{"title":"果糖-铜的联系:添加糖通过铜缺乏诱导脂肪肝和胰岛素抵抗","authors":"J. DiNicolantonio, Dennis F. Mangan, J. O’Keefe","doi":"10.4102/JIR.V3I1.43","DOIUrl":null,"url":null,"abstract":"Background: Evidence suggests that the overconsumption of added sugars can induce fatty liver disease and insulin resistance. Aim: To propose a hypothesis that added sugars induce copper deficiency which can lead to hepatic iron overload, fatty liver disease, insulin resistance and eventually non-alcoholic steatohepatitis. Setting: On average, the intake of added sugars in humans is higher than levels that have been found to impair copper status in animals. Methods: Narrative review. Results: Fructose-induced copper deficiency may be a leading cause of fatty liver disease and insulin resistance. Conclusion: The reduction in the intake of added sugars may improve copper status and reduce the risk of fatty liver disease and insulin resistance.","PeriodicalId":32155,"journal":{"name":"Journal of Insulin Resistance","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2018-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"3","resultStr":"{\"title\":\"The fructose–copper connection: Added sugars induce fatty liver and insulin resistance via copper deficiency\",\"authors\":\"J. DiNicolantonio, Dennis F. Mangan, J. O’Keefe\",\"doi\":\"10.4102/JIR.V3I1.43\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Background: Evidence suggests that the overconsumption of added sugars can induce fatty liver disease and insulin resistance. Aim: To propose a hypothesis that added sugars induce copper deficiency which can lead to hepatic iron overload, fatty liver disease, insulin resistance and eventually non-alcoholic steatohepatitis. Setting: On average, the intake of added sugars in humans is higher than levels that have been found to impair copper status in animals. Methods: Narrative review. Results: Fructose-induced copper deficiency may be a leading cause of fatty liver disease and insulin resistance. Conclusion: The reduction in the intake of added sugars may improve copper status and reduce the risk of fatty liver disease and insulin resistance.\",\"PeriodicalId\":32155,\"journal\":{\"name\":\"Journal of Insulin Resistance\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2018-09-26\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Insulin Resistance\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4102/JIR.V3I1.43\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Insulin Resistance","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4102/JIR.V3I1.43","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The fructose–copper connection: Added sugars induce fatty liver and insulin resistance via copper deficiency
Background: Evidence suggests that the overconsumption of added sugars can induce fatty liver disease and insulin resistance. Aim: To propose a hypothesis that added sugars induce copper deficiency which can lead to hepatic iron overload, fatty liver disease, insulin resistance and eventually non-alcoholic steatohepatitis. Setting: On average, the intake of added sugars in humans is higher than levels that have been found to impair copper status in animals. Methods: Narrative review. Results: Fructose-induced copper deficiency may be a leading cause of fatty liver disease and insulin resistance. Conclusion: The reduction in the intake of added sugars may improve copper status and reduce the risk of fatty liver disease and insulin resistance.