The role of insufficient copper in lipid synthesis and fatty-liver disease.
The role of insufficient copper in lipid synthesis and fatty-liver disease.
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DOI：
10.1002/iub.1613
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发表时间：
2017-04
期刊：
影响因子：
4.6
通讯作者：
Burkhead JL
中科院分区：
文献类型：
--
作者：
Morrell A;Tallino S;Yu L;Burkhead JL
在真核生物中，必需的过渡金属铜在脂质代谢、氧化还原平衡、铁动员和许多其他关键过程中是重要的。铜稳态被破坏的遗传性疾病，包括门克斯病和威尔逊病，表明铜平衡对人类健康的重要性。铜供应不足的严重后果由门克斯病（Menkes Disease）说明，门克斯病是由X连锁的ATP 7A基因突变引起的，该基因编码一种蛋白质，该蛋白质将铜从肠上皮细胞转运到血流中并穿过血脑屏障。由于饮食质量差或吸收不良导致的铜供应不足会破坏几种分子水平的途径和过程。尽管已经描述了许多铜分布机制，并且已经在人类疾病以及动物模型中表征了铜处理中断的后果，但是由于营养不良或吸收不良而导致的次优铜的生理后果尚未得到广泛研究。最近的研究表明，铜不足可能是重要的一些常见疾病，包括肥胖症，缺血性心脏病和代谢综合征。具体而言，已报道边缘性铜缺乏症（CuD）是以脂质代谢紊乱为特征的疾病（如非酒精性脂肪肝（NAFLD））的潜在病因。在这篇综述中，我们讨论了现有的数据表明，一个显着的一部分北美人口可能会消耗不足的铜，CuD可能促进脂质生物合成的潜在机制，以及CuD和饮食果糖之间的相互作用在NAFLD的病因。
The essential transition metal copper is important in lipid metabolism, redox balance, iron mobilization and many other critical processes in eukaryotic organisms. Genetic diseases where copper homeostasis is disrupted, including Menkes Disease and Wilson Disease, indicate the importance of copper balance to human health. The severe consequences of insufficient copper supply are illustrated by Menkes Disease, caused by mutation in the X-linked ATP7A gene encoding a protein that transports copper from intestinal epithelia into the bloodstream and across the blood-brain barrier. Inadequate copper supply to the body due to poor diet quality or malabsorption can disrupt several molecular level pathways and processes. Though much of the copper distribution machinery has been described and consequences of disrupted copper handling have been characterized in human disease as well as animal models, physiological consequences of sub-optimal copper due to poor nutrition or malabsorption have not been extensively studied. Recent work indicates that insufficient copper may be important in a number of common diseases including obesity, ischemic heart disease, and metabolic syndrome. Specifically, marginal copper deficiency (CuD) in has been reported as a potential etiologic factor in diseases characterized by disrupted lipid metabolism such as non-alcoholic fatty-liver disease (NAFLD). In this review, we discuss the available data suggesting that a significant portion of the North American population may consume insufficient copper, the potential mechanisms by which CuD may promote lipid biosynthesis, and the interaction between CuD and dietary fructose in the etiology of NAFLD.
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DOI：
10.5049/ebp.2014.12.1.1
发表时间：
2014-06
期刊：
Electrolyte & blood pressure : E & BP
影响因子：
--
作者：
Kang DH;Ha SK
通讯作者：
Ha SK
影响因子：
13.5
作者：
Ishimoto, Takuji;Lanaspa, Miguel A.;Rivard, Christopher J.;Roncal-Jimenez, Carlos A.;Orlicky, David J.;Cicerchi, Christina;McMahan, Rachel H.;Abdelmalek, Manal F.;Rosen, Hugo R.;Jackman, Matthew R.;MacLean, Paul S.;Diggle, Christine P.;Asipu, Aruna;Inaba, Shinichiro;Kosugi, Tomoki;Sato, Waichi;Maruyama, Shoichi;Sanchez-Lozada, Laura G.;Sautin, Yuri Y.;Hill, James O.;Bonthron, David T.;Johnson, Richard J.
通讯作者：
Johnson, Richard J.
影响因子：
7.1
作者：
Cockell, Kevin A.;Bertinato, Jesse;L'Abbe, Mary R.
通讯作者：
L'Abbe, Mary R.
DOI：
10.1016/0305-0491(89)90250-2
发表时间：
1989-01-01
影响因子：
2.2
作者：
GAYNES, BI;WATKINS, JB
通讯作者：
WATKINS, JB
影响因子：
13.5
作者：
Abdelmalek, Manal F.;Suzuki, Ayako;Guy, Cynthia;Unalp-Arida, Aynur;Colvin, Ryan;Johnson, Richard J.;Diehl, Anna Mae
通讯作者：
Diehl, Anna Mae