Relationship between non-alcoholic fatty liver disease and inflammation in patients with non-alcoholic fatty liver


1 Department of Community Nutrition, Metabolic Liver Diseases Research Center, School of Nutrition and Food Sciences, Isfahan Endocrine and Metabolism Research Center, Isfahan University of Medical Sciences, Isfahan, Iran

2 Department of Community Nutrition, Metabolic Liver Diseases Research Center, School of Nutrition and Food Sciences, Isfahan Endocrine and Metabolism Research Center, Isfahan University of Medical Sciences, Isfahan; Department of Food Security Research Center and Community Nutrition, Isfahan Endocrine and Metabolism Research Center, Isfahan University of Medical Sciences, Isfahan, Iran

3 Department of Clinical Nutrition, Isfahan Endocrine and Metabolism Research Center, Isfahan University of Medical Sciences, Isfahan, Iran


Background: Non-alcoholic fatty liver is the most chronic liver disease that eventually can become cirrhosis. One of the underlying assumptions for the fatty liver created by inflammation of the hepatocytes. We aimed to assess the association between non-alcoholic fatty liver disease (NAFLD) and sub-clinical inflammation.
Materials and Methods: This is a cross-sectional study which was conducted on 55 patients over 30 years, with NAFLD. Fatty liver grade was assessed using liver ultrasound. Liver enzymes (alanine aminotransferase, aspartate aminotransferase), anthropometric characteristics and inflammatory marker C-reactive protein (CRP) were measured. Qualitative variables (sex and fatty liver grade) and quantitative variables such as were compared with independent t-test and Chi-square test. Relationship between fatty liver grade and inflammatory index was assessed with SPSS software (version 20; SPSS, Inc. Chicago, IL, USA).

Results: Non-alcoholic fatty liver grades were associated with CRP level and this relationship remains in statistically significant level even after adjusting the effects of confounding variables such as age, sex and body mass index of participants (P = 0.016).

Conclusion: In this cross-sectional study, presentation of NAFLD showed a significant correlation with sub-clinical systemic inflammation and CRP level.


