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Article: Effects of sorbitol dehydrogenase deficiency on nerve conduction in experimental diabetic mice

TitleEffects of sorbitol dehydrogenase deficiency on nerve conduction in experimental diabetic mice
Authors
Issue Date1998
PublisherAmerican Diabetes Association. The Journal's web site is located at http://diabetes.diabetesjournals.org/
Citation
Diabetes, 1998, v. 47 n. 6, p. 961-966 How to Cite?
Abstract
In this report, we made use of sorbitol dehydrogenase (SDH)-deficient mutant mice (C57BL/LiA) to test whether there is a close correlation between the level of polyol accumulation and the degree of reduction in motor nerve conduction velocity (MNCV) associated with diabetes. The C57BL/LiA mouse has SDH deficiency due to a G-to-A mutation at the +1 position of intron 8, thus producing only aberrant SDH transcripts. These C57BL/LiA mice should have higher levels of polyol accumulation in the peripheral nerve because of the inability to further metabolize sorbitol to fructose. Here, we confirm by Western blot analysis and high-performance liquid chromatography that these mice lack SDH in the sciatic nerve and other various tissues, whereas normal mice possess SDH. These C57BL/LiA mice do not display any obvious phenotype that includes peripheral neuropathy in the normal laboratory environment and breed normally as described previously, although the tissues that normally contain SDH accumulate more sorbitol. This finding suggested that C57BL/LiA mouse strain is a valid model for studying the role in diabetic neuropathy of the polyol pathway, which consists of two enzymes-aldose reductase for converting glucose to sorbitol and SDH for converting sorbitol to fructose. Sorbitol levels in the sciatic nerve of diabetic C57BL/10N, nondiabetic, and diabetic C57BL/LiA mice were increased 4.3-, 16.6-, and 38.1-fold, respectively, above that of nondiabetic C57BL/10N. The fructose level in the sciatic nerve was increased 2.4-fold in diabetic C57BL/10N mice compared with that of nondiabetic and diabetic C57BL/LiA mice. Diabetic SDH-deficient mice showed an MNCV reduction similar in magnitude to that of diabetic C57BL/10N mice, despite greater nerve sorbitol accumulation and the lack of fructose in the former. The present data suggest that the levels of sorbitol and fructose in the sciatic nerve of mice do not correlate with the severity of MNCV deficit associated with diabetes.
Persistent Identifierhttp://hdl.handle.net/10722/49398
ISSN
2013 Impact Factor: 8.474
2013 SCImago Journal Rankings: 4.749
References

 

Author Affiliations
  1. The University of Hong Kong
  2. University of California, San Diego
DC FieldValueLanguage
dc.contributor.authorNg, DTFen_HK
dc.contributor.authorLee, FKen_HK
dc.contributor.authorSong, ZTen_HK
dc.contributor.authorCalcutt, NAen_HK
dc.contributor.authorLee, LWen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2008-06-12T06:41:31Z-
dc.date.available2008-06-12T06:41:31Z-
dc.date.issued1998en_HK
dc.identifier.citationDiabetes, 1998, v. 47 n. 6, p. 961-966en_HK
dc.identifier.issn0012-1797en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49398-
dc.description.abstractIn this report, we made use of sorbitol dehydrogenase (SDH)-deficient mutant mice (C57BL/LiA) to test whether there is a close correlation between the level of polyol accumulation and the degree of reduction in motor nerve conduction velocity (MNCV) associated with diabetes. The C57BL/LiA mouse has SDH deficiency due to a G-to-A mutation at the +1 position of intron 8, thus producing only aberrant SDH transcripts. These C57BL/LiA mice should have higher levels of polyol accumulation in the peripheral nerve because of the inability to further metabolize sorbitol to fructose. Here, we confirm by Western blot analysis and high-performance liquid chromatography that these mice lack SDH in the sciatic nerve and other various tissues, whereas normal mice possess SDH. These C57BL/LiA mice do not display any obvious phenotype that includes peripheral neuropathy in the normal laboratory environment and breed normally as described previously, although the tissues that normally contain SDH accumulate more sorbitol. This finding suggested that C57BL/LiA mouse strain is a valid model for studying the role in diabetic neuropathy of the polyol pathway, which consists of two enzymes-aldose reductase for converting glucose to sorbitol and SDH for converting sorbitol to fructose. Sorbitol levels in the sciatic nerve of diabetic C57BL/10N, nondiabetic, and diabetic C57BL/LiA mice were increased 4.3-, 16.6-, and 38.1-fold, respectively, above that of nondiabetic C57BL/10N. The fructose level in the sciatic nerve was increased 2.4-fold in diabetic C57BL/10N mice compared with that of nondiabetic and diabetic C57BL/LiA mice. Diabetic SDH-deficient mice showed an MNCV reduction similar in magnitude to that of diabetic C57BL/10N mice, despite greater nerve sorbitol accumulation and the lack of fructose in the former. The present data suggest that the levels of sorbitol and fructose in the sciatic nerve of mice do not correlate with the severity of MNCV deficit associated with diabetes.en_HK
dc.format.extent418 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherAmerican Diabetes Association. The Journal's web site is located at http://diabetes.diabetesjournals.org/en_HK
dc.relation.ispartofDiabetesen_HK
dc.rightsThis is an author-created, uncopyedited electronic version of an article accepted for publication in Diabetes [http://diabetes.diabetesjournals.org/] The American Diabetes Association (ADA), publisher of Diabetes, is not responsible for any errors or omissions in this version of the manuscript or any version derived from it by third parties. The definitive publisher-authenticated version is available online at [http://diabetes.diabetesjournals.org/]en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshCataract - genetics - pathology - physiopathologyen_HK
dc.subject.meshDiabetes Mellitus, Experimental - enzymology - physiopathologyen_HK
dc.subject.meshL-Iditol 2-Dehydrogenase - biosynthesis - deficiency - geneticsen_HK
dc.subject.meshNeural Conduction - genetics - physiologyen_HK
dc.subject.meshPoint Mutationen_HK
dc.titleEffects of sorbitol dehydrogenase deficiency on nerve conduction in experimental diabetic miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0012-1797&volume=47&issue=6&spage=961&epage=966&date=1998&atitle=Effects+of+sorbitol+dehydrogenase+deficiency+on+nerve+conduction+in+experimental+diabetic+miceen_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.2337/diabetes.47.6.961en_HK
dc.identifier.pmid9604875en_HK
dc.identifier.scopuseid_2-s2.0-2642616217en_HK
dc.identifier.hkuros34271-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-2642616217&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume47en_HK
dc.identifier.issue6en_HK
dc.identifier.spage961en_HK
dc.identifier.epage966en_HK
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridNg, DTF=20535251900en_HK
dc.identifier.scopusauthoridLee, FK=7403111561en_HK
dc.identifier.scopusauthoridSong, ZT=55455634500en_HK
dc.identifier.scopusauthoridCalcutt, NA=7007127505en_HK
dc.identifier.scopusauthoridLee, LW=7404388974en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK

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