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

J. DiNicolantonio, Dennis F. Mangan, J. O’Keefe
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引用次数: 3

摘要

背景:有证据表明,过量摄入添加糖可诱发脂肪肝和胰岛素抵抗。目的:提出添加糖诱导铜缺乏的假说,铜缺乏可导致肝铁超载、脂肪性肝病、胰岛素抵抗并最终导致非酒精性脂肪性肝炎。环境:平均而言,人类添加糖的摄入量高于已经发现的损害动物体内铜状态的水平。方法:叙述回顾。结果:果糖引起的铜缺乏可能是脂肪肝和胰岛素抵抗的主要原因。结论:减少添加糖的摄入可改善铜状态,降低脂肪肝和胰岛素抵抗的风险。
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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.
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