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亚精胺改善饮食诱导肥胖小鼠的肠道屏障完整性和肠道微生物群功能。

Spermidine improves gut barrier integrity and gut microbiota function in diet-induced obese mice.

机构信息

College of Biotechnology and Bioengineering, Zhejiang University of Technology , Hangzhou, China.

Research Institute of Poyang Lake, Jiangxi Academy of Sciences , Nanchang, China.

出版信息

Gut Microbes. 2020 Nov 9;12(1):1-19. doi: 10.1080/19490976.2020.1832857.

DOI:10.1080/19490976.2020.1832857
PMID:33151120
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7668533/
Abstract

Obesity is associated with impaired intestinal barrier function and dysbiosis of the gut microbiota. Spermidine, a polyamine that acts as an autophagy inducer, has important benefits in patients with aging-associated diseases and metabolic dysfunction. However, the mechanism of spermidine on obesity remains unclear. Here, we show that spermidine intake is negatively correlated with obesity in both humans and mice. Spermidine supplementation causes a significant loss of weight and improves insulin resistance in diet-induced obese (DIO) mice. These effects are associated with the alleviation of metabolic endotoxemia and enhancement of intestinal barrier function, which might be mediated through autophagy pathway and TLR4-mediated microbial signaling transduction. Moreover, spermidine causes the significant alteration of microbiota composition and function. Microbiota depletion compromises function, while transplantation of spermidine-altered microbiota confers protection against obesity. These changes might partly be driven by an SCFA-producing bacterium, , which was decreased in obese subjects and subsequently increased by spermidine. Notably, the change of is significantly correlated with enhanced gut barrier function induced by spermidine. Our results indicate that spermidine supplementation may serve as a viable therapy for obesity.

摘要

肥胖与肠道屏障功能受损和肠道微生物群落失调有关。亚精胺作为一种自噬诱导剂,在与衰老相关的疾病和代谢功能障碍患者中有重要的益处。然而,亚精胺对肥胖的作用机制尚不清楚。在这里,我们表明亚精胺的摄入与人类和小鼠的肥胖呈负相关。亚精胺补充剂可显著减轻体重,改善饮食诱导肥胖(DIO)小鼠的胰岛素抵抗。这些作用与代谢内毒素血症的缓解和肠道屏障功能的增强有关,这可能是通过自噬途径和 TLR4 介导的微生物信号转导介导的。此外,亚精胺导致微生物群落组成和功能的显著改变。微生物群耗竭会损害功能,而移植亚精胺改变的微生物群可预防肥胖。这些变化可能部分是由一种产生 SCFA 的细菌,即,在肥胖患者中减少,随后被亚精胺增加。值得注意的是,的变化与亚精胺诱导的增强肠道屏障功能显著相关。我们的研究结果表明,亚精胺补充可能是肥胖的一种可行治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/aec867f05a4a/KGMI_A_1832857_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/062844051b76/KGMI_A_1832857_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/ce7563a323d9/KGMI_A_1832857_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/69b8271afe86/KGMI_A_1832857_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/f3def96d2e70/KGMI_A_1832857_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/d0414cf9e5d0/KGMI_A_1832857_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/f98577c1e133/KGMI_A_1832857_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/36590d5096a3/KGMI_A_1832857_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/aec867f05a4a/KGMI_A_1832857_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/062844051b76/KGMI_A_1832857_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/ce7563a323d9/KGMI_A_1832857_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/69b8271afe86/KGMI_A_1832857_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/f3def96d2e70/KGMI_A_1832857_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/d0414cf9e5d0/KGMI_A_1832857_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/f98577c1e133/KGMI_A_1832857_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/36590d5096a3/KGMI_A_1832857_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a563/7668533/aec867f05a4a/KGMI_A_1832857_F0008_OC.jpg

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