Lipid Metabolism 2013
DOI: 10.5772/51819
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The Role of Copper as a Modifier of Lipid Metabolism

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Cited by 16 publications
(7 citation statements)
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“…This is another proof that the deficit of Cu in the rat diet may negatively affect the body by weakening the antioxidant defence. Also, low level of Cu in the diet may adversely affect lipid metabolism and lead to an increase in the TG, TC or LDL levels in serum (Kaya et al, 2006;Burkhead and Lutsenko, 2013;Megahed et al, 2014). However, the results of our research do not confirm these reports.…”
Section: Discussioncontrasting
confidence: 91%
“…This is another proof that the deficit of Cu in the rat diet may negatively affect the body by weakening the antioxidant defence. Also, low level of Cu in the diet may adversely affect lipid metabolism and lead to an increase in the TG, TC or LDL levels in serum (Kaya et al, 2006;Burkhead and Lutsenko, 2013;Megahed et al, 2014). However, the results of our research do not confirm these reports.…”
Section: Discussioncontrasting
confidence: 91%
“…16,17 On the other hand, misregulation of copper is also implicated in human genetic disorders like Menkes 1820 and Wilson’s 2123 diseases; neurodegenerative diseases 24 such as Alzheimer’s, 2528 Parkinson’s, 29 prion, 30,31 and Huntington’s 32 diseases and familial amyotrophic lateral sclerosis; 33 and metabolic disorders such as obesity and diabetes. 3438 More recently, copper has also been found to regulate cancers that operate through widely observed oncogenic BRAF mutations 6,39,40 and influence tumour growth. In addition to the canonical, tightly bound pool of copper, the observation of a reversibly and relatively loosely bound (“labile”) pool of copper in cells, 4144 likely buffered by low molecular weight ligands like glutathione (GSH), is particularly intriguing, presaging that copper and related transition metals in these more bioavailable forms can also participate in dynamic cell signalling pathways.…”
Section: Introductionmentioning
confidence: 99%
“…Both hepatic iron excess, as seen in the P3 specimens, and depletion, as detected in the P4 rats, can cause mitochondrial dysfunction and impair the glico-lipidic control [ 57 , 58 ]. Glico-lipidic imbalance can also occur in the case of copper depletion, as observed in the P4 rats, finally leading to non-alcoholic fatty liver disease [ 59 , 60 ]. Moreover, manganese accumulation not only causes liver dysfunction, but the excess not excreted into the bile is transported to the central nervous system, causing neurotoxicity [ 61 ].…”
Section: Discussionmentioning
confidence: 99%