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微生物群-肝脏-胆汁盐轴,一种与亚硒酸钠和纳米硒补充剂对青春期大鼠脂肪组织发育的相反作用相关的新机制。

Microbiota-Liver-Bile Salts Axis, a Novel Mechanism Involved in the Contrasting Effects of Sodium Selenite and Selenium-Nanoparticle Supplementation on Adipose Tissue Development in Adolescent Rats.

作者信息

Ojeda María Luisa, Nogales Fátima, Carrasco López José A, Gallego-López María Del Carmen, Carreras Olimpia, Alcudia Ana, Pajuelo Eloísa

机构信息

Departamento de Fisiología, Facultad de Farmacia, Universidad de Sevilla, 41012 Sevilla, Spain.

Departamento de Microbiología y Parasitología, Facultad de Farmacia, Universidad de Sevilla, 41012 Sevilla, Spain.

出版信息

Antioxidants (Basel). 2023 May 19;12(5):1123. doi: 10.3390/antiox12051123.

DOI:10.3390/antiox12051123
PMID:37237989
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10215413/
Abstract

Adolescence is a period during which body composition changes deeply. Selenium (Se) is an excellent antioxidant trace element related to cell growth and endocrine function. In adolescent rats, low Se supplementation affects adipocyte development differently depending on its form of administration (selenite or Se nanoparticles (SeNPs). Despite this effect being related to oxidative, insulin-signaling and autophagy processes, the whole mechanism is not elucidated. The microbiota-liver-bile salts secretion axis is related to lipid homeostasis and adipose tissue development. Therefore, the colonic microbiota and total bile salts homeostasis were explored in four experimental groups of male adolescent rats: control, low-sodium selenite supplementation, low SeNP supplementation and moderate SeNPs supplementation. SeNPs were obtained by reducing Se tetrachloride in the presence of ascorbic acid. Supplementation was received orally through water intake; low-Se rats received twice more Se than control animals and moderate-Se rats tenfold more. Supplementation with low doses of Se clearly affected anaerobic colonic microbiota profile and bile salts homeostasis. However, these effects were different depending on the Se administration form. Selenite supplementation primarily affected liver by decreasing farnesoid X receptor hepatic function, leading to the accumulation of hepatic bile salts together to increase in the ratio Firmicutes/Bacteroidetes and glucagon-like peptide-1 (GLP-1) secretion. In contrast, low SeNP levels mainly affected microbiota, moving them towards a more prominent Gram-negative profile in which the relative abundance of and was clearly enhanced and the Firmicutes/Bacteroidetes ratio decreased. This bacterial profile is directly related to lower adipose tissue mass. Moreover, low SeNP administration did not modify bile salts pool in serum circulation. In addition, specific gut microbiota was regulated upon administration of low levels of Se in the forms of selenite or SeNPs, which are properly discussed. On its side, moderate-SeNPs administration led to great dysbiosis and enhanced the abundance of pathogenic bacteria, being considered toxic. These results strongly correlate with the deep change in adipose mass previously found in these animals, indicating that the microbiota-liver-bile salts axis is also mechanistically involved in these changes.

摘要

青春期是身体成分发生深刻变化的时期。硒(Se)是一种与细胞生长和内分泌功能相关的优秀抗氧化微量元素。在青春期大鼠中,低剂量硒补充剂对脂肪细胞发育的影响因其给药形式(亚硒酸盐或硒纳米颗粒(SeNPs))而异。尽管这种影响与氧化、胰岛素信号传导和自噬过程有关,但其完整机制尚未阐明。微生物群-肝脏-胆汁盐分泌轴与脂质稳态和脂肪组织发育有关。因此,在雄性青春期大鼠的四个实验组中研究了结肠微生物群和总胆汁盐稳态:对照组、低剂量亚硒酸钠补充组、低剂量SeNP补充组和中等剂量SeNP补充组。通过在抗坏血酸存在下还原四氯化硒获得SeNPs。通过饮水口服补充;低硒大鼠摄入的硒是对照动物的两倍,中等硒大鼠摄入的硒是对照动物的十倍。低剂量硒补充剂明显影响厌氧结肠微生物群谱和胆汁盐稳态。然而,这些影响因硒的给药形式而异。补充亚硒酸盐主要通过降低法尼醇X受体肝功能影响肝脏,导致肝脏胆汁盐积累,同时增加厚壁菌门/拟杆菌门的比例和胰高血糖素样肽-1(GLP-1)分泌。相比之下,低剂量SeNP主要影响微生物群,使其向更突出的革兰氏阴性菌谱转变,其中 和 的相对丰度明显增加,厚壁菌门/拟杆菌门比例降低。这种细菌谱与较低的脂肪组织量直接相关。此外,低剂量SeNP给药并未改变血清循环中的胆汁盐池。此外,以亚硒酸盐或SeNPs形式给予低水平硒时,特定的肠道微生物群会受到调节,对此进行了适当讨论。另一方面,中等剂量SeNP给药导致严重的生态失调并增加了病原菌的丰度,被认为具有毒性。这些结果与之前在这些动物中发现的脂肪量的深刻变化密切相关,表明微生物群-肝脏-胆汁盐轴在这些变化中也有机制性参与。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d034/10215413/3601e7926071/antioxidants-12-01123-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d034/10215413/c53385a9cf00/antioxidants-12-01123-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d034/10215413/83d9fb5ff981/antioxidants-12-01123-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d034/10215413/3601e7926071/antioxidants-12-01123-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d034/10215413/c53385a9cf00/antioxidants-12-01123-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d034/10215413/a3da974ec9b4/antioxidants-12-01123-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d034/10215413/9ad383469644/antioxidants-12-01123-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d034/10215413/3601e7926071/antioxidants-12-01123-g005.jpg

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