果寡糖作用于肠道-骨骼轴,改善年轻成年 C57BL/6 雌性小鼠的骨骼,而与 Tregs 无关,并改变骨细胞。

IF 3.4 Q2 ENDOCRINOLOGY & METABOLISM
JBMR Plus Pub Date : 2024-02-21 eCollection Date: 2024-05-01 DOI:10.1093/jbmrpl/ziae021
Proapa Islam, John A Ice, Sanmi E Alake, Pelumi Adedigba, Bethany Hatter, Kara Robinson, Stephen L Clarke, Ashlee N Ford Versypt, Jerry Ritchey, Edralin A Lucas, Brenda J Smith
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引用次数: 0

摘要

用益生菌和益生元来靶向肠道-骨骼轴被认为是降低骨质疏松症风险的一种有前途的策略。肠道衍生的短链脂肪酸(SCFA)通过Tregs介导益生菌对骨骼的影响,但目前还不清楚益生元是否通过类似的机制发挥作用。我们研究了酸樱桃(TC)和果寡糖(FOS)这两种不同的益生元如何影响骨骼,以及这种反应是否需要Tregs。八周龄的 C57BL/6 雌性小鼠喂食补充了 10% w/w TC、FOS 或对照组饮食(Con;AIN-93M)的饮食,并接受同型对照或 CD25 Ab 以抑制 Tregs。与TC和对照饮食(Con)相比,FOS饮食增加了脊椎骨(约40%)和胫骨近端(约30%)的BMC、密度和骨小梁体积,与CD25治疗无关。两种益生元都能增加粪便中的 SCFAs(P .01),但 FOS 的反应更大。为了确定 FOS 如何影响骨细胞,我们检测了参与成骨细胞和破骨细胞分化和活性的基因以及骨细胞表达的基因。FOS 增加了成骨细胞分化调节因子(骨形态发生蛋白 2 [Bmp2]、Wnt 家族成员 10b [Wnt10b] 和 Osterix [Osx])和 1 型胶原蛋白的表达。)破骨细胞调节因子则没有变化。FOS 还增加了与成骨细胞相关的基因的表达,包括 Phex、基质细胞外磷酸化蛋白(Mepe)和牙本质基质酸性磷酸化蛋白 1(Dmp-1)。不过,随着成骨细胞数量和密度的增加,FOS 也会增加编码硬骨素的基因 Sost。这些研究结果表明,与TC相比,FOS对年轻成年雌性小鼠骨质和骨结构的影响更大,而且其对成骨细胞和骨细胞的影响并不依赖于Tregs。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Fructooligosaccharides act on the gut-bone axis to improve bone independent of Tregs and alter osteocytes in young adult C57BL/6 female mice.

Targeting the gut-bone axis with probiotics and prebiotics is considered as a promising strategy to reduce the risk of osteoporosis. Gut-derived short chain fatty acids (SCFA) mediate the effects of probiotics on bone via Tregs, but it is not known whether prebiotics act through a similar mechanism. We investigated how 2 different prebiotics, tart cherry (TC) and fructooligosaccharide (FOS), affect bone, and whether Tregs are required for this response. Eight-wk-old C57BL/6 female mice were fed with diets supplemented with 10% w/w TC, FOS, or a control diet (Con; AIN-93M) diet, and they received an isotype control or CD25 Ab to suppress Tregs. The FOS diet increased BMC, density, and trabecular bone volume in the vertebra (~40%) and proximal tibia (~30%) compared to the TC and control diets (Con), irrespective of CD25 treatment. Both prebiotics increased (P < .01) fecal SCFAs, but the response was greater with FOS. To determine how FOS affected bone cells, we examined genes involved in osteoblast and osteoclast differentiation and activity as well as genes expressed by osteocytes. The FOS increased the expression of regulators of osteoblast differentiation (bone morphogenetic protein 2 [Bmp2], Wnt family member 10b [Wnt10b] and Osterix [Osx]) and type 1 collagen). Osteoclasts regulators were unaltered. The FOS also increased the expression of genes associated with osteocytes, including (Phex), matrix extracellular phosphoglycoprotein (Mepe), and dentin matrix acidic phosphoprotein 1 (Dmp-1). However, Sost, the gene that encodes for sclerostin was also increased by FOS as the number and density of osteocytes increased. These findings demonstrate that FOS has a greater effect on the bone mass and structure in young adult female mice than TC and that its influence on osteoblasts and osteocytes is not dependent on Tregs.

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来源期刊
JBMR Plus
JBMR Plus Medicine-Orthopedics and Sports Medicine
CiteScore
5.80
自引率
2.60%
发文量
103
审稿时长
8 weeks
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