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

查看全文 作　　者：Qian [1]Ge;Xinxin [2]Xie;Xiangjun [1]Chen;Rongfeng [3]Huang;Cheng-Xue [2,4]Rui;Qianna [1]Zhen;Renzhi [1]Hu;Min [3]Wu;Xiaoqiu [3]Xiao;Xi [2]Li 高影响力作者 机构地区：[1]Department of Endocrinology,The First Affiliated Hospital of Chongqing Medical University,Chongqing 400016,PR China;[2]The Biology Science Institutes,Chongqing Medical University,Chongqing 400016,PR China;[3]The Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases,The First Affiliated Hospital of Chongqing Medical University,Chongqing 400016,PR China;[4]de Duve Institute,Catholic University of Louvain,Brussels 1200,Belgium高影响力机构 出　　处：《Genes & Diseases》索引2022年第9卷第4期,共15页高影响力期刊 基　　金：This work was supported by the National Key R&D Program of China(No.2018YFA0800401);the National Natural Science Foundation of China(No.81200629,81570763,81770861 and 31571401);the Fundamental Science and Advanced Technology Research of Chongqing(Major Project,No.CSTC2015jcyjB0146);the Chongqing Science and Technology Foundation(No.cstc2018jcyjAX0232);the Science and Technology Research Program of Chongqing Municipal Education Commission(No.KJZD-K201800402). 摘　　要：The regulation ofβ-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 isletβ-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 ofβ-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 inhibitedβ-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 increaseβ-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 forβ-cell mass in nondiabetic obesity through inhibitingβ-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 impairedβ-cell proliferation and a new potential target for increasingβ-cell mass in obesity and T2DM. 关 键 词：β-Cell EXOSOME OBESITY Proliferation Type 2 diabetes mellitus
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