Effects of dietary calcium on atherosclerosis, aortic calcification, and icterus in rabbits fed a supplemental cholesterol diet.

Effects of dietary calcium on atherosclerosis, aortic calcification, and icterus in rabbits fed a supplemental cholesterol diet.
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DOI:
10.1186/1476-511x-5-16
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发表时间:
2006-06-23
影响因子:
4.5
通讯作者:
Culley NC
Culley NC
中科院分区:
医学3区
文献类型:
--
作者:
Hsu HH;Culley NC

文献摘要

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血管钙化与心肌梗死、主动脉壁不稳定和僵硬以及生物修复失败有关。虽然在致动脉粥样硬化饮食中增加钙(Ca)含量已被证明可以减少家兔的动脉粥样硬化,但钙补充和缺乏是否会影响动脉粥样硬化相关的主动脉钙化仍然未知。用含有0.5%胆固醇和2%花生油的新西兰白兔公窝饲喂致动脉粥样硬化饮食。饲料中钙的含量由原来的1%调整为0.5%或3%。取家兔胸主动脉段进行组织学评价和Ca、Pi测定。补钙组维持4个月,缺钙组维持2个半月。分别使用内膜与内侧区域和钙化与内膜区域的比例来半量化病变积累和钙化。黄疸是根据皮肤、巩膜和粘膜的黄化程度以及肝脂质沉积和/或胆道阻塞的明显迹象来判断的。对16只配对的幼崽进行统计分析,结果表明,添加钙显著降低了41%的病变(p < 0.05),显著抑制了62%的钙化(p < 0.05)。对11只配对的幼崽进行统计分析发现,钙缺乏显著增加了2.7倍的病变(p < 0.05),并且饮食中钙含量正常的兄弟姐妹组没有出现轻微但显著的钙化。钙补充使血清胆固醇显著降低30% (p < 0.05)。缺钙使血清胆固醇升高57% (p < 0.001)。钙缺乏家兔的血清胆固醇和低密度脂蛋白胆固醇水平比高钙家兔高2倍。钙的补充降低了主动脉中可溶性钙和Pi的含量,表明这可能是钙补充对钙化的影响的基础。缺钙使黄疸增加33% (p < 0.05),影响肝脏对胆固醇的清除率,而补钙使黄疸减少43% (p < 0.001)。在致动脉粥样硬化饮食中补充钙可以抑制动脉粥样硬化、主动脉钙化和黄疸,而缺乏钙的饮食则会促进这些疾病的发生。
Vascular calcification is implicated in myocardial infarction, instability and rigidity of the aortic wall, and bioprosthetic failures. Although an increase in the calcium (Ca) content in atherogenic diets has been shown to decrease atherosclerosis in rabbits, whether Ca supplementation and deficiency can affect atherosclerosis-related aortic calcification remains unknown. New Zealand White male rabbit littermates were fed an atherogenic diet containing 0.5% cholesterol and 2% peanut oil. The Ca content of the diet, which normally contains 1%, was adjusted to 0.5 or 3%. Segments of thoracic aortas were dissected from rabbits for histological evaluations and Ca and Pi determinations. Rabbits with calcium supplementation were maintained for 4 months, whereas those with calcium deficiency were maintained for 2 1/2 months due to severe icterus beyond this stage. The ratios of intimal to medial areas and calcified to intimal areas were used to semi-quantify lesion accumulation and calcification, respectively. Icterus was estimated from the extent of yellowing of the skin, sclera, and mucous membranes along with gross evidence of hepatic lipidosis and/or biliary obstructions. Statistical analysis of 16 matched littermates shows that Ca supplementation significantly decreased the lesions by 41% (p < 0.05) and markedly inhibited calcification by 62% (p < 0.05). Statistical analysis of 11 matched littermates shows that Ca deficiency significantly increased the lesions by 2.7-fold (p < 0.05) and that the diet caused a small but significant calcification not seen in the sibling groups with normal dietary Ca. Ca supplementation caused a significant 30% decrease in serum cholesterol (p < 0.05). Calcium deficiency increased serum cholesterol by 57% (p < 0.001). Serum cholesterol and LDL-cholesterol levels in Ca deficient rabbits were 2-fold higher than those with high Ca diets. Ca supplementation decreased soluble Ca and Pi content in aortas, suggesting that this effect may underlie the effects of Ca supplementation on calcification. Calcium deficiency increased icterus by 33% (p < 0.05), which may affect hepatic clearance of cholesterol, while calcium supplementation decreased it by 43% (p < 0.001). Ca supplementation to an atherogenic diet inhibits atherosclerosis, aortic calcification, and icterus, whereas a Ca deficient-diet promotes them.