Linked Life Data

20728534

Source:http://linkedlifedata.com/resource/pubmed/id/20728534

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2010-10-11
pubmed:abstractText
Carbonyl reductase 1 (CBR1) plays an important role in the detoxification of reactive lipid aldehydes. Oxidative stress has been implicated in the pathogenesis of pancreatic ?-cell failure. However, the functional role of CBR1 in pancreatic ?-cell failure has not been studied yet. Therefore, we investigated the role of CBR1 in pancreatic ?-cell failure under glucotoxic and glucolipotoxic conditions. Under both conditions, knockdown of CBR1 by specific siRNA increased ?-cell apoptosis, expression of lipogenic enzymes (such as ACC, FAS, and ABCA1), intracellular lipid accumulation, oxidative stress, ER stress, and nuclear SREBP1c, but decreased glucose-stimulated insulin secretion. In contrast, overexpression of CBR1 showed the opposite effects. The antioxidants N-acetyl-l-cysteine and Tiron, as well as the FAS inhibitor cerulenin, reversed the effects of CBR1 knockdown. Interestingly, the expression level and enzyme activity of CBR1 were significantly decreased in pancreatic islets of db/db mice, compared with those of wild-type mice. In conclusion, CBR1 protects pancreatic ?-cells against oxidative stress and promotes their survival in glucotoxicity and glucolipotoxicity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1873-4596
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
30
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1522-33
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Carbonyl reductase 1 protects pancreatic ?-cells against oxidative stress-induced apoptosis in glucotoxicity and glucolipotoxicity.
pubmed:affiliation
Medical Science and Engineering Research Center for Bioreaction to Reactive Oxygen Species and Biomedical Science Institute (BK-21), Department of Biochemistry and Molecular Biology, School of Medicine, Kyung Hee University, Seoul 130-701, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't