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学科主题: 临床医学
题名:
Stimulating beta cell replication and improving islet graft function by GPR119 agonists
作者: Gao, Jie1,2,3; Tian, Lei1,2,4; Weng, Guobin1,2,5; Bhagroo, Nicholas V.6; Sorenson, Robert L.6; O′ Brien, Timothy D.7; Luo, Jian8; Guo, Zhiguang1,2
关键词: GLP-1 ; GPR119 ; islet graft function ; islet transplantation ; beta-cell regeneration ; beta-cell replication
刊名: TRANSPLANT INTERNATIONAL
发表日期: 2011-11-01
DOI: 10.1111/j.1432-2277.2011.01332.x
卷: 24, 期:11, 页:1124-1134
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Surgery ; Transplantation
研究领域[WOS]: Surgery ; Transplantation
关键词[WOS]: GLUCAGON-LIKE PEPTIDE-1 ; PROTEIN-COUPLED RECEPTOR ; DIABETIC NOD MICE ; GLYCEMIC CONTROL ; IMMUNOSUPPRESSIVE REGIMEN ; SINGLE-DONOR ; TRANSPLANTATION ; PROLIFERATION ; SECRETION ; GROWTH
英文摘要:

G protein-coupled receptor 119 (GPR119) is predominantly expressed in beta cells and intestinal L cells. In this study, we investigated whether oleoylethanolamide (OEA), a GPR119 endogenous ligand, and PSN632408, a GPR119 synthetic agonist, can stimulate beta-cell replication in vitro and in vivo and improve islet graft function in diabetic mice. We found that OEA and PSN632408 significantly increased numbers of insulin(+)/5-bromo-2′-deoxyuridine (BrdU)(+) beta cells in cultured mouse islets in a dose-dependent manner. All diabetic recipient mice, given marginal syngeneic islet transplants with OEA or PSN632408 or vehicle, achieved normoglycemia at 4 weeks after transplantation. However, normoglycemia was achieved significantly faster in OEA- or PSN632408-treated diabetic mice than in vehicle-treated diabetic mice (P < 0.05). The percentage of insulin(+)/BrdU(+) beta cells in islet grafts in OEA- and PSN632408-treated mice was significantly higher than in vehicle-treated mice (P < 0.01). Our data demonstrated that OEA and PSN632408 can stimulate beta-cell replication in vitro and in vivo and improve islet graft function. Targeting GPR119 is a novel therapeutic approach to increase beta-cell mass and to improve islet graft function by stimulating beta-cell replication.

语种: 英语
WOS记录号: WOS:000295835500015
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/57695
Appears in Collections:北京大学第二临床医学院_肝胆外科_期刊论文

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作者单位: 1.NGM Biopharmaceut Inc, San Francisco, CA USA
2.Univ Minnesota, Dept Surg, Minneapolis, MN 55455 USA
3.Univ Minnesota, Schulze Diabet Inst, Minneapolis, MN 55455 USA
4.Peking Univ, Peoples Hosp, Dept Hepatobiliary Surg, Beijing 100871, Peoples R China
5.Guangxi Med Univ, Affiliated Hosp 1, Dept Surg, Nanning, Peoples R China
6.Ningbo Univ, Yinzhou Hosp 2, Dept Urol, Ningbo 315211, Zhejiang, Peoples R China
7.Univ Minnesota, Dept Genet Cell Biol & Dev, Minneapolis, MN USA
8.Univ Minnesota, Dept Vet Populat Med, Minneapolis, MN USA

Recommended Citation:
Gao, Jie,Tian, Lei,Weng, Guobin,et al. Stimulating beta cell replication and improving islet graft function by GPR119 agonists[J]. TRANSPLANT INTERNATIONAL,2011,24(11):1124-1134.
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