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低聚木糖预防肝脂肪变性和脂肪组织炎症:粪便微生物组的分类和代谢组学模式与双聚类相关。

Xylo-Oligosaccharides in Prevention of Hepatic Steatosis and Adipose Tissue Inflammation: Associating Taxonomic and Metabolomic Patterns in Fecal Microbiomes with Biclustering.

机构信息

Faculty of Sport and Health Sciences, University of Jyväskylä, FI-40014 Jyväskylä, Finland.

Department of Psychology, University of Jyväskylä, FI-40014 Jyväskylä, Finland.

出版信息

Int J Environ Res Public Health. 2021 Apr 12;18(8):4049. doi: 10.3390/ijerph18084049.

DOI:10.3390/ijerph18084049
PMID:33921370
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8068902/
Abstract

We have shown that prebiotic xylo-oligosaccharides (XOS) increased beneficial gut microbiota (GM) and prevented high fat diet-induced hepatic steatosis, but the mechanisms associated with these effects are not clear. We studied whether XOS affects adipose tissue inflammation and insulin signaling, and whether the GM and fecal metabolome explain associated patterns. XOS was supplemented or not with high (HFD) or low (LFD) fat diet for 12 weeks in male Wistar rats ( = 10/group). Previously analyzed GM and fecal metabolites were biclustered to reduce data dimensionality and identify interpretable groups of co-occurring genera and metabolites. Based on our findings, biclustering provides a useful algorithmic method for capturing such joint signatures. On the HFD, XOS-supplemented rats showed lower number of adipose tissue crown-like structures, increased phosphorylation of AKT in liver and adipose tissue as well as lower expression of hepatic miRNAs. XOS-supplemented rats had more fecal glycine and less hypoxanthine, isovalerate, branched chain amino acids and aromatic amino acids. Several bacterial genera were associated with the metabolic signatures. In conclusion, the beneficial effects of XOS on hepatic steatosis involved decreased adipose tissue inflammation and likely improved insulin signaling, which were further associated with fecal metabolites and GM.

摘要

我们已经证明,益生元木低聚糖(XOS)可以增加有益的肠道微生物群(GM)并预防高脂肪饮食引起的肝脂肪变性,但与这些效果相关的机制尚不清楚。我们研究了 XOS 是否会影响脂肪组织炎症和胰岛素信号转导,以及 GM 和粪便代谢组是否可以解释相关模式。12 周内,雄性 Wistar 大鼠分别用高(HFD)或低(LFD)脂肪饮食补充或不补充 XOS(每组 = 10 只)。先前分析的 GM 和粪便代谢物被双聚类以降低数据的维度,并确定可解释的共同出现的属和代谢物组。根据我们的发现,双聚类为捕获这种联合特征提供了一种有用的算法方法。在 HFD 上,补充 XOS 的大鼠脂肪组织中的冠状结构数量减少,肝脏和脂肪组织中 AKT 的磷酸化增加,以及肝 miRNA 的表达降低。补充 XOS 的大鼠粪便中甘氨酸增多,次黄嘌呤、异戊酸、支链氨基酸和芳香族氨基酸减少。一些细菌属与代谢特征有关。总之,XOS 对肝脂肪变性的有益作用涉及减少脂肪组织炎症,并可能改善胰岛素信号转导,这与粪便代谢物和 GM 进一步相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/a92ba5e6c1cc/ijerph-18-04049-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/338366b84c11/ijerph-18-04049-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/7b6ab9a51c35/ijerph-18-04049-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/8e70b44cfe34/ijerph-18-04049-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/1b43ec511b18/ijerph-18-04049-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/6ef9bad3f13e/ijerph-18-04049-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/02968dc040b9/ijerph-18-04049-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/2ae37b1c869c/ijerph-18-04049-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/bfa7264b55bd/ijerph-18-04049-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/7aa0c7adccff/ijerph-18-04049-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/a92ba5e6c1cc/ijerph-18-04049-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/338366b84c11/ijerph-18-04049-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/7b6ab9a51c35/ijerph-18-04049-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/8e70b44cfe34/ijerph-18-04049-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/1b43ec511b18/ijerph-18-04049-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/6ef9bad3f13e/ijerph-18-04049-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/02968dc040b9/ijerph-18-04049-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/2ae37b1c869c/ijerph-18-04049-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/bfa7264b55bd/ijerph-18-04049-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/7aa0c7adccff/ijerph-18-04049-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e380/8068902/a92ba5e6c1cc/ijerph-18-04049-g010.jpg

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