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Title 

Increased vulnerability to beta-cell destruction and diabetes in mice lacking NAD(P)H:quinone oxidoreductase 1

Authors 

Seung Hoon YeoJung Ran NohYong Hoon KimGil Tae GangSang Woo KimKyoung Shim KimJung Hwan HwangM ShongChul Ho Lee

Publisher 

Elsevier

Issue Date 

2013

Citation 

Toxicology Letters, vol. 219, no. 1, pp. 35-41

Keywords 

β-cellApoptosisDiabetesMiceNQO1Streptozotocin

Abstract 

NAD(P)H:quinone oxidoreductase 1 (NQO1) has been known to protect cells against stressors, including the diabetogenic reagent streptozotocin (STZ). The present study demonstrated that NQO1 deficiency resulted in increased pancreatic β-cell death induced by multiple low dose of STZ (MLDS) injections. NQO1 knockout (KO) mice showed hyperglycemia, body weight loss, impaired glucose clearance rate and a lower plasma insulin level after MLDS treatment. Moreover, β-cell mass and pancreatic insulin content were significantly lower in KO mice than in wild-type (WT) mice after MLDS treatment. Five days after the first STZ treatment, the islets of KO mice had substantially more TUNEL-positive β-cells than those of WT mice, but there was no difference in the regeneration of β-cells between KO mice and WT mice. At the same time, MLDS-treated KO mice showed significantly increased apoptotic markers in β-cells, including cleaved caspase 3, Smac/DIABLO and AIF (apoptosis inducing factor) in the cytoplasm. These results suggest that mice deficient in NQO1 are vulnerable to MLDS-induced β-cell destruction and diabetes, caused by increase of β-cell apoptosis in pancreas.

ISSN 

0378-4274

Link 

http://dx.doi.org/10.1016/j.toxlet.2013.02.013

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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