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铜-果糖相互作用:非酒精性脂肪性肝病发病机制中的新机制。

Copper-Fructose Interactions: A Novel Mechanism in the Pathogenesis of NAFLD.

机构信息

Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Louisville School of Medicine, Louisville, KY 40202, USA.

Hepatobiology&Toxicology Center, University of Louisville School of Medicine, Louisville, KY 40202, USA.

出版信息

Nutrients. 2018 Nov 21;10(11):1815. doi: 10.3390/nu10111815.

DOI:10.3390/nu10111815
PMID:30469339
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6266129/
Abstract

Compelling epidemiologic data support the critical role of dietary fructose in the epidemic of obesity, metabolic syndrome and nonalcoholic fatty liver disease (NAFLD). The metabolic effects of fructose on the development of metabolic syndrome and NAFLD are not completely understood. High fructose intake impairs copper status, and copper-fructose interactions have been well documented in rats. Altered copper-fructose metabolism leads to exacerbated experimental metabolic syndrome and NAFLD. A growing body of evidence has demonstrated that copper levels are low in NAFLD patients. Moreover, hepatic and serum copper levels are inversely correlated with the severity of NAFLD. Thus, high fructose consumption and low copper availability are considered two important risk factors in NAFLD. However, the causal effect of copper-fructose interactions as well as the effects of fructose intake on copper status remain to be evaluated in humans. The aim of this review is to summarize the role of copper-fructose interactions in the pathogenesis of the metabolic syndrome and discuss the potential underlying mechanisms. This review will shed light on the role of copper homeostasis and high fructose intake and point to copper-fructose interactions as novel mechanisms in the fructose induced NAFLD.

摘要

有强有力的流行病学数据支持,饮食中的果糖在肥胖症、代谢综合征和非酒精性脂肪性肝病(NAFLD)的流行中起着关键作用。果糖对代谢综合征和 NAFLD 发展的代谢影响尚不完全清楚。高果糖摄入会损害铜的状态,并且铜-果糖相互作用在大鼠中已有充分的记载。铜-果糖代谢的改变会导致实验性代谢综合征和 NAFLD 的恶化。越来越多的证据表明,NAFLD 患者的铜水平较低。此外,肝脏和血清铜水平与 NAFLD 的严重程度呈负相关。因此,高果糖摄入和铜供应不足被认为是 NAFLD 的两个重要危险因素。然而,铜-果糖相互作用的因果关系以及果糖摄入对铜状态的影响仍有待在人体中进行评估。本综述的目的是总结铜-果糖相互作用在代谢综合征发病机制中的作用,并讨论潜在的潜在机制。这篇综述将阐明铜动态平衡和高果糖摄入的作用,并指出铜-果糖相互作用是果糖诱导的 NAFLD 的新机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/67d1/6266129/eb45d4ac1155/nutrients-10-01815-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/67d1/6266129/f5f98e370d14/nutrients-10-01815-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/67d1/6266129/c2683531a258/nutrients-10-01815-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/67d1/6266129/850acfb4cf28/nutrients-10-01815-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/67d1/6266129/eb45d4ac1155/nutrients-10-01815-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/67d1/6266129/f5f98e370d14/nutrients-10-01815-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/67d1/6266129/c2683531a258/nutrients-10-01815-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/67d1/6266129/850acfb4cf28/nutrients-10-01815-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/67d1/6266129/eb45d4ac1155/nutrients-10-01815-g004.jpg

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Risk factors for development of nonalcoholic fatty liver disease after pancreatoduodenectomy.胰十二指肠切除术后非酒精性脂肪性肝病发生的危险因素。
Ann Gastroenterol Surg. 2017 Jul 20;1(3):226-231. doi: 10.1002/ags3.12024. eCollection 2017 Sep.
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Lifelong reduction in complex IV induces tissue-specific metabolic effects but does not reduce lifespan or healthspan in mice.
非酒精性脂肪性肝病中铜状态及其与腹部肥胖指数和肝功能的关系:一项病例对照研究
BMC Res Notes. 2024 Dec 19;17(1):370. doi: 10.1186/s13104-024-07025-x.
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Dietary therapy of murine primary biliary cholangitis induces hepatocellular steatosis: A cautionary tale.饮食疗法治疗原发性胆汁性胆管炎可诱导肝细胞脂肪变性:一个警示故事。
Liver Int. 2024 Oct;44(10):2834-2846. doi: 10.1111/liv.16060. Epub 2024 Aug 5.
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Examining the Pathogenesis of MAFLD and the Medicinal Properties of Natural Products from a Metabolic Perspective.从代谢角度审视MAFLD的发病机制及天然产物的药用特性。
Metabolites. 2024 Apr 12;14(4):218. doi: 10.3390/metabo14040218.
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