Fructose as a key player in the development of fatty liver disease

查看全文 作　　者：Metin [1]Basaranoglu;Gokcen [2]Basaranoglu;Tevfik [3]Sabuncu;Hakan [1]Sentürk

机构地区：[1]Department of Gastroenterology and Hepatology,Bezmialem Vakif University,Istanbul 34400,Turkey;[2]Department of Anaesthesiology,Bezmialem Vakif University,Istanbul 34400,Turkey;[3]Department of Endocrinology,Harran University,Sanliurfa 68000,Turkey

出　　处：《World Journal of Gastroenterology》索引2013年第19卷第8期,共7页

摘　　要：We aimed to investigate whether increased consumption of fructose is linked to the increased prevalence of fatty liver.The prevalence of nonalcoholic steatohepatitis(NASH) is 3% and 20% in nonobese and obese subjects,respectively.Obesity is a low-grade chronic inflam-m-atory condition and obesity-related cytokines such as interleukin-6,adiponectin,leptin,and tumor necrosis factor-α may play important roles in the developm-ent of nonalcoholic fatty liver disease(NAFLD).Additionally,the prevalence of NASH associated with both cirrhosis and hepatocellular carcinom-a was reported to be high am-ong patients with type 2 diabetes with or without obesity.Our research group previously showed that consumption of fructose is associated with adverse alterations of plasma lipid profiles and metabolic changes in m-ice,the Am-erican Lifestyle-Induced Obesity Syndrom-e m-odel,which included consum-ption of a high-fructose corn syrup in amounts relevant to that consum-ed by som-e Am-ericans.The observation reinforces the concerns about the role of fructose in the obesity epidem-ic.Increased availability of fructose(e.g.,high-fructose corn syrup) increases not only abnorm-al glucose flux but also fructose m-etabolism-in the hepatocyte.Thus,the anatomic position of the liver places it in a strategic buffering position for absorbed carbohydrates and am-ino acids.Fructose was previously accepted as a beneficial dietary com-ponent because it does not stim-ulate insulin secretion.However,since insulin signaling plays an important role in central m-echanism-s of NAFLD,this property of fructose m-ay be undesirable.Fructose has a selective hepatic m-etabolism,and provokes a hepatic stress response involving activation of c-Jun N-term-inal kinases and subsequent reduced hepatic insulin signaling.As high fat diet alone produces obesity,insulin resistance,and som-e degree of fatty liver with m-inim-al inflam-m-ation and no fibrosis,the fast food diet which includes fructose and fats produces a gene expression signature of increased hepatic fibrosis,inflam-m-ation,endoplasm-ic reticulumstress and lipoapoptosis.Hepatic de novo lipogenesis(fatty acid and triglyceride synthesis) is increased in patients with NAFLD.Stable-isotope studies showed that increased de novo lipogenesis(DNL) in patients with NAFLD contributed to fat accum-ulation in the liver and the developm-ent of NAFLD.Specifically,DNL was responsible for 26% of accum-ulated hepatic triglycerides and 15%-23% of secreted very low-density lipoprotein triglycerides in patients with NAFLD com-pared to an estim-ated less than 5% DNL in healthy subjects and 10% DNL in obese people with hyperinsulinem-ia.In conclusion,understanding the underlying causes of NAFLD form-s the basis for rational preventive and treatm-ent strategies of this m-ajor form-of chronic liver disease. 关键词：NONALCOHOLIC FATTY liver Diabetes INSULIN resistance CYTOKINES OBESITY FRUCTOSE

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Fructose as a key player in the development of fatty liver disease

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