File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Effects of sorbitol dehydrogenase deficiency on nerve conduction in experimental diabetic mice
  • Basic View
  • Metadata View
  • XML View
TitleEffects of sorbitol dehydrogenase deficiency on nerve conduction in experimental diabetic mice
 
AuthorsNg, DTF
Lee, FK
Song, ZT
Calcutt, NA2
Lee, LW
Chung, SSM
Chung, SK1
 
Issue Date1998
 
PublisherAmerican Diabetes Association. The Journal's web site is located at http://diabetes.diabetesjournals.org/
 
CitationDiabetes, 1998, v. 47 n. 6, p. 961-966 [How to Cite?]
DOI: http://dx.doi.org/10.2337/diabetes.47.6.961
 
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.
 
ISSN0012-1797
2012 Impact Factor: 7.895
2012 SCImago Journal Rankings: 3.810
 
DOIhttp://dx.doi.org/10.2337/diabetes.47.6.961
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorNg, DTF
 
dc.contributor.authorLee, FK
 
dc.contributor.authorSong, ZT
 
dc.contributor.authorCalcutt, NA
 
dc.contributor.authorLee, LW
 
dc.contributor.authorChung, SSM
 
dc.contributor.authorChung, SK
 
dc.date.accessioned2008-06-12T06:41:31Z
 
dc.date.available2008-06-12T06:41:31Z
 
dc.date.issued1998
 
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.
 
dc.description.naturepublished_or_final_version
 
dc.format.extent418 bytes
 
dc.format.mimetypetext/html
 
dc.identifier.citationDiabetes, 1998, v. 47 n. 6, p. 961-966 [How to Cite?]
DOI: http://dx.doi.org/10.2337/diabetes.47.6.961
 
dc.identifier.doihttp://dx.doi.org/10.2337/diabetes.47.6.961
 
dc.identifier.epage966
 
dc.identifier.hkuros34271
 
dc.identifier.issn0012-1797
2012 Impact Factor: 7.895
2012 SCImago Journal Rankings: 3.810
 
dc.identifier.issue6
 
dc.identifier.openurl
 
dc.identifier.pmid9604875
 
dc.identifier.scopuseid_2-s2.0-2642616217
 
dc.identifier.spage961
 
dc.identifier.urihttp://hdl.handle.net/10722/49398
 
dc.identifier.volume47
 
dc.languageeng
 
dc.publisherAmerican Diabetes Association. The Journal's web site is located at http://diabetes.diabetesjournals.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofDiabetes
 
dc.relation.referencesReferences in Scopus
 
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/]
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshCataract - genetics - pathology - physiopathology
 
dc.subject.meshDiabetes Mellitus, Experimental - enzymology - physiopathology
 
dc.subject.meshL-Iditol 2-Dehydrogenase - biosynthesis - deficiency - genetics
 
dc.subject.meshNeural Conduction - genetics - physiology
 
dc.subject.meshPoint Mutation
 
dc.titleEffects of sorbitol dehydrogenase deficiency on nerve conduction in experimental diabetic mice
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Ng, DTF</contributor.author>
<contributor.author>Lee, FK</contributor.author>
<contributor.author>Song, ZT</contributor.author>
<contributor.author>Calcutt, NA</contributor.author>
<contributor.author>Lee, LW</contributor.author>
<contributor.author>Chung, SSM</contributor.author>
<contributor.author>Chung, SK</contributor.author>
<date.accessioned>2008-06-12T06:41:31Z</date.accessioned>
<date.available>2008-06-12T06:41:31Z</date.available>
<date.issued>1998</date.issued>
<identifier.citation>Diabetes, 1998, v. 47 n. 6, p. 961-966</identifier.citation>
<identifier.issn>0012-1797</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/49398</identifier.uri>
<description.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.</description.abstract>
<format.extent>418 bytes</format.extent>
<format.mimetype>text/html</format.mimetype>
<language>eng</language>
<publisher>American Diabetes Association. The Journal&apos;s web site is located at http://diabetes.diabetesjournals.org/</publisher>
<relation.ispartof>Diabetes</relation.ispartof>
<rights>This 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/]</rights>
<rights>Creative Commons: Attribution 3.0 Hong Kong License</rights>
<subject.mesh>Cataract - genetics - pathology - physiopathology</subject.mesh>
<subject.mesh>Diabetes Mellitus, Experimental - enzymology - physiopathology</subject.mesh>
<subject.mesh>L-Iditol 2-Dehydrogenase - biosynthesis - deficiency - genetics</subject.mesh>
<subject.mesh>Neural Conduction - genetics - physiology</subject.mesh>
<subject.mesh>Point Mutation</subject.mesh>
<title>Effects of sorbitol dehydrogenase deficiency on nerve conduction in experimental diabetic mice</title>
<type>Article</type>
<identifier.openurl>http://library.hku.hk:4550/resserv?sid=HKU:IR&amp;issn=0012-1797&amp;volume=47&amp;issue=6&amp;spage=961&amp;epage=966&amp;date=1998&amp;atitle=Effects+of+sorbitol+dehydrogenase+deficiency+on+nerve+conduction+in+experimental+diabetic+mice</identifier.openurl>
<description.nature>published_or_final_version</description.nature>
<identifier.doi>10.2337/diabetes.47.6.961</identifier.doi>
<identifier.pmid>9604875</identifier.pmid>
<identifier.scopus>eid_2-s2.0-2642616217</identifier.scopus>
<identifier.hkuros>34271</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-2642616217&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>47</identifier.volume>
<identifier.issue>6</identifier.issue>
<identifier.spage>961</identifier.spage>
<identifier.epage>966</identifier.epage>
<publisher.place>United States</publisher.place>
<bitstream.url>http://hub.hku.hk/bitstream/10722/49398/1/34271.htm</bitstream.url>
</item>
Author Affiliations
  1. The University of Hong Kong
  2. University of California, San Diego