High fructose feeding induces copper deficiency in Sprague-Dawley rats: a novel mechanism for obesity related fatty liver.
High fructose feeding induces copper deficiency in Sprague-Dawley rats: a novel mechanism for obesity related fatty liver.
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DOI：
10.1016/j.jhep.2011.05.030
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发表时间：
2012-02
影响因子：
25.7
通讯作者：
McClain, Craig J.
中科院分区：
文献类型：
--
作者：
Song, Ming;Schuschke, Dale A.;Zhou, Zhanxiang;Chen, Theresa;Pierce, William M., Jr.;Wang, Renwei;Johnson, W. Thomas;McClain, Craig J.
膳食铜缺乏与代谢综合征的多种表现有关，包括高脂血症和脂肪肝。据报道，果糖喂养会加剧缺铜的并发症。在这项研究中，我们研究了铜缺乏是否在果糖诱导的脂肪肝中发挥作用，并探讨了潜在的潜在机制。雄性断奶的 Sprague-Dawley 大鼠被喂食充足的铜或略微缺乏铜的饮食 4 周。还随意给予去离子水或含有30%果糖(w/v)的去离子水。评估铜和铁状态、肝损伤和脂肪变性、十二指肠铜转运蛋白-1（Ctr-1）。果糖喂养进一步损害了铜的状态并导致铁过载。暴露于果糖的边缘铜缺乏大鼠显着诱导肝损伤和脂肪积累，血浆天冬氨酸转氨酶（AST）和肝甘油三酯的显着升高证明了这一点。在喂食果糖的边缘铜缺乏大鼠中，肝脏肉毒碱棕榈酰辅酶 A 转移酶 I (CPT I) 表达显着受到抑制，而肝脂肪酸合酶 (FAS) 显着上调。边缘铜缺乏和果糖喂养会抑制肝脏抗氧化防御系统，并增加脂质过氧化。此外，边缘铜缺乏使十二指肠 Ctr-1 表达显着增加，而果糖喂养则消除了这种增加。我们的数据表明，高果糖诱发的非酒精性脂肪肝（NAFLD）可能部分归因于膳食铜不足。果糖喂养中观察到的十二指肠 Ctr1 表达受损可能会导致铜吸收减少，进而导致铜缺乏。
Dietary copper deficiency is associated with a variety of manifestations of the metabolic syndrome, including hyperlipidemia and fatty liver. Fructose feeding has been reported to exacerbate complications of copper deficiency. In this study, we investigated whether copper deficiency plays a role in fructose-induced fatty liver and explored the potential underlying mechanism(s). Male weanling Sprague-Dawley rats were fed either an adequate copper or a marginally copper deficient diet for 4 weeks. Deionized water or deionized water containing 30% fructose (w/v) was also given ad lib. Copper and iron status, hepatic injury and steatosis, duodenum copper transporter-1(Ctr-1) were assessed. Fructose feeding further impaired copper status and led to iron overload. Liver injury and fat accumulation were significantly induced in marginal copper deficient rats exposed to fructose as evidenced by robust increased plasma aspartate aminotransferase (AST) and hepatic triglyceride. Hepatic carnitine palmitoyl-CoA transferase I (CPT I) expression was significantly inhibited, whereas hepatic fatty acid synthase (FAS) was markedly up-regulated in marginal copper deficient rats fed with fructose. Hepatic antioxidant defense system was suppressed and lipid peroxidation was increased by marginal copper deficiency and fructose feeding. Moreover, duodenum Ctr-1 expression was significantly increased by marginal copper deficiency, whereas this increase was abrogated by fructose feeding. Our data suggest that high fructose-induced nonalcoholic fatty liver disease (NAFLD) may be due, in part, to inadequate dietary copper. Impaired duodenum Ctr1 expression seen in fructose feeding may lead to decreased copper absorption, and subsequent copper deficiency.
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影响因子：
29.4
作者：
Day, CP
通讯作者：
Day, CP
影响因子：
3.8
作者：
Jaeschke, H;Gores, GJ;Lemasters, JJ
通讯作者：
Lemasters, JJ
影响因子：
4.4
作者：
Fields, M;Lewis, CG;Lure, MD
通讯作者：
Lure, MD
影响因子：
25.7
作者：
Ouyang, Xiaosen;Cirillo, Pietro;Abdelmalek, Manal F.
通讯作者：
Abdelmalek, Manal F.
DOI：
10.3181/00379727-175-41832
发表时间：
1984-01-01
影响因子：
--
作者：
FIELDS, M;FERRETTI, RJ;SMITH, JC
通讯作者：
SMITH, JC