Circulating exosome-like vesicles of humans with nondiabetic obesity impaired islet β-cell proliferation, which was associated with decreased Omentin-1 protein cargo

Qian Ge; Xinxin Xie; Xiangjun Chen; Rongfeng Huang; Cheng-Xue Rui; Qianna Zhen; Renzhi Hu; Min Wu; Xiaoqiu Xiao; Xi Li

doi:10.1016/j.gendis.2020.12.011

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Circulating exosome-like vesicles of humans with nondiabetic obesity impaired islet β-cell proliferation, which was associated with decreased Omentin-1 protein cargo

Full-length article | 更新时间：2022-06-24

- Circulating exosome-like vesicles of humans with nondiabetic obesity impaired islet β-cell proliferation, which was associated with decreased Omentin-1 protein cargo
- Circulating exosome-like vesicles of humans with nondiabetic obesity impaired islet β-cell proliferation, which was associated with decreased Omentin-1 protein cargo
- Genes & Diseases 2022年9卷第4期
- 作者机构：
  
  1. Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University,Chongqing,PR China,400016
  2. The Biology Science Institutes, Chongqing Medical University,Chongqing,PR China,400016
  3. The Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University,Chongqing,PR China,400016
  4. de Duve Institute, Catholic University of Louvain,Brussels,Belgium,1200
- 作者简介：
- 基金信息：
- DOI：10.1016/j.gendis.2020.12.011
  中图分类号：
- 纸质出版日期：2022，
  
  网络出版日期：2022-7-1，
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Qian Ge, Xinxin Xie, Xiangjun Chen, 等. Circulating exosome-like vesicles of humans with nondiabetic obesity impaired islet β-cell proliferation, which was associated with decreased Omentin-1 protein cargo[J]. Genes & Diseases, 2022,9(4).

Qian Ge, Xinxin Xie, Xiangjun Chen, et al. Circulating exosome-like vesicles of humans with nondiabetic obesity impaired islet β-cell proliferation, which was associated with decreased Omentin-1 protein cargo[J]. Genes & Diseases, 2022,9(4).
Qian Ge, Xinxin Xie, Xiangjun Chen, 等. Circulating exosome-like vesicles of humans with nondiabetic obesity impaired islet β-cell proliferation, which was associated with decreased Omentin-1 protein cargo[J]. Genes & Diseases, 2022,9(4). DOI： 10.1016/j.gendis.2020.12.011.

Qian Ge, Xinxin Xie, Xiangjun Chen, et al. Circulating exosome-like vesicles of humans with nondiabetic obesity impaired islet β-cell proliferation, which was associated with decreased Omentin-1 protein cargo[J]. Genes & Diseases, 2022,9(4). DOI： 10.1016/j.gendis.2020.12.011.

摘要

Abstract

The regulation of β-cell mass in the status of nondiabetic obesity remains not well understood. We aimed to investigate the role of circulating exosome-like vesicles (ELVs) isolated from humans with simple obesity in the regulation of islet β-cell mass. Between June 2017 and July 2019

81 subjects with simple obesity and 102 healthy volunteers with normal weight were recruited. ELVs were isolated by ultra-centrifugation. The proliferations of β-cells and islets were measured by 5-ethynl-2′-deoxyuridine (EdU). Protein components in ELVs were identified by Quantitative Proteomic Analysis and verified by Western blot and ELISA. The role of specific exosomal protein was analyzed by gain-of-function approach in ELVs released by 3T3-L1 preadipocytes. Circulating ELVs from subjects with simple obesity inhibited β-cell proliferation

in vitro

without affecting its apoptosis

secretion

and inflammation. The protein levels of Rictor and Omentin-1 were downregulated in circulating ELVs from subjects with simple obesity and associated with the obesity-linked pathologic conditions. The ELV-carried Omentin-1 and Omentin-1 protein

per se

were validated to increase β-cell proliferation and activate Akt signaling pathway. Moreover

Omentin-1 in ELVs was downregulated by insulin. The circulating ELVs may act as a negative regulator for β-cell mass in nondiabetic obesity through inhibiting β-cell proliferation. This effect was associated with downregulated Omentin-1 protein in ELVs. This newly identified ELV-carried protein could be a mediator linking insulin resistance to impaired β-cell proliferation and a new potential target for increasing β-cell mass in obesity and T2DM.

关键词

Keywords

β-CellExosomeObesityProliferationType 2 diabetes mellitus

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