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

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Title
Increased vulnerability to beta-cell destruction and diabetes in mice lacking NAD(P)H:quinone oxidoreductase 1
Author(s)
Seung Hoon Yeo; Jung Ran NohYong Hoon Kim; Gil Tae Gang; Sang Woo Kim; Kyoung Shim KimJung Hwan Hwang; M Shong; Chul Ho Lee
Bibliographic Citation
Toxicology Letters, vol. 219, no. 1, pp. 35-41
Publication Year
2013
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.
Keyword
β-cellApoptosisDiabetesMiceNQO1Streptozotocin
ISSN
0378-4274
Publisher
Elsevier
DOI
http://dx.doi.org/10.1016/j.toxlet.2013.02.013
Type
Article
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
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