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Hepatic steatosis: Innocent bystander or guilty party?

泰恩河畔纽卡斯尔 水蛭 医学杂志 艺术史 媒体研究 艺术 图书馆学 社会学 计算机科学 万维网
作者
Christopher P. Day,Oliver James
出处
期刊:Hepatology [Lippincott Williams & Wilkins]
卷期号:27 (6): 1463-1466 被引量:395
标识
DOI:10.1002/hep.510270601
摘要

HepatologyVolume 27, Issue 6 p. 1463-1466 Concise ReviewFree Access Hepatic steatosis: Innocent bystander or guilty party? Christopher P. Day Ph.D., M.D., Corresponding Author Christopher P. Day Ph.D., M.D. Centre for Liver Research, Floor 4, William Leech Building Medical School, Framlington Place, Newcastle upon Tyne, UKCentre for LiverResearch, Floor 4, William Leech Building, Medical School, Framlington Place, Newcastle upon Tyne, NE2 4HH UK. Fax: 44-191-222-0723===Search for more papers by this authorOliver F.W. James, Oliver F.W. James Centre for Liver Research, Floor 4, William Leech Building Medical School, Framlington Place, Newcastle upon Tyne, UKSearch for more papers by this author Christopher P. Day Ph.D., M.D., Corresponding Author Christopher P. Day Ph.D., M.D. Centre for Liver Research, Floor 4, William Leech Building Medical School, Framlington Place, Newcastle upon Tyne, UKCentre for LiverResearch, Floor 4, William Leech Building, Medical School, Framlington Place, Newcastle upon Tyne, NE2 4HH UK. Fax: 44-191-222-0723===Search for more papers by this authorOliver F.W. James, Oliver F.W. James Centre for Liver Research, Floor 4, William Leech Building Medical School, Framlington Place, Newcastle upon Tyne, UKSearch for more papers by this author First published: 30 December 2003 https://doi.org/10.1002/hep.510270601Citations: 302AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat REFERENCES 1 Day CP, Yeaman SJ. The biochemistry of alcoholic fatty liver. Biochim Biophys Acta 1994; 1215: 33–48. 2 Fromenty B, Pessayre D. Inhibition of mitochondrial beta-oxidation as a mechanism of hepatotoxicity. 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Evidence that oxidative stress plays a role in steatohepatitis produced in a rat nutritional model [Abstract]. Hepatology 1996; 24: 240A. 21 Pinto HC, Felipe P, Baptista A, Fernandes A, Camilo E, Ramalho F, Moura MC. Hepatic steatosis and lipid peroxidation in human chronic liver diseases [Abstract]. Hepatology 1996; 24: 311A. 22 Weltman MD, Farrell GC, Hall P, Ingelman-Sundberg M, Liddle C. Hepatic cytochrome P450 2E1 is increased in patients with non-alcoholic steatohepatitis. Hepatology 1998; 27: 128–133.MEDLINE 23 Weltman MD, Farrell GC, Liddle C. Increased CYP2E1 expression in a rat nutritional model of hepatic steatosis with inflammation. Gastroenterology 1996; 111: 1645–1653.MEDLINE 24 Zangar RC, Novak RF. Effects of fatty acids and ketone bodies on cytochromes P450 2B, 4A, and 2E1 expression in primary cultured rat hepatocytes. Arch Biochem Biophys 1997; 337: 217–224.MEDLINE 25 Osmundsen H, Bremer J, Pedersen JI. Metabolic aspects of peroxisomal β-oxidation. Biochim Biopys Acta 1991; 1085: 141–158. 26 George DK, Goldwurm S, Macdonald GA, Cowley LL, Walker NI, Ward PJ, Jazwinska EC, et al. Increased hepatic iron concentration in nonalcoholic steatohepatitis is associated with increased fibrosis. Gastroenterology 1998; 114: 311–318.MEDLINE 27 Cotrim HP, Parana R, Portugal M, Lyra L, Andrade Z, Freitas LAR. Nonalcoholic steatohepatitis (NASH) and industrial toxins. Follow up of patients removed from one industrial area [Abstract]. Hepatology 1997; 26: 149A. 28 McClain CJ, Hill D, Schmidt J, Diehl AM. Cytokines and alcoholic liver disease. Semin Liver Dis 1993; 13: 170–182.MEDLINE 29 Haines NW, Baker AL, Boyer JL, Glagov S, Schneir H, Jaspan J, Ferguson DJ. Prognostic indicators of hepatic injury following jejunoileal bypass performed for refractory obesity: a prospective study. Hepatology 1981; 1: 161–165.MEDLINE 30 Drenick EJ, Fisler J, Johnson D. Hepatic steatosis after intestinal bypass. Prevention and reversal by metronidazole irrespective of protein-calorie malnutrition. Gastroenterology 1982; 82: 534–548. 31 Yang SQ, Lin HZ, Lane MD, Clemens M, Diehl AM. Obesity increases sensitivity to endotoxin liver injury: implications for the pathogenesis of steatohepatitis. Proc Natl Acad Sci U S A 1997; 94: 2557–2562.MEDLINE 32 Kern PA, Saghizadeh M, Ong JM, Bosch RJ, Deem R, Simsolo RB. The expression of tumor necrosis factor in human adipose tissue. Regulation by obesity, weight loss and relationship to lipoprotein lipase. J Clin Invest 1995; 95: 2111–2119.MEDLINE 33 Hotamisligil GS, Peraldi P, Budavari A, Ellis R, White MF, Spiegelman BM. IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-α- and obesity-induced insulin resistance. Science 1996; 271: 665–668.MEDLINE 34 Yamakawa T, Tanaka S-I, Yamakawa Y, Kiuchi Y, Isoda F, Kawamoto S, Sokuda K, et al. Augmented production of tumor necrosis factor-alpha in obese mice. Immunol Immunopathol 1995; 75: 51–56. 35 Fromenty B, Grimbert S, Mansouri A, Beaugrand M, Erlinger S, Rotig A, Pessayre D. Hepatic mitochondrial DNA deletion in alcoholics: association with microvesicular steatosis. Gastroenterology 1995; 108: 193–200.MEDLINE 36 DiLuzio NR, Costales F. Inhibition of ethanol and carbon tetrachloride induced fatty liver by antoxidants. Exp Mol Pathol 1965; 4: 141–154. 37 Letteron P, Duchatelle V, Berson A, Fromenty B, Fisch C, Degott C, Benhamou JP, et al. Increased ethane exhalation, an in vivo index of lipid peroxidation, in alcohol-abusers. Gut 1993; 34: 409–414.MEDLINE 38 Jaeschke H, Wang Y, Essani NA. Reactive oxygen species activate the transcription factor NF-KB in the liver by induction of lipid peroxidation [Abstract]. Hepatology 1996; 24: 238A. 39 Caraceni P, Ryu HS, Subbotin V, De Maria N, Colantoni A, Roberts L, Trevisani F, et al. Rat hepatocytes isolated from alcohol-induced fatty liver have an increased sensitivity to anoxic injury. 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