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内皮细胞 IGF-1 受体介导与肠道壁的串扰，以调节肥胖中的微生物组。

Endothelial IGF-1 receptor mediates crosstalk with the gut wall to regulate microbiota in obesity.

机构信息

Faculty of Medicine and Health, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, UK.

Faculty of Engineering, School of Mechanical Engineering, University of Leeds, Leeds, UK.

出版信息

EMBO Rep. 2021 May 5;22(5):e50767. doi: 10.15252/embr.202050767. Epub 2021 May 2.

DOI:10.15252/embr.202050767
PMID:33934497
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8097321/
Abstract

Changes in composition of the intestinal microbiota are linked to the development of obesity and can lead to endothelial cell (EC) dysfunction. It is unknown whether EC can directly influence the microbiota. Insulin-like growth factor-1 (IGF-1) and its receptor (IGF-1R) are critical for coupling nutritional status and cellular growth; IGF-1R is expressed in multiple cell types including EC. The role of ECIGF-1R in the response to nutritional obesity is unexplored. To examine this, we use gene-modified mice with EC-specific overexpression of human IGF-1R (hIGFREO) and their wild-type littermates. After high-fat feeding, hIGFREO weigh less, have reduced adiposity and have improved glucose tolerance. hIGFREO show an altered gene expression and altered microbial diversity in the gut, including a relative increase in the beneficial genus Akkermansia. The depletion of gut microbiota with broad-spectrum antibiotics induces a loss of the favourable metabolic differences seen in hIGFREO mice. We show that IGF-1R facilitates crosstalk between the EC and the gut wall; this crosstalk protects against diet-induced obesity, as a result of an altered gut microbiota.

摘要

肠道微生物群组成的变化与肥胖的发展有关，并可能导致内皮细胞（EC）功能障碍。目前尚不清楚 EC 是否可以直接影响微生物群。胰岛素样生长因子-1（IGF-1）及其受体（IGF-1R）对于将营养状况和细胞生长联系起来至关重要；IGF-1R 在内皮细胞等多种细胞类型中表达。ECIGF-1R 在对营养性肥胖的反应中的作用尚未得到探索。为了研究这一点，我们使用基因修饰的小鼠，其内皮细胞中过表达人 IGF-1R（hIGFREO）及其野生型同窝仔鼠。高脂喂养后，hIGFREO 体重减轻，脂肪减少，葡萄糖耐量改善。hIGFREO 在肠道中表现出基因表达和微生物多样性的改变，包括有益属 Akkermansia 的相对增加。广谱抗生素耗尽肠道微生物群会导致 hIGFREO 小鼠中观察到的有利代谢差异丧失。我们表明，IGF-1R 促进 EC 与肠道壁之间的串扰；这种串扰通过改变肠道微生物群来防止饮食引起的肥胖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/286c/8097321/a891bbddb33e/EMBR-22-e50767-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/286c/8097321/cd24e088845f/EMBR-22-e50767-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/286c/8097321/503efc32b4cf/EMBR-22-e50767-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/286c/8097321/184e67e82772/EMBR-22-e50767-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/286c/8097321/34c1ab6137ca/EMBR-22-e50767-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/286c/8097321/5d6974b3cdcf/EMBR-22-e50767-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/286c/8097321/a891bbddb33e/EMBR-22-e50767-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/286c/8097321/cd24e088845f/EMBR-22-e50767-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/286c/8097321/503efc32b4cf/EMBR-22-e50767-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/286c/8097321/184e67e82772/EMBR-22-e50767-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/286c/8097321/34c1ab6137ca/EMBR-22-e50767-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/286c/8097321/5d6974b3cdcf/EMBR-22-e50767-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/286c/8097321/a891bbddb33e/EMBR-22-e50767-g007.jpg

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