymorphism affects liver fibrosis in non-alcoholic fatty liver disease. PLoS One. 2014;9(2):e87523.
Canesin G, et al. Heme-derived metabolic signals dictate immune responses. Front Immunol. 2020;11:66.
Chang PF, et al. Heme oxygenase-1 gene promoter polymorphism and the risk of pediatric nonalcoholic fatty liver disease. Int J Obes. 2015;39(8):1236–40.
Raffaele M, et al. Inhibition of Heme oxygenase antioxidant activity exacerbates hepatic steatosis and fibrosis in vitro. Antioxidants (Basel). 2019;8(8):277.
Canesin G, et al. Heme oxygenase-1 mitigates liver injury and fibrosis via modulation of LNX1/Notch1 pathway in myeloid cells. iScience. 2022;25(9):104983.
Mehta R, et al. The role of mitochondrial genomics in patients with non-alcoholic steatohepatitis (NASH). BMC Med Genet. 2016;17(1):63.
Anty R, et al. A new composite model including metabolic syndrome, alanine aminotransferase and cytokeratin-18 for the diagnosis of non-alcoholic steatohepatitis in morbidly obese patients. Aliment Pharmacol Ther. 2010;32(11–12):1315–22.
Yu SJ, et al. Visceral obesity predicts significant fibrosis in patients with nonalcoholic fatty liver disease. Medicine (Baltimore). 2015;94(48):e2159.
Chang Y, et al. Weight gain within the normal weight range predicts ultrasonographically detected fatty liver in healthy Korean men. Gut. 2009;58(10):1419–25.
Quek J, et al. Global prevalence of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis in the overweight and obese population: a systematic review and meta-analysis. Lancet Gastroenterol Hepatol. 2023;8(1):20–30.
Polyzos SA, Kountouras J, Zavos C. Nonalcoholic fatty liver disease: the pathogenetic roles of insulin resistance and adipocytokines. Curr Mol Med. 2009;9(3):299–314.
Bugianesi E, et al. Insulin resistance in nonalcoholic fatty liver disease. Curr Pharm Des. 2010;16(17):1941–51.
Polyzos SA, et al. The potential adverse role of leptin resistance in nonalcoholic fatty liver disease a hypothesis based on critical review of the literature. J Clin Gastroenterol. 2011;45(1):50–4.
Amiri Dash Atan N, et al. Type 2 diabetes mellitus and non-alcoholic fatty liver disease: a systematic review and meta-analysis. Gastroenterol Hepatol Bed Bench. 2017;10(Suppl1):S1–7.
Golabi P, et al. The worldwide prevalence of non-alcoholic steatohepatitis (NASH) in patients with type 2 diabetes mellitus (DM). J Hepatol. 2018;68:S841.
Powell EE, Wong VW, Rinella M. Non-alcoholic fatty liver disease. Lancet. 2021;397(10290):2212–24.
Ortiz-Lopez C, et al. Prevalence of prediabetes and diabetes and metabolic profile of patients with nonalcoholic fatty liver disease (NAFLD). Diabetes Care. 2012;35(4):873–8.
Serin Y, Acar Tek N. Effect of circadian rhythm on metabolic processes and the regulation of energy balance. Ann Nutr Metab. 2019;74(4):322–30.
Adamovich Y, et al. Circadian clocks and feeding time regulate the oscillations and levels of hepatic triglycerides. Cell Metab. 2014;19(2):319–30.
Jacobi D, et al. Hepatic Bmal1 regulates rhythmic mitochondrial dynamics and promotes metabolic fitness. Cell Metab. 2015;22(4):709–20.
Rudic RD, et al. BMAL1 and CLOCK, two essential components of the circadian clock, are involved in glucose homeostasis. PLoS Biol. 2004;2(11):e377.
Marcheva B, et al. Disruption of the CLOCK components CLOCK and BMAL1 leads to hypoinsulinaemia and diabetes. Nature. 2010;466(7306):627–31.
Perumpail BJ, et al. Clinical epidemiology and disease burden of nonalcoholic fatty liver disease. World J Gastroenterol. 2017;23(47):8263–76.
Yang J, et al. Sleep factors in relation to metabolic dysfunction-associated fatty liver disease in middle-aged and elderly Chinese. J Clin Endocrinol Metab. 2022;107(10):2874–82.
Langin D, Arner P. Importance of TNFalpha and neutral lipases in human adipose tissue lipolysis. Trends Endocrinol Metab. 2006;17(8):314–20.
Kim CW, et al. Sleep duration and quality in relation to non-alcoholic fatty liver disease in middle-aged workers and their spouses. J Hepatol. 2013;59(2):351–7.
