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一种短链果糖低聚糖作为益生元,通过成骨机制促进去卵巢大鼠的峰值骨量并维持其骨量。

A prebiotic, short-chain fructo-oligosaccharides promotes peak bone mass and maintains bone mass in ovariectomized rats by an osteogenic mechanism.

机构信息

Division of Endocrinology, CSIR-Central Drug Research Institute, Sector-10, Jankipuram Extension, Sitapur Road, Lucknow, 226031, India.

Division of Pharmaceutics, CSIR-Central Drug Research Institute, Sector-10, Jankipuram Extension, Sitapur Road, Lucknow, 226031, India.

出版信息

Biomed Pharmacother. 2020 Sep;129:110448. doi: 10.1016/j.biopha.2020.110448. Epub 2020 Jul 7.

DOI:10.1016/j.biopha.2020.110448
PMID:32776872
Abstract

In preclinical studies, fructooligosaccharide (FOS) showed beneficial skeletal effects but its effect on peak bone mass (PBM) and bone loss caused by estrogen (E2) deficiency has not been studied, and we set out to study these effects in rats. Short-chain (sc)-FOS had no effect on body weight, body composition, and energy metabolism of ovary intact (sham) and ovariectomized (OVX) rats. scFOS did not affect serum and urinary calcium and phosphorus levels, and on calcium absorption, although an increasing trend was noted in the sham group. Sham and OVX rats given scFOS had better skeletal parameters than their respective controls. scFOS treatment resulted in a higher bone anabolic response but had no effect on the catabolic parameters. scFOS increased serum levels of a short-chain fatty acid, butyrate which is known to have osteogenic effect. Our study for the first time demonstrates that in rats scFOS at the human equivalent dose enhances PBM and protects against E2 deficiency-induced bone loss by selective enhancement of new bone formation, and implicates butyrate in this process.

摘要

在临床前研究中,低聚果糖(FOS)对骨骼有有益的影响,但它对峰值骨量(PBM)和雌激素(E2)缺乏引起的骨丢失的影响尚未得到研究,我们着手研究其在大鼠中的这些作用。短链(sc)-FOS 对卵巢完整(假手术)和卵巢切除(OVX)大鼠的体重、身体成分和能量代谢没有影响。scFOS 不影响血清和尿钙和磷水平,也不影响钙吸收,尽管假手术组有增加的趋势。给予 scFOS 的假手术和 OVX 大鼠的骨骼参数均优于各自的对照组。scFOS 治疗导致骨合成反应增加,但对分解代谢参数没有影响。scFOS 增加了短链脂肪酸丁酸盐的血清水平,而丁酸盐已知具有成骨作用。我们的研究首次表明,在大鼠中,以人体等效剂量给予 scFOS 可增强 PBM,并通过选择性增强新骨形成来预防 E2 缺乏引起的骨丢失,而丁酸盐参与了这一过程。

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