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饮食型 2 抗性淀粉通过调节高脂肪饮食老龄小鼠的微生物群和代谢物来改善全身炎症和肠道通透性。

Dietary type 2 resistant starch improves systemic inflammation and intestinal permeability by modulating microbiota and metabolites in aged mice on high-fat diet.

机构信息

Department of Gastroenterology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310016, Zhejiang Province, China.

Institute of Gastroenterology, Zhejiang University, Hangzhou 310016, Zhejiang Province, China.

出版信息

Aging (Albany NY). 2020 May 25;12(10):9173-9187. doi: 10.18632/aging.103187.

DOI:10.18632/aging.103187
PMID:32452830
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7288951/
Abstract

Type 2 resistant starch (RS2) is a fermentable dietary fiber conferring health benefits. We investigated the effects of RS2 on host, gut microbiota, and metabolites in aged mice on high-fat diet. In eighteen-month old mice randomly assigned to control, high-fat (HF), or high-fat+20% RS2 (HFRS) diet for 16 weeks, RS2 reversed the weight gain and hepatic steatosis induced by high-fat diet. Serum and fecal LPS, colonic IL-2 and hepatic IL-4 mRNA expressions decreased while colonic mucin 2 mRNA and protein expressions increased in the HFRS compared to the HF and the control group. 16s rRNA sequencing of fecal microbial DNA demonstrated that RS2 decreased the abundance of pathogen taxa associated with obesity, inflammation, and aging including ( phylum), , , , , and Additionally, RS2 increased the colonic butyric acid by 2.6-fold while decreasing the isobutyric and isovaleric acid levels by half compared to the HF group. Functional analyses based on Clusters of Orthologous Groups showed that RS2 increased carbohydrate while decreasing amino acid metabolism. These findings demonstrate that RS2 can reverse weight gain, hepatic steatosis, inflammation, and increased intestinal permeability in aged mice on high-fat diet mediated by changes in gut microbiome and metabolites.

摘要

2 型抗性淀粉(RS2)是一种可发酵膳食纤维,具有健康益处。我们研究了 RS2 对高脂肪饮食老年小鼠的宿主、肠道微生物群和代谢物的影响。在 18 个月大的小鼠中,随机分为对照组、高脂肪组(HF)或高脂肪+20% RS2 组(HFRS),喂养 16 周。与 HF 组和对照组相比,RS2 逆转了高脂肪饮食引起的体重增加和肝脂肪变性。HFRS 组血清和粪便 LPS、结肠 IL-2 和肝 IL-4 mRNA 表达降低,而结肠黏蛋白 2 mRNA 和蛋白表达增加。粪便微生物 DNA 的 16s rRNA 测序表明,RS2 降低了与肥胖、炎症和衰老相关的病原体分类群的丰度,包括 (门)、、、、、和 。此外,与 HF 组相比,RS2 使结肠丁酸增加 2.6 倍,而异丁酸和异戊酸水平降低一半。基于同源基因簇的功能分析表明,RS2 增加了碳水化合物代谢,而减少了氨基酸代谢。这些发现表明,RS2 通过改变肠道微生物群和代谢物,可以逆转高脂肪饮食老年小鼠的体重增加、肝脂肪变性、炎症和增加的肠道通透性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ced/7288951/04331bd0941e/aging-12-103187-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ced/7288951/a511cd5e2703/aging-12-103187-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ced/7288951/643aba2d3711/aging-12-103187-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ced/7288951/709b1b63e681/aging-12-103187-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ced/7288951/ea11525182df/aging-12-103187-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ced/7288951/04331bd0941e/aging-12-103187-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ced/7288951/a511cd5e2703/aging-12-103187-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ced/7288951/643aba2d3711/aging-12-103187-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ced/7288951/709b1b63e681/aging-12-103187-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ced/7288951/ea11525182df/aging-12-103187-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ced/7288951/04331bd0941e/aging-12-103187-g005.jpg

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