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Protection of pancreatic β-cells against glucotoxicity by short-term treatment with GLP-1

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Author(s)
Sun-Hyun ParkJae-Hyung ParkHye-Min ShimAnn-Yae NaKi-Churl BaeJeung-Geun LimDae-Kyu Song
Keimyung Author(s)
Park, Jae HyungSong, Dae KyuBae, Ki CheorLim, Jeong Geun
Department
Dept. of Physiology (생리학)
Dept. of Orthopedic Surgery (정형외과학)
Dept. of Neurology (신경과학)
Journal Title
Biochemical and Biophysical Research Communications
Issued Date
2015
Volume
459
Issue
4
Abstract
Glucagon-like peptide-1 (GLP-1) reduces pancreatic β-cell apoptosis in type 2 diabetes. Glucotoxiciy is a main cause of β-cell apoptosis in type 2 diabetes. The aims of this study were to investigate the anti-apoptotic mechanisms of GLP-1 against glucotoxicity and whether physiological short-term treatment with GLP-1 can protect β-cells from glucotoxicity-induced apoptosis. GLP-1 treatment for only 30 min alleviated high glucose-induced β-cell apoptosis. The effect of GLP-1 was related with phosphoinositide 3-kinase (PI3K)/AKT-S473 phosphorylation. The increase in pAKT-S473 led to suppression of FoxO-1. GLP-1-induced AKT-S473 activation and FoxO-1 suppression were abolished by the selective inactivation of mTOR complex (mTORC) 2 using small interfering RNA directed towards the rapamycin-insensitive companion of mTOR. The protective effect of GLP-1 on β-cell apoptosis was also abolished by the selective inactivation of mTORC2. Hence, the protective effect of GLP-1 against glucotoxicity may be mediated by FoxO-1 suppression through the PI3K/mTORC2/AKT-S473 phosphorylation. This report provides evidence that short-term treatment with GLP-1 is beneficial to protect against glucotoxicity-induced β-cell apoptosis.

Keywords
Glucagon-like peptide-1;
Glucotoxiciy;
FoxO-1;
mTOR complex 2;
Pancreatic β-cell;
Type 2 diabetes
Keimyung Author(s)(Kor)
박재형
송대규
배기철
임정근
Publisher
School of Medicine
Citation
Sun-Hyun Park et al. (2015). Protection of pancreatic β-cells against glucotoxicity by short-term
treatment with GLP-1. Biochemical and Biophysical Research Communications, 459(4), 561–567. doi: 10.1016/j.bbrc.2015.02.139
Type
Article
ISSN
0006-291X
Source
https://linkinghub.elsevier.com/retrieve/pii/S0006291X15003861
DOI
10.1016/j.bbrc.2015.02.139
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/35169
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Neurology (신경과학)
1. School of Medicine (의과대학) > Dept. of Orthopedic Surgery (정형외과학)
1. School of Medicine (의과대학) > Dept. of Physiology (생리학)
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