Hepatic iron overload may contribute to hypertriglyceridemia and hypercholesterolemia in copper-deficient rats
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Cited by (29)
Nutrition
2019, The Laboratory RatHigh fructose feeding induces copper deficiency in Sprague-Dawley rats: A novel mechanism for obesity related fatty liver
2012, Journal of HepatologyCitation Excerpt :A very recent study suggested that iron overload was associated with increased cholesterol synthesis [32]. Moreover, restricting iron intake in copper deficient animals improved fatty liver [9,10,33]. Our data clearly showed that hepatic and whole body iron levels moved in the opposite direction of copper levels, suggesting that iron overload secondary to copper deficiency is another likely mechanism by which copper deficiency induces fatty liver.
Antiatherogenic effects of zinc are associated with copper in iron-overloaded hypercholesterolemic rabbits
2008, Nutrition ResearchCitation Excerpt :We speculate that this effect may be related to reduction of the serum copper level in these groups and support previous findings regarding the positive association between body copper status and lipid metabolism [34,35]. None of enzymes in lipid metabolism are known to be cuproenzymes, but it is thought that hepatic iron accumulation [36] and impairment in cellular antioxidant capacity resulted from copper deficiency [37] may be counted for the hyperlipidemia under this nutritional state. Our data from rabbits given the HC + FeO can be confirmed by this hypothesis, whereas the findings obtained from the rabbits treated with the HC + Zn (higher antioxidant status and higher serum lipid levels) and the HC + FeO + Cu (lower antioxidant status and lower serum lipid levels) may contrast with such hypothesis.
Copper, oxidative stress, and human health
2005, Molecular Aspects of MedicineCitation Excerpt :When rat cardiac myocytes were treated with the Cu chelator diethyldithiocarbamic acid, intracellular superoxide concentrations increased, and apoptosis was triggered suggesting a possible role for oxidative stress in myocardial remodeling (Siwik et al., 1999). Increased lipid peroxidation (estimated by thiobarbituric acid reactive substances (TBARs) or malondialdehyde) has been observed in Cu deficient plasma, liver, heart, aorta, and erythrocytes (Chen et al., 1994; Fields and Lewis, 1997; Lynch et al., 1997; Nelson et al., 1992; Saari, 2000). Whole body lipid oxidative damage as assessed by breath ethane, a hydrocarbon by-product of lipid peroxidation, is increased with Cu deficiency (Saari et al., 1990).
Copper induces the expression of cholesterogenic genes in human macrophages
2003, AtherosclerosisAspirin reduces blood cholesterol in copper-deficient rats: A potential antioxidant agent?
2001, Metabolism: Clinical and Experimental