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钙饮食含量、PTH(1-34)治疗与大鼠模型中骨稳态平衡的相互作用:小梁骨作为关键。

Interaction among Calcium Diet Content, PTH (1-34) Treatment and Balance of Bone Homeostasis in Rat Model: The Trabecular Bone as Keystone.

机构信息

Department of Biomedical, Metabolic and Neural Sciences, Section of Human Morphology, University of Modena and Reggio Emilia, 41124 Modena, Italy.

Department of Laboratory Medicine and Pathological Anatomy, Azienda USL of Modena, 41126 Modena, Italy.

出版信息

Int J Mol Sci. 2019 Feb 11;20(3):753. doi: 10.3390/ijms20030753.

DOI:10.3390/ijms20030753
PMID:30754633
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6387065/
Abstract

The present study is the second step (concerning normal diet restoration) of the our previous study (concerning the calcium-free diet) to determine whether normal diet restoration, with/without concomitant PTH (1-34) administration, can influence amounts and deposition sites of the total bone mass. Histomorphometric evaluations and immunohistochemical analysis for Sclerostin expression were conducted on the vertebral bodies and femurs in the rat model. The final goals are (i) to define timing and manners of bone mass changes when calcium is restored to the diet, (ii) to analyze the different involvement of the two bony architectures having different metabolism (i.e., trabecular versus cortical bone), and (iii) to verify the eventual role of PTH (1-34) administration. Results evidenced the greater involvement of the trabecular bone with respect to the cortical bone, in response to different levels of calcium content in the diet, and the effect of PTH, mostly in the recovery of trabecular bony architecture. The main findings emerged from the present study are (i) the importance of the interplay between mineral homeostasis and skeletal homeostasis in modulating and guiding bone's response to dietary/metabolic alterations and (ii) the evidence that the more involved bony architecture is the trabecular bone, the most susceptible to the dynamical balance of the two homeostases.

摘要

本研究是我们之前关于无钙饮食研究的第二步(涉及正常饮食恢复),旨在确定正常饮食恢复(伴或不伴 PTH(1-34)给药)是否会影响总骨量的数量和沉积部位。在大鼠模型中对椎体和股骨进行组织形态计量学评估和 Sclerostin 表达的免疫组织化学分析。最终目标是:(i) 确定当钙恢复到饮食中时骨量变化的时间和方式;(ii) 分析具有不同代谢的两种骨结构(即小梁骨与皮质骨)的不同参与程度;(iii) 验证 PTH(1-34)给药的可能作用。结果表明,饮食中钙含量的不同会导致骨小梁比皮质骨更多地参与其中,而 PTH 的作用主要在于恢复小梁骨结构。本研究的主要发现是:(i) 矿物质稳态和骨骼稳态之间的相互作用在调节和指导骨骼对饮食/代谢变化的反应方面具有重要意义;(ii) 证据表明,参与程度更高的骨结构是小梁骨,对两种稳态的动态平衡更为敏感。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0fc/6387065/a50fdb4dae43/ijms-20-00753-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0fc/6387065/3b1ec4184e56/ijms-20-00753-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0fc/6387065/c60010ee61cb/ijms-20-00753-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0fc/6387065/546dc9ecc04a/ijms-20-00753-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0fc/6387065/6923943a4964/ijms-20-00753-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0fc/6387065/0c5677aeb5f2/ijms-20-00753-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0fc/6387065/a50fdb4dae43/ijms-20-00753-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0fc/6387065/3b1ec4184e56/ijms-20-00753-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0fc/6387065/c60010ee61cb/ijms-20-00753-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0fc/6387065/546dc9ecc04a/ijms-20-00753-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0fc/6387065/6923943a4964/ijms-20-00753-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0fc/6387065/0c5677aeb5f2/ijms-20-00753-g011.jpg
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