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在超重、肥胖和患有代谢综合征的胰岛素抵抗个体中,粪便中失调杆菌属的浓度与血浆脂质组相关。

Fecal Dysosmobacter spp. concentration is linked to plasma lipidome in insulin-resistant individuals with overweight, obesity and metabolic syndrome.

作者信息

Petitfils Camille, Depommier Clara, Delzenne Nathalie M, Everard Amandine, Van Hul Matthias, Cani Patrice D

机构信息

Metabolism and Nutrition Research Group (MNUT), Louvain Drug Research Institute (LDRI), UCLouvain, Université catholique de Louvain, Brussels, Belgium.

Walloon Excellence in Life Sciences and BIOtechnology (WELBIO), WELBIO Department, WEL Research Institute, Wavre, Belgium.

出版信息

Lipids Health Dis. 2025 Jun 6;24(1):203. doi: 10.1186/s12944-025-02629-z.

DOI:10.1186/s12944-025-02629-z
PMID:40481506
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12142885/
Abstract

BACKGROUND

Obesity is reaching epidemic proportions worldwide. This excessive increase of adipose tissue is a risk factor for the development of multiple diseases and premature death. Amongst associated diseases, metabolic syndrome is one of the main comorbidities of obesity. In this context, the gut microbiota has been recognized as both shaping and responding to host energy metabolism. Recently metabolomics has emerged as a powerful tool to capture a snapshot of the metabolites present in a specific tissue, providing new insights into host-microbiota interactions. Integrating metabolomics with gut microbiota studies could help us better understand how specific species impact on host metabolomic profile. Dysosmobacter welbionis has been identified as a promising next generation beneficial bacteria with potential effects on fat mass and glucose metabolism in mice, and fecal Dysosmobacter spp. concentration was inversely correlated to body mass index fasting glucose and plasmatic HbA1c in humans.

METHODS

Concentration of Dysosmobacter spp. was quantified by qPCR in the stools of insulin resistant overweight/obese participants with a metabolic syndrome and plasma metabolites were analyzed using untargeted metabolomics. Correlations between Dysosmobacter spp. fecal abundance and the 1169 identified plasma metabolites were uncovered using Spearman correlations followed by a false discovery rate correction.

RESULTS

Interestingly, among the detected metabolites, Dysosmobacter spp. was exclusively associated with lipid molecules. Fecal concentration of Dysosmobacter spp. was positively associated with plasmatic levels of five phosphatidylcholines, arachidonate, two monoacylglycerols, twelve diacylglycerols, three lysophosphatidylethanolamines, one phosphatidylinositol and three lysophosphatidylinositols, as well as glycerophosphoethanolamines, glycerophosphatidylcholine and PC(P-16:0). The correlation was particularly interesting with acylcholine and lysophosphatidylcholine metabolites as, respectively, 6/8 and 8/10 detected molecules were positively associated with Dysosmobacter spp.

CONCLUSION

These results suggest that Dysosmobacter spp. plays a specific role in host lipid metabolism. This finding aligns with previous in vivo studies highlighting lipid profile alterations in multiple tissues of mice treated with this bacterium. Further studies are needed to elucidate the underlying mechanisms and assess its potential therapeutic applications.

摘要

背景

肥胖在全球正达到流行程度。脂肪组织的这种过度增加是多种疾病发生和过早死亡的危险因素。在相关疾病中,代谢综合征是肥胖的主要合并症之一。在这种情况下,肠道微生物群已被认为既塑造宿主能量代谢又对其作出反应。最近,代谢组学已成为一种强大的工具,可捕捉特定组织中存在的代谢物的快照,为宿主 - 微生物群相互作用提供新的见解。将代谢组学与肠道微生物群研究相结合可以帮助我们更好地理解特定物种如何影响宿主代谢组学特征。韦氏菌属已被鉴定为一种有前景的下一代有益细菌,对小鼠的脂肪量和葡萄糖代谢有潜在影响,并且人类粪便中韦氏菌属的浓度与体重指数、空腹血糖和血浆糖化血红蛋白呈负相关。

方法

通过qPCR对患有代谢综合征的胰岛素抵抗超重/肥胖参与者的粪便中韦氏菌属的浓度进行定量,并使用非靶向代谢组学分析血浆代谢物。使用Spearman相关性,然后进行错误发现率校正,揭示韦氏菌属粪便丰度与1169种已鉴定的血浆代谢物之间的相关性。

结果

有趣的是,在检测到的代谢物中,韦氏菌属仅与脂质分子相关。韦氏菌属的粪便浓度与五种磷脂酰胆碱、花生四烯酸、两种单酰甘油、十二种二酰甘油、三种溶血磷脂酰乙醇胺、一种磷脂酰肌醇和三种溶血磷脂酰肌醇以及甘油磷酸乙醇胺、甘油磷脂酰胆碱和PC(P - 16:0)的血浆水平呈正相关。与酰胆碱和溶血磷脂酰胆碱代谢物的相关性特别有趣,因为分别有6/8和8/10检测到的分子与韦氏菌属呈正相关。

结论

这些结果表明韦氏菌属在宿主脂质代谢中起特定作用。这一发现与先前的体内研究一致,这些研究强调了用这种细菌处理的小鼠多个组织中的脂质谱改变。需要进一步研究以阐明潜在机制并评估其潜在的治疗应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/662d/12142885/e23511ba4b81/12944_2025_2629_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/662d/12142885/2971a85374bb/12944_2025_2629_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/662d/12142885/ae527dd27494/12944_2025_2629_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/662d/12142885/e23511ba4b81/12944_2025_2629_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/662d/12142885/2971a85374bb/12944_2025_2629_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/662d/12142885/ae527dd27494/12944_2025_2629_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/662d/12142885/e23511ba4b81/12944_2025_2629_Fig3_HTML.jpg

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