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大西洋鲑鱼()中无矿物质的骨骼及其二次矿化:从磷缺乏症中恢复。

Bone without minerals and its secondary mineralization in Atlantic salmon (): the recovery from phosphorus deficiency.

机构信息

Ghent University, Biology Department, Ledeganckstraat 35, 9000 Ghent, Belgium

Institute of Marine Research (IMR), Matre Aquaculture Research Station, N-5984, Matredal, Norway.

出版信息

J Exp Biol. 2019 Feb 8;222(Pt 3):jeb188763. doi: 10.1242/jeb.188763.

Abstract

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 bones' mineral composition and mechanical properties. For 7 weeks, post-smolt Atlantic salmon () 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.

摘要

钙和磷(P)是骨骼的主要矿物质,P 缺乏会导致矿物质不足的骨骼(佝偻病)和畸形。本研究使用 P 缺乏的三文鱼模型来验证三个假设。首先,长期的膳食 P 缺乏不会导致除佝偻病以外的其他病理。其次,非矿化骨的二次矿化是可能的。第三,二次矿化可以恢复骨骼的矿物质组成和机械性能。7 周龄大西洋三文鱼()在接受正常 P 含量(RP)或 50%降低 P 含量(LP)饮食 7 周后,继续接受正常饮食(RP-RP)。LP 动物继续接受 LP 饮食(LP-LP)、正常 P 饮食(LP-RP)或高 P 饮食(LP-HP)。16 周后,所有组的动物都保持了未变形的脊柱。尽管没有矿化,但 LP-LP 动物仍在继续骨形成。9 周的 RP 饮食在很大程度上恢复了椎骨的矿物质含量和机械性能。矿化在骨内深处并远离成骨细胞重新开始。LP-RP 和 LP-HP 动物的 P 缺乏史可追溯到椎体终板的低矿化骨环,但没有发生预示椎体压缩或融合的组织改变。大量未矿化的三文鱼骨有再矿化的能力。如果 16 周的 P 缺乏作为单一因素不是导致典型椎体畸形的原因,那么其他因素仍有待确定。这种无矿物质的功能性骨骼的例子可能解释了为什么一些硬骨鱼物种能够拥有极其低矿化的骨骼。

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