Browning JD, Szczepaniak LS, Dobbins R, Nuremberg P, Horton JD, Cohen JC, et al. Prevalence of hepatic steatosis in an urban population in the United States: Impact of ethnicity. Hepatology 2004;40:1387-95.  Back to cited text no. 1
Ludwig J, Viggiano T, Mill B, Ott B. Non alcoholic steatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease. Mayo Clin Proc. 1980;55:434-438.  Back to cited text no. 2
Farrell GC, Larter CZ. Nonalcoholic fatty liver disease: From steatosis to cirrhosis. Hepatology 2006;43:S99-112.  Back to cited text no. 3
Adams LA, Angulo P. Recent concepts in non-alcoholic fatty liver disease. Diabet Med 2005;22:1129-33.  Back to cited text no. 4
Adams LA, Lymp JF, St Sauver J, Sanderson SO, Lindor KD, Feldstein A, et al. The natural history of nonalcoholic fatty liver disease: A population-based cohort study. Gastroenterology 2005;129:113-21.  Back to cited text no. 5
Ahmed MH, Byrne CD. Current treatment of non-alcoholic fatty liver disease. Diabetes Obes Metab 2009;11:188-95.  Back to cited text no. 6
Angulo P, Lindor KD. Non-alcoholic fatty liver disease. J Gastroenterol Hepatol 2002;17 Suppl:S186-90.  Back to cited text no. 7
Bansilal S, Farkouh ME, Fuster V. Role of insulin resistance and hyperglycemia in the development of atherosclerosis. Am J Cardiol 2007;99:6B-14.  Back to cited text no. 8
Bass M, Merriman R. Fatty acid metabolism and lipotoxicity in the pathogenesis of NAFLD/NASH. In: Fatty Liver Disease: NASH and Related Disorders. J Gastroenterol Hepatol 2010;21:109-22.  Back to cited text no. 9
Bataller R, Sancho-Bru P, Ginès P, Lora JM, Al-Garawi A, Solé M, et al. Activated human hepatic stellate cells express the renin-angiotensin system and synthesize angiotensin II. Gastroenterology 2003;125:117-25.  Back to cited text no. 10
Blake G, Ridker P. Inflammatory bio-markers and NAFLD. J Intern Med 2010;4:283-94.  Back to cited text no. 11
Massaro KS, Costa SF, Leone C, Chamone DA. Procalcitonin (PCT) and C-reactive protein (CRP) as severe systemic infection markers in febrile neutropenic adults. BMC Infect Dis 2007;7:137.  Back to cited text no. 12
Yudkin JS, Stehouwer CD, Emeis JJ, Coppack SW. C-reactive protein in healthy subjects: Associations with obesity, insulin resistance, and endothelial dysfunction: A potential role for cytokines originating from adipose tissue? Arterioscler Thromb Vasc Biol 1999;19:972-8.  Back to cited text no. 13
Danesh J, Whincup P, Walker M, Lennon L, Thomson A, Appleby P, et al. Low grade inflammation and coronary heart disease: Prospective study and updated meta-analyses. BMJ 2000;321:199-204.  Back to cited text no. 14
Farrell GC. Non-alcoholic steatohepatitis: What is it, and why is it important in the Asia-Pacific region? J Gastroenterol Hepatol 2003;18:124-38.  Back to cited text no. 15
Angulo P. Nonalcoholic fatty liver disease. N Engl J Med 2002;346:1221-31.  Back to cited text no. 16
Chitturi S, Abeygunasekera S, Farrell GC, Holmes-Walker J, Hui JM, Fung C, et al. NASH and insulin resistance: Insulin hypersecretion and specific association with the insulin resistance syndrome. Hepatology 2002;35:373-9.  Back to cited text no. 17
Targher G, Bertolini L, Rodella S, Lippi G, Franchini M, Zoppini G, et al. NASH predicts plasma inflammatory biomarkers independently of visceral fat in men. Obesity (Silver Spring) 2008;16:1394-9.  Back to cited text no. 18
Nigam P1, Bhatt SP, Misra A, Vaidya M, Dasgupta J, Chadha DS. Non-alcoholic fatty liver disease is closely associated with sub-clinical inflammation: A case-control study on Asian Indians in North India. J Hepatol 2006;44:1167-74.  Back to cited text no. 19
Oruc N, Ozutemiz O, Yuce G, Akarca US, Ersoz G, Gunsar F, et al. Serum procalcitonin and CRP levels in non-alcoholic fatty liver disease: A case control study. BMC Gastroenterol 2009;9:16.  Back to cited text no. 20
Uchihara M, Izumi N. High-sensitivity C-reactive protein (hs-CRP): A promising biomarker for the screening of non-alcoholic steatohepatitis (NASH). Nihon Rinsho 2006;64:1133-8.  Back to cited text no. 21
Haukeland JW, Damås JK, Konopski Z, Løberg EM, Haaland T, Goverud I, et al. Systemic inflammation in nonalcoholic fatty liver disease is characterized by elevated levels of CCL2. J Hepatol 2006;44:1167-74.  Back to cited text no. 22
Gandhe MB, M L, Srinivasan AR. Evaluation of body mass index (BMI) percentile cut-off levels with reference to insulin resistance: A comparative study on south Indian obese and non-obese adolescents. J Clin Diagn Res 2013;7:1579-82.  Back to cited text no. 23
Lupattelli G, De Vuono S, Boni M, Helou R, Raffaele Mannarino M, Rita Roscini A, et al. Insulin resistance and not BMI is the major determinant of early vascular impairment in patients with morbid obesity. J Atheroscler Thromb 2013;20:924-33.  Back to cited text no. 24
Kao PC, Shiesh SC, Wu TJ. Serum C-reactive protein as a marker for wellness assessment. Ann Clin Lab Sci 2006;36:163-9.  Back to cited text no. 25
Anty R, Bekri S, Luciani N, Saint-Paul MC, Dahman M, Iannelli A, et al. The inflammatory C-reactive protein is increased in both liver and adipose tissue in severely obese patients independently from metabolic syndrome, Type 2 diabetes, and NASH. Am J Gastroenterol 2006;101:1824-33.  Back to cited text no. 26
Yoneda M, Mawatari H, Fujita K, Iida H, Yonemitsu K, Kato S, et al. High-sensitivity C-reactive protein is an independent clinical feature of nonalcoholic steatohepatitis (NASH) and also of the severity of fibrosis in NASH. J Gastroenterol 2007;42:573-82.  Back to cited text no. 27
Riquelme A, Arrese M, Soza A, Morales A, Baudrand R, Pérez-Ayuso RM, et al. Non-alcoholic fatty liver disease and its association with obesity, insulin resistance and increased serum levels of C-reactive protein in Hispanics. Liver Int 2009;29:82-8.  Back to cited text no. 28
Mohamed-Ali V, Goodrick S, Rawesh A, Katz DR, Miles JM, Yudkin JS, et al. Subcutaneous adipose tissue releases interleukin-6, but not tumor necrosis factor-alpha, in vivo. J Clin Endocrinol Metab 1997;82:4196-200.  Back to cited text no. 29
Wieckowska A, Papouchado BG, Li Z, Lopez R, Zein NN, Feldstein AE. Increased hepatic and circulating interleukin-6 levels in human nonalcoholic steatohepatitis. Am J Gastroenterol 2008;103:1372-9.  Back to cited text no. 30