Fouhy F, et al. Composition of the early intestinal microbiota: knowledge, knowledge gaps and the use of high-throughput sequencing to address these gaps. Gut Microbes. 2012;3(3):203–20.
Le Roy T, et al. Intestinal microbiota determines development of non-alcoholic fatty liver disease in mice. Gut. 2013;62(12):1787–94.
Henao-Mejia J, et al. Inflammasome-mediated dysbiosis regulates progression of NAFLD and obesity. Nature. 2012;482(7384):179–85.
Leung C, et al. The role of the gut microbiota in NAFLD. Nat Rev Gastroenterol Hepatol. 2016;13(7):412–25.
Kirpich IA, Marsano LS, McClain CJ. Gut-liver axis, nutrition, and non-alcoholic fatty liver disease. Clin Biochem. 2015;48(13–14):923–30.
Wahlstrom A, et al. Intestinal crosstalk between bile acids and microbiota and its impact on host metabolism. Cell Metab. 2016;24(1):41–50.
Sayin SI, et al. Gut microbiota regulates bile acid metabolism by reducing the levels of Tauro-beta-muricholic acid, a naturally occurring FXR antagonist. Cell Metab. 2013;17(2):225–35.
Staley C, Khoruts A, Sadowsky MJ. Contemporary applications of fecal microbiota transplantation to treat intestinal diseases in humans. Arch Med Res. 2017;48(8):766–73.
Arab JP, et al. Bile acids and nonalcoholic fatty liver disease: molecular insights and therapeutic perspectives. Hepatology. 2017;65(1):350–62.
Jennifer Gallacher SM. Practical diagnosis and staging of nonalcoholic fatty liver disease: a narrative review. Hepatology. 2018;3:108. https://doi.org/10.33590/emj/10314271.
Tahan V, et al. Serum gamma-glutamyltranspeptidase distinguishes non-alcoholic fatty liver disease at high risk. Hepato-Gastroenterology. 2008;55(85):1433–8.
Dyson JK, Anstee QM, McPherson S. Non-alcoholic fatty liver disease: a practical approach to diagnosis and staging. Frontline Gastroenterol. 2014;5(3):211–8.
Borrelli A, et al. Role of gut microbiota and oxidative stress in the progression of non-alcoholic fatty liver disease to hepatocarcinoma: current and innovative therapeutic approaches. Redox Biol. 2018;15:467–79.
Giboney PT. Mildly elevated liver transaminase levels in the asymptomatic patient. Am Fam Physician. 2005;71(6):1105–10.
Brunt EM, et al. Nonalcoholic fatty liver disease (NAFLD) activity score and the histopathologic diagnosis in NAFLD: distinct clinicopathologic meanings. Hepatology. 2011;53(3):810–20.
Jacobs A, et al. An overview of mouse models of nonalcoholic steatohepatitis: from past to present. Curr Protoc Mouse Biol. 2016;6(2):185–200.
Ito M, et al. Longitudinal analysis of murine steatohepatitis model induced by chronic exposure to high-fat diet. Hepatol Res. 2007;37(1):50–7.
Speakman JR. Use of high-fat diets to study rodent obesity as a model of human obesity. Int J Obes. 2019;43(8):1491–2.
Fakhoury-Sayegh N, et al. Characteristics of nonalcoholic fatty liver disease induced in Wistar rats following four different diets. Nutr Res Pract. 2015;9(4):350–7.
Chen K, et al. Advancing the understanding of NAFLD to hepatocellular carcinoma development: from experimental models to humans. Biochim Biophys Acta Rev Cancer. 2019;1871(1):117–25.
Vonghia L, et al. CD4+ROR gamma t++ and Tregs in a mouse model of diet-induced nonalcoholic steatohepatitis. Mediat Inflamm. 2015;2015:239623.
Lustig RH, Schmidt LA, Brindis CD. The toxic truth about sugar. Nature. 2012;482(7383):27–9.
Nomura K, Yamanouchi T. The role of fructose-enriched diets in mechanisms of nonalcoholic fatty liver disease. J Nutr Biochem. 2012;23(3):203–8.
Abe N, et al. Longitudinal characterization of diet-induced genetic murine models of non-alcoholic steatohepatitis with metabolic, histological, and transcriptomic hallmarks of human patients. Biol Open. 2019;8(5):bio041251.
Bray GA, Nielsen SJ, Popkin BM. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr. 2004;79(4):537–43.
Korinkova L, et al. Pathophysiology of NAFLD and NASH in experimental models: the role of food intake regulating peptides. Front Endocrinol (Lausanne). 2020;11:597583.
