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首页> 外文期刊>The Journal of Experimental Biology >Bone without minerals and its secondary mineralization in Atlantic salmon (Salmo salar): the recovery from phosphorus deficiency
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Bone without minerals and its secondary mineralization in Atlantic salmon (Salmo salar): the recovery from phosphorus deficiency

机译:没有矿物质的骨骼及其在大西洋鲑鱼(沙摩酱)中的次生矿化:磷缺乏的恢复

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Calcium and phosphorus (P) are the main bone minerals, and P deficiency can cause hypomineralized bones (osteomalacia) and malformations. This study used a P-deficient salmon model to falsify three hypotheses. First, an extended period of dietary P deficiency does not cause pathologies other than osteomalacia. Second, secondary mineralization of non-mineralized bone is possible. Third, secondary mineralization can restore the bone's mineral composition and mechanical properties. For 7 weeks, post-smolt Atlantic salmon (Salmo salar) received diets with regular P content (RP) or with a 50% lowered P content (LP). For additional 9 weeks, RP animals continued on the regular diet (RP-RP). LP animals continued on the LP diet (LP-LP), on a regular P diet (LP-RP) or on a high P diet (LP-HP). After 16 weeks, animals in all groups maintained a non-deformed vertebral column. LP-LP animals continued bone formation albeit without mineralization. Nine weeks of RP diet largely restored the mineral content and mechanical properties of vertebral bodies. Mineralization resumed deep inside the bone and away from osteoblasts. The history of P deficiency was traceable in LP-RP and LP-HP animals as a ring of low-mineralized bone in the vertebral body endplates, but no tissue alterations occurred that foreshadow vertebral body compression or fusion. Large quantities of non-mineralized salmon bone have the capacity to re-mineralize. If 16 weeks of P deficiency as a single factor is not causal for typical vertebral body malformations, other factors remain to be identified. This example of functional bone without minerals may explain why some teleost species can afford to have an extremely low mineralized skeleton.
机译:钙和磷(P)是主要的骨矿物质,P缺乏可引起支离骨髓(骨癌)和畸形。本研究使用了P缺陷的鲑鱼模型来伪造三个假设。首先,延长的膳食P缺乏症不会引起骨癌以外的病理学。其次,非矿化骨的二次矿化是可能的。第三,继发性矿化可以恢复骨骼的矿物成分和机械性能。持续7周,后面的大西洋鲑鱼(Salmo Salar)接受了常规P含量(RP)或50%降低的P含量(LP)饮食。另外9周,RP动物继续常规饮食(RP-RP)。 LP动物继续对LP饮食(LP-LP),定期P饮食(LP-RP)或在高磷饮食(LP-HP)。 16周后,所有组中的动物都维持了一种非变形的椎体柱。 LP-LP动物仍在没有矿化而继续骨形成。九周的RP饮食在很大程度上恢复了椎体的矿物质含量和力学性能。矿化在骨内部恢复,远离成骨细胞。 P缺乏症的历史在LP-RP和LP-HP动物中可追溯,作为椎体端板的低矿化骨环,但没有发生组织改变,即预示椎体压缩或融合。大量的非矿化鲑鱼骨具有重新矿化的能力。如果作为单个因素的16周的P缺乏不是典型的椎体畸形的因果,则仍有待确定的其他因素。没有矿物质的功能骨骼的这个例子可以解释为什么一些紧邻物种可以负担得起极低的矿化骨架。

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