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乙醇诱导骨质疏松症中肠道微生物群和代谢物谱的改变与骨代谢降低有关。

Altered gut microbiota and metabolites profile are associated with reduced bone metabolism in ethanol-induced osteoporosis.

机构信息

Graduate School, Heilongjiang University of Chinese Medicine, Harbin, China.

The First Affiliated Hospital of Zhejiang University of Chinese Medicine, Hangzhou, China.

出版信息

Cell Prolif. 2022 Jul;55(7):e13245. doi: 10.1111/cpr.13245. Epub 2022 Jun 10.

DOI:10.1111/cpr.13245
PMID:35688648
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9251047/
Abstract

OBJECTIVE

Chronic heavy drinking causes ethanol-induced osteoporosis (EIO). The present study aimed to explore the role of GM in EIO.

MATERIAL AND METHODS

A rat EIO model was established by chronic ethanol intake. Taking the antibiotic application as the matched group of dysbacteriosis, an integrated 16S rRNA sequencing and liquid chromatography-tandem mass spectrometry-based metabolomics in serum and faeces were applied to explore the association of differential metabolic phenotypes and screen out the candidate metabolites detrimental to ossification. The colon organoids were used to track the source of 5-HT and the effect of 5-HT on bone formation was examined in vitro.

RESULTS

Compared with antibiotics application, ethanol-gavaged decreased the BMD in rats. We found that both ethanol and antibiotic intake affected the composition of GM, but ethanol intake increased the ratio of Firmicutes to Bacteroidetes. Elevated serotonin was proved to be positively correlated with the changes of the composition of GM and faecal metabolites and inhibited the proliferation and mineralization of osteogenesis-related cells. However, the direct secretory promotion of serotonin was absent in the colon organoids exposed to ethanol.

CONCLUSION

This study demonstrated that ethanol consumption led to osteoporosis and intestinal-specific dysbacteriosis. Conjoint analysis of the genetic profiles of GM and metabolic phenotypes in serum and faeces allowed us to understand the endogenous metabolite, 5-HT, as detrimental regulators in the gut-bone axis to impair bone formation.

摘要

目的

慢性大量饮酒可导致乙醇诱导性骨质疏松症（EIO）。本研究旨在探讨 GM 在 EIO 中的作用。

材料与方法

通过慢性乙醇摄入建立大鼠 EIO 模型。以抗生素应用作为菌群失调的匹配组，应用整合的 16S rRNA 测序和基于液相色谱-串联质谱的血清和粪便代谢组学，探讨差异代谢表型的相关性，并筛选出不利于成骨的候选代谢物。使用结肠类器官追踪 5-HT 的来源，并在体外研究 5-HT 对骨形成的影响。

结果

与抗生素应用相比，乙醇灌胃降低了大鼠的 BMD。我们发现，乙醇和抗生素摄入均影响 GM 的组成，但乙醇摄入增加了厚壁菌门与拟杆菌门的比例。已证实，升高的 5-HT 与 GM 组成和粪便代谢物的变化呈正相关，并抑制成骨相关细胞的增殖和矿化。然而，在暴露于乙醇的结肠类器官中，5-HT 并未直接促进其分泌。

结论

本研究表明，乙醇摄入可导致骨质疏松症和肠道特异性菌群失调。对 GM 的遗传特征和血清及粪便代谢表型的联合分析，使我们能够了解内源性代谢物 5-HT 作为肠道-骨骼轴中损害骨形成的有害调节剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e2/9251047/67fa3063302a/CPR-55-e13245-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e2/9251047/67fa3063302a/CPR-55-e13245-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e2/9251047/227c5f5b5a51/CPR-55-e13245-g005.jpg
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