Corbin KD, Zeisel SH. Choline metabolism provides novel insights into nonalcoholic fatty liver disease and its progression. Curr Opin Gastroenterol. 2012;28(2):159–65.
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.
Leclercq IA, et al. CYP2E1 and CYP4A as microsomal catalysts of lipid peroxides in murine nonalcoholic steatohepatitis. J Clin Invest. 2000;105(8):1067–75.
Kirsch R, et al. Rodent nutritional model of non-alcoholic steatohepatitis: species, strain and sex difference studies. J Gastroenterol Hepatol. 2003;18(11):1272–82.
Machado MV, et al. Mouse models of diet-induced nonalcoholic steatohepatitis reproduce the heterogeneity of the human disease. PLoS One. 2015;10(5):e0127991.
Trak-Smayra V, et al. Pathology of the liver in obese and diabetic ob/ob and db/db mice fed a standard or high-calorie diet. Int J Exp Pathol. 2011;92(6):413–21.
Yang SQ, et al. Obesity increases sensitivity to endotoxin liver injury: implications for the pathogenesis of steatohepatitis. Proc Natl Acad Sci U S A. 1997;94(6):2557–62.
Campfield LA, Smith FJ, Burn P. The OB protein (leptin) pathway – a link between adipose tissue mass and central neural networks. Horm Metab Res. 1996;28(12):619–32.
Sahai A, et al. Obese and diabetic db/db mice develop marked liver fibrosis in a model of nonalcoholic steatohepatitis: role of short-form leptin receptors and osteopontin. Am J Physiol Gastrointest Liver Physiol. 2004;287(5):G1035–43.
Pelleymounter MA, et al. Effects of the obese gene product on body weight regulation in ob/ob mice. Science. 1995;269(5223):540–3.
Wang B, Chandrasekera PC, Pippin JJ. Leptin- and leptin receptor-deficient rodent models: relevance for human type 2 diabetes. Curr Diabetes Rev. 2014;10(2):131–45.
Pawlak M, Lefebvre P, Staels B. Molecular mechanism of PPAR alpha action and its impact on lipid metabolism, inflammation and fibrosis in non-alcoholic fatty liver disease. J Hepatol. 2015;62(3):720–33.
Liss KHH, Finck BN. PPARs and nonalcoholic fatty liver disease. Biochimie. 2017;136:65–74.
Gao Q, et al. PPAR alpha-deficient Ob/Ob obese mice become more obese and manifest severe hepatic steatosis due to decreased fatty acid oxidation. Am J Pathol. 2015;185(5):1396–408.
Stec DE, et al. Loss of hepatic PPAR alpha promotes inflammation and serum hyperlipidemia in diet-induced obesity. Am J Phys Regul Integr Comp Phys. 2019;317(5):R733–45.
Ipsen DH, Lykkesfeldt J, Tveden-Nyborg P. Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease. Cell Mol Life Sci. 2018;75(18):3313–27.
Pei K, et al. An overview of lipid metabolism and nonalcoholic fatty liver disease. Biomed Res Int. 2020;2020:1.
Bence KK, Birnbaum MJ. Metabolic drivers of non-alcoholic fatty liver disease. Mol Metabol. 2020;50:50.
Rada P, et al. Understanding lipotoxicity in NAFLD pathogenesis: is CD36 a key driver? Cell Death Dis. 2020;11(9):802.
Wilson CG, et al. Hepatocyte-specific disruption of CD36 attenuates fatty liver and improves insulin sensitivity in HFD-fed mice. Endocrinology. 2016;157(2):570–85.
Cusi K, et al. Long-term pioglitazone treatment for patients with nonalcoholic steatohepatitis and prediabetes or type 2 diabetes mellitus: a randomized trial. Ann Intern Med. 2016;165(5):305–15.
Sanyal AJ, et al. Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. N Engl J Med. 2010;362(18):1675–85.
Chalasani N, et al. The diagnosis and management of nonalcoholic fatty liver disease: practice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2018;67(1):328–57.
Loomba R, et al. Clinical trial: pilot study of metformin for the treatment of non-alcoholic steatohepatitis. Aliment Pharmacol Ther. 2009;29(2):172–82.
Uygun A, et al. Metformin in the treatment of patients with non-alcoholic steatohepatitis. Aliment Pharmacol Ther. 2004;19(5):537–44.
Athyros VG, et al. Safety and efficacy of long-term statin treatment for cardiovascular events in patients with coronary heart disease and abnormal liver tests in the Greek Atorvastatin and Coronary Heart Disease Evaluation (GREACE) study: a post-hoc analysis. Lancet. 2010;376(9756):1916–22.
Kuchay MS, et al. Effect of Empagliflozin on liver fat in patients with type 2 diabetes and nonalcoholic fatty liver disease: a randomized controlled trial (E-LIFT trial). Diabetes Care. 2018;41(8):1801–8.
