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

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Author(s)
박재형송대규배기철임정근
Alternative Author(s)
Park, Jae HyungSong, Dae KyuBae, Ki CheorLim, Jeong Geun
Publication Year
2015
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
Department
Dept. of Physiology (생리학)
Dept. of Orthopedic Surgery (정형외과학)
Dept. of Neurology (신경과학)
Publisher
School of Medicine
Citation
Biochemical and Biophysical Research Communications, Vol.459(4) : 561-567, 2015
Type
Article
ISSN
0006-291X
DOI
10.1016/j.bbrc.2015.02.139
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/35169
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