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视黄醇代谢信号通路参与肥胖小鼠中微生物群调节的脂肪沉积。

Retinol metabolism signaling participates in microbiota-regulated fat deposition in obese mice.

作者信息

Han Hui, Zhang Shunfen, Wang Mengyu, Yi Bao, Zhao Yong, Schroyen Martine, Zhang Hongfu

机构信息

State Key Laboratory of Animal Nutrition, Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing, China; Precision Livestock and Nutrition Unit, Gembloux Agro-Bio Tech, University of Liège, Gembloux, Belgium.

State Key Laboratory of Animal Nutrition, Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing, China.

出版信息

J Nutr Biochem. 2025 Feb;136:109787. doi: 10.1016/j.jnutbio.2024.109787. Epub 2024 Oct 25.

Abstract

Obesity is a global pandemic threatening public health, excess fat accumulation and overweight are its characteristics. In this study, the interplay between gut microbiota and retinol metabolism in modulating fat accumulation was verified. We observed gut microbiota depletion reduced the body weight and the ratios of white adipose tissues (WATs) to body weight in high-fat diet (HFD) fed-mice. The kyoto encyclopedia of genes and genomes (KEGG) analysis and protein-protein interaction (PPI) network of RNA-seq results indicated that retinol metabolism signaling may be involved in the microbiota-regulated fat deposition. Furthermore, activated retinol metabolism signaling by all-trans retinoic acid (atRA) supplementation reduced body weight and WAT accumulation in obese mice. 16S rRNA gene sequencing of the ileal microbiota suggested that atRA supplementation increased the microbial diversity and induced the growth of beneficial bacteria including Parabacteroides, Bacteroides, Clostridium_XVIII, Bifidobacterium, Enterococcus, Bacillus, Leuconostoc, and Lactobacillus in obese mice. Spearman correlation showed that the microbiota altered by atRA were associated with body and WAT weights. Together, this study reveals the interaction between the gut microbiota and retinol metabolism signaling in regulating adipose accumulation and obesity. It is expected of this finding to provide new insights to prevent and develop therapeutic measures of obesity-related metabolic syndrome.

摘要

肥胖是一种威胁公众健康的全球性流行病,其特征是脂肪过度堆积和超重。在本研究中,验证了肠道微生物群与视黄醇代谢在调节脂肪堆积中的相互作用。我们观察到,在高脂饮食喂养的小鼠中,肠道微生物群的减少降低了体重以及白色脂肪组织(WAT)与体重的比率。京都基因与基因组百科全书(KEGG)分析以及RNA测序结果的蛋白质-蛋白质相互作用(PPI)网络表明,视黄醇代谢信号可能参与微生物群调节的脂肪沉积。此外,通过补充全反式维甲酸(atRA)激活视黄醇代谢信号可降低肥胖小鼠的体重和WAT堆积。回肠微生物群的16S rRNA基因测序表明,补充atRA可增加微生物多样性,并诱导肥胖小鼠体内包括副拟杆菌、拟杆菌、 XVIII梭菌、双歧杆菌、肠球菌、芽孢杆菌、明串珠菌和乳杆菌在内的有益细菌生长。Spearman相关性分析表明,atRA改变的微生物群与体重和WAT重量相关。总之,本研究揭示了肠道微生物群与视黄醇代谢信号在调节脂肪堆积和肥胖中的相互作用。预期这一发现可为预防和制定肥胖相关代谢综合征的治疗措施提供新的见解。

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