Armstrong MJ, et al. Liraglutide safety and efficacy in patients with non-alcoholic steatohepatitis (LEAN): a multicentre, double-blind, randomised, placebo-controlled phase 2 study. Lancet. 2016;387(10019):679–90.
Schauer PR, et al. Bariatric surgery versus intensive medical therapy in obese patients with diabetes. N Engl J Med. 2012;366(17):1567–76.
Sanyal AJ, et al. Challenges and opportunities in drug and biomarker development for nonalcoholic steatohepatitis: findings and recommendations from an American Association for the Study of Liver Diseases-U.S. Food and Drug Administration Joint Workshop. Hepatology. 2015;61(4):1392–405.
Belfort R, et al. A placebo-controlled trial of pioglitazone in subjects with nonalcoholic steatohepatitis. N Engl J Med. 2006;355(22):2297–307.
National Institute for Health and Care Excellence. Non-alcoholic fatty liver disease: assessment and management. National Institute for Health and Care Excellence (NICE), London, UK: 2016.
Promrat K, et al. Randomized controlled trial testing the effects of weight loss on nonalcoholic steatohepatitis. Hepatology. 2010;51(1):121–9.
Lincoff AM, et al. Pioglitazone and risk of cardiovascular events in patients with type 2 diabetes mellitus – a meta-analysis of randomized trials. JAMA. 2007;298(10):1180–8.
Loke YK, Singh S, Furberg CD. Long-term use of thiazolidinediones and fractures in type 2 diabetes: a meta-analysis. Can Med Assoc J. 2009;180(1):32–9.
Karimian G, et al. Vitamin E attenuates the progression of non-alcoholic fatty liver disease caused by partial hepatectomy in mice. PLoS One. 2015;10(11):e0143121.
Bugianesi E, et al. A randomized controlled trial of metformin versus vitamin E or prescriptive diet in nonalcoholic fatty liver disease. Am J Gastroenterol. 2005;100(5):1082–90.
Cohen DE, Anania FA, Chalasani N. An assessment of statin safety by hepatologists. Am J Cardiol. 2006;97(8a):77c–81c.
Abraldes JG, et al. Addition of simvastatin to standard therapy for the prevention of variceal rebleeding does not reduce rebleeding but increases survival in patients with cirrhosis. Gastroenterology. 2016;150(5):1160–1170 e3.
Armstrong MJ, et al. Glucagon-like peptide 1 decreases lipotoxicity in non-alcoholic steatohepatitis. J Hepatol. 2016;64(2):399–408.
Ito D, et al. Comparison of Ipragliflozin and pioglitazone effects on nonalcoholic fatty liver disease in patients with type 2 diabetes: a randomized, 24-week, open-label, active-controlled trial. Diabetes Care. 2017;40(10):1364–72.
Fakhry TK, et al. Bariatric surgery improves nonalcoholic fatty liver disease: a contemporary systematic review and meta-analysis. Surg Obes Relat Dis. 2019;15(3):502–11.
Esquivel CM, et al. Laparoscopic sleeve gastrectomy resolves NAFLD: another formal indication for bariatric surgery? Obes Surg. 2018;28(12):4022–33.
Aller R, et al. Effect on liver enzymes of biliopancreatic diversion: 4 years of follow-up. Ann Nutr Metab. 2015;66(2–3):132–6.
Acknowledgments
JHC is supported by NRF-2021R1I1A2041463 and KGM5392212, and SFK is supported by the American Heart Association 20SFRN35210662
Author information
Authors and Affiliations
Corresponding authors
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2023 Springer Nature Switzerland AG
About this entry
Cite this entry
Kim, S.F., Choi, J.H. (2023). Non-alcoholic Fatty Liver Disease. In: Ahima, R.S. (eds) Metabolic Syndrome. Springer, Cham. https://doi.org/10.1007/978-3-319-12125-3_36-2
Download citation
DOI: https://doi.org/10.1007/978-3-319-12125-3_36-2
Received:
Accepted:
Published:
Publisher Name: Springer, Cham
Print ISBN: 978-3-319-12125-3
Online ISBN: 978-3-319-12125-3
eBook Packages: Springer Reference MedicineReference Module Medicine
Publish with us
Chapter history
-
Latest
Non-alcoholic Fatty Liver Disease- Published:
- 19 September 2023
DOI: https://doi.org/10.1007/978-3-319-12125-3_36-2
-
Original
Non-alcoholic Fatty Liver Disease- Published:
- 15 July 2015
DOI: https://doi.org/10.1007/978-3-319-12125-3_36-1