Mohamad H Yousef, Alhareth Al Juboori, Abdulmajeed A Albarrak, Jamal A Ibdah, Veysel Tahan
{"title":"无大“肚”的脂肪肝:非肥胖患者非酒精性脂肪肝的放大回顾","authors":"Mohamad H Yousef, Alhareth Al Juboori, Abdulmajeed A Albarrak, Jamal A Ibdah, Veysel Tahan","doi":"10.4291/wjgp.v8.i3.100","DOIUrl":null,"url":null,"abstract":"Nonalcoholic fatty liver disease (NAFLD) is well described as a common cause of chronic liver disease, mostly in the obese population. It refers to a spectrum of chronic liver disease that starts with simple steatosis than progresses to nonalcoholic steatohepatitis and cirrhosis in patients without significant alcohol consumption. NAFLD in the non-obese population has been increasingly reported and studied recently. The pathogenesis of nonobese NAFLD is poorly understood and is related to genetic predisposition, most notably patatin-like phospholipase domain-containing 33 G allele polymorphism that leads to intrahepatic triglyceride accumulation and insulin resistance. Non-obese NAFLD is associated with components of metabolic syndrome and, especially, visceral obesity which seems to be an important etiological factor in this group. Dietary factors and, specifically, a high fructose diet seem to play a role. Cardiovascular events remain the main cause of mortality and morbidity in NAFLD, including in the non-obese population. There is not enough data regarding treatment in non-obese NAFLD patients, but similar to NAFLD in obese subjects, lifestyle changes that include dietary modification, physical activity, and weight loss remain the mainstay of treatment.","PeriodicalId":23760,"journal":{"name":"World Journal of Gastrointestinal Pathophysiology","volume":"8 3","pages":"100-107"},"PeriodicalIF":0.0000,"publicationDate":"2017-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/bf/69/WJGP-8-100.PMC5561430.pdf","citationCount":"22","resultStr":"{\"title\":\"Fatty liver without a large \\\"belly\\\": Magnified review of non-alcoholic fatty liver disease in non-obese patients.\",\"authors\":\"Mohamad H Yousef, Alhareth Al Juboori, Abdulmajeed A Albarrak, Jamal A Ibdah, Veysel Tahan\",\"doi\":\"10.4291/wjgp.v8.i3.100\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Nonalcoholic fatty liver disease (NAFLD) is well described as a common cause of chronic liver disease, mostly in the obese population. It refers to a spectrum of chronic liver disease that starts with simple steatosis than progresses to nonalcoholic steatohepatitis and cirrhosis in patients without significant alcohol consumption. NAFLD in the non-obese population has been increasingly reported and studied recently. The pathogenesis of nonobese NAFLD is poorly understood and is related to genetic predisposition, most notably patatin-like phospholipase domain-containing 33 G allele polymorphism that leads to intrahepatic triglyceride accumulation and insulin resistance. Non-obese NAFLD is associated with components of metabolic syndrome and, especially, visceral obesity which seems to be an important etiological factor in this group. Dietary factors and, specifically, a high fructose diet seem to play a role. Cardiovascular events remain the main cause of mortality and morbidity in NAFLD, including in the non-obese population. There is not enough data regarding treatment in non-obese NAFLD patients, but similar to NAFLD in obese subjects, lifestyle changes that include dietary modification, physical activity, and weight loss remain the mainstay of treatment.\",\"PeriodicalId\":23760,\"journal\":{\"name\":\"World Journal of Gastrointestinal Pathophysiology\",\"volume\":\"8 3\",\"pages\":\"100-107\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2017-08-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/bf/69/WJGP-8-100.PMC5561430.pdf\",\"citationCount\":\"22\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"World Journal of Gastrointestinal Pathophysiology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4291/wjgp.v8.i3.100\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"World Journal of Gastrointestinal Pathophysiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4291/wjgp.v8.i3.100","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Fatty liver without a large "belly": Magnified review of non-alcoholic fatty liver disease in non-obese patients.
Nonalcoholic fatty liver disease (NAFLD) is well described as a common cause of chronic liver disease, mostly in the obese population. It refers to a spectrum of chronic liver disease that starts with simple steatosis than progresses to nonalcoholic steatohepatitis and cirrhosis in patients without significant alcohol consumption. NAFLD in the non-obese population has been increasingly reported and studied recently. The pathogenesis of nonobese NAFLD is poorly understood and is related to genetic predisposition, most notably patatin-like phospholipase domain-containing 33 G allele polymorphism that leads to intrahepatic triglyceride accumulation and insulin resistance. Non-obese NAFLD is associated with components of metabolic syndrome and, especially, visceral obesity which seems to be an important etiological factor in this group. Dietary factors and, specifically, a high fructose diet seem to play a role. Cardiovascular events remain the main cause of mortality and morbidity in NAFLD, including in the non-obese population. There is not enough data regarding treatment in non-obese NAFLD patients, but similar to NAFLD in obese subjects, lifestyle changes that include dietary modification, physical activity, and weight loss remain the mainstay of treatment.