Prohaska J R, Korte J J, Bailey W R
J Nutr. 1985 Dec;115(12):1702-7. doi: 10.1093/jn/115.12.1702.
Experiments were conducted with suckling male C57BL mice and Sprague-Dawley rats to investigate the relationship between copper deficiency and elevated serum cholesterol. Brindled mice, which have a genetic defect that affects copper distribution, were compared to their normal brothers. Dietary copper deficiency was produced in dams heterozygous for the brindled gene, in normal mouse dams and in rat dams. The subsequent male offspring were compared to those from copper-supplemented dams. Copper deficiency, as assessed by liver copper levels or ceruloplasmin activity, was demonstrated in 12-d-old rats, brindled mice, and in genotypically normal mice from dams fed the copper-deficient diet. However, serum cholesterol levels were not elevated in these "copper-deficient" rats or mice. In one experiment serum cholesterol levels of brindled mice were significantly lower than that of their littermate controls. An additional study was done with older mice. Their dams were fed a low copper diet from parturition throughout lactation, and the pups were fed the same copper-deficient diet for 4 wk after weaning. The 7-wk-old male copper-deficient mice had liver copper levels below 1 microgram/g, but no elevation in serum cholesterol was observed. The failure to demonstrate a rise in serum cholesterol in these perinatal models may be due in part to less severe hepatic copper deficiency because of neonatal copper reserves in liver.
使用哺乳期雄性C57BL小鼠和Sprague-Dawley大鼠进行实验，以研究铜缺乏与血清胆固醇升高之间的关系。将具有影响铜分布的遗传缺陷的斑驳小鼠与其正常的兄弟进行比较。在携带斑驳基因的杂合子母鼠、正常母鼠和大鼠母鼠中造成饮食性铜缺乏。将随后的雄性后代与来自补充铜的母鼠的后代进行比较。通过肝脏铜水平或铜蓝蛋白活性评估，在12日龄大鼠、斑驳小鼠以及来自喂食缺铜饮食的母鼠的基因正常小鼠中证实存在铜缺乏。然而，这些“缺铜”大鼠或小鼠的血清胆固醇水平并未升高。在一项实验中，斑驳小鼠的血清胆固醇水平显著低于其同窝对照。对年龄较大的小鼠进行了另一项研究。它们的母鼠从分娩到整个哺乳期都喂食低铜饮食，幼崽在断奶后4周喂食相同的缺铜饮食。7周龄的雄性缺铜小鼠肝脏铜水平低于1微克/克，但未观察到血清胆固醇升高。在这些围产期模型中未能证明血清胆固醇升高，部分原因可能是由于肝脏中的新生儿铜储备，导致肝脏铜缺乏不太严重。
