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Article: Demonstration that polyol accumulation is responsible for diabetic cataract by the use of transgenic mice expressing the aldose reductase gene in the lens

TitleDemonstration that polyol accumulation is responsible for diabetic cataract by the use of transgenic mice expressing the aldose reductase gene in the lens
Authors
Issue Date1995
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings Of The National Academy Of Sciences Of The United States Of America, 1995, v. 92 n. 7, p. 2780-2784 How to Cite?
AbstractAldose reductase (AR) has been implicated in the etiology of diabetic cataract, as well as in other complications. However, the role of AR in these complications remains controversial because the strongest supporting evidence is drawn from the use of AR inhibitors for which specificity in vivo cannot be ascertained. To settle this issue we developed transgenic mice that overexpress AR in their lens epithelial cells and found that they become susceptible to the development of diabetic and galactose cataracts. When the sorbitol dehydrogenase-deficient mutation is also present in these transgenic mice, greater accumulation of sorbitol and further acceleration of diabetic cataract develop. These genetic studies demonstrated convincingly that accumulation of polyols from the reduction of hexose by AR leads to the formation of sugar cataracts.
Persistent Identifierhttp://hdl.handle.net/10722/146621
ISSN
2015 Impact Factor: 9.423
2015 SCImago Journal Rankings: 6.883
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLee, AYWen_HK
dc.contributor.authorChung, SKen_HK
dc.contributor.authorChung, SSMen_HK
dc.date.accessioned2012-05-08T03:21:19Z-
dc.date.available2012-05-08T03:21:19Z-
dc.date.issued1995en_HK
dc.identifier.citationProceedings Of The National Academy Of Sciences Of The United States Of America, 1995, v. 92 n. 7, p. 2780-2784en_HK
dc.identifier.issn0027-8424en_HK
dc.identifier.urihttp://hdl.handle.net/10722/146621-
dc.description.abstractAldose reductase (AR) has been implicated in the etiology of diabetic cataract, as well as in other complications. However, the role of AR in these complications remains controversial because the strongest supporting evidence is drawn from the use of AR inhibitors for which specificity in vivo cannot be ascertained. To settle this issue we developed transgenic mice that overexpress AR in their lens epithelial cells and found that they become susceptible to the development of diabetic and galactose cataracts. When the sorbitol dehydrogenase-deficient mutation is also present in these transgenic mice, greater accumulation of sorbitol and further acceleration of diabetic cataract develop. These genetic studies demonstrated convincingly that accumulation of polyols from the reduction of hexose by AR leads to the formation of sugar cataracts.en_HK
dc.languageengen_US
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.orgen_HK
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of Americaen_HK
dc.subject.meshAldehyde Reductase - Biosynthesis - Geneticsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlotting, Southernen_US
dc.subject.meshCataract - Metabolismen_US
dc.subject.meshCrosses, Geneticen_US
dc.subject.meshDna, Complementary - Analysisen_US
dc.subject.meshDiabetes Mellitus, Experimental - Metabolismen_US
dc.subject.meshDiabetic Retinopathy - Metabolismen_US
dc.subject.meshFemaleen_US
dc.subject.meshGalactitol - Metabolismen_US
dc.subject.meshGalactose - Toxicityen_US
dc.subject.meshGalactosemias - Metabolismen_US
dc.subject.meshGenotypeen_US
dc.subject.meshHumansen_US
dc.subject.meshLens, Crystalline - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred Balb Cen_US
dc.subject.meshMice, Transgenicen_US
dc.subject.meshPolymerase Chain Reactionen_US
dc.titleDemonstration that polyol accumulation is responsible for diabetic cataract by the use of transgenic mice expressing the aldose reductase gene in the lensen_HK
dc.typeArticleen_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1073/pnas.92.7.2780en_HK
dc.identifier.pmid7708723-
dc.identifier.pmcidPMC42302-
dc.identifier.scopuseid_2-s2.0-0028946316en_HK
dc.identifier.hkuros1851-
dc.identifier.volume92en_HK
dc.identifier.issue7en_HK
dc.identifier.spage2780en_HK
dc.identifier.epage2784en_HK
dc.identifier.isiWOS:A1995QP88900076-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLee, AYW=55477259800en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK

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