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Conference Paper: Myo-inositol is important for neuromuscular functions

TitleMyo-inositol is important for neuromuscular functions
Authors
Keywordsenergy
hormones
ions
lipids
neuromuscular functions
others
signal transduction
transporters
Issue Date2004
PublisherBlackwell Publishing Ltd.
Citation
The 6th Biennial Meeting of the Asian-Pacific Society for Neurochemistry, Hong Kong, 4-7 February 2004. In Journal of Neurochemistry, 2004, v. 88 n. S1, p. 85 Abstract no. P33-20 How to Cite?
AbstractSodium/myo-inositol co-transporter (SMIT) is a membrane protein responsiblefor importing myo-inositol (MI) into the cell. MI is a precursor ofphosphatidylinositol, and also serves as an osmolyte to maintain propercellular osmolarity. To understand the function of SMIT, we generated SMITknockout mice. Homozygous SMIT knockout mice died soon after birth butmaternal MI feeding prevented the lethality, suggesting that there may be otherless efficient transporters to facilitate the cellular uptake of MI. Adult SMITknockout mice that did not receive MI supplement after weaning, had 1/10 thesciatic nerve MI level compared with the wildtype and showed a dramaticreduction in their motor nerve conduction velocity (MNCV). SMIT knockoutmice that received continuous MI supplement showed a small but significantincrease in their sciatic nerve MI content and improved MNCV. Skeletal muscleMI level was also decreased in SMIT knockout mice and continuous MI feedingbrought MI content back to normal. Gastrocnemius mass was reduced in SMITknockout mice and was increased by continuous MI feeding. Functionally,homozygous SMIT knockout mice not receiving MI supplement after weaningshowed a reduction in the length of time that they could hang onto the wire,indicating neuromuscular problem. Depletion of nerve MI may impairphosphatidylinositols synthesis and turnover, and eventually impair proteinkinase C (PKC) and Na+/K+ATPase activity leading to neuropathy. There was asignificant decrease in sciatic nerve PKC activity in SMIT knockout micesuggesting MI depletion in sciatic nerve impaired PKC signaling cascadecausing peripheral neuropathy. The present data suggest that MI is important inmaintaining normal neuromuscular function.
Persistent Identifierhttp://hdl.handle.net/10722/88038
ISSN
2015 Impact Factor: 3.842
2015 SCImago Journal Rankings: 2.021

 

DC FieldValueLanguage
dc.contributor.authorChau, JFLen_HK
dc.contributor.authorLee, MKen_HK
dc.contributor.authorChung, SKen_HK
dc.contributor.authorChung, SSMen_HK
dc.date.accessioned2010-09-06T09:37:50Z-
dc.date.available2010-09-06T09:37:50Z-
dc.date.issued2004en_HK
dc.identifier.citationThe 6th Biennial Meeting of the Asian-Pacific Society for Neurochemistry, Hong Kong, 4-7 February 2004. In Journal of Neurochemistry, 2004, v. 88 n. S1, p. 85 Abstract no. P33-20en_HK
dc.identifier.issn0022-3042en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88038-
dc.description.abstractSodium/myo-inositol co-transporter (SMIT) is a membrane protein responsiblefor importing myo-inositol (MI) into the cell. MI is a precursor ofphosphatidylinositol, and also serves as an osmolyte to maintain propercellular osmolarity. To understand the function of SMIT, we generated SMITknockout mice. Homozygous SMIT knockout mice died soon after birth butmaternal MI feeding prevented the lethality, suggesting that there may be otherless efficient transporters to facilitate the cellular uptake of MI. Adult SMITknockout mice that did not receive MI supplement after weaning, had 1/10 thesciatic nerve MI level compared with the wildtype and showed a dramaticreduction in their motor nerve conduction velocity (MNCV). SMIT knockoutmice that received continuous MI supplement showed a small but significantincrease in their sciatic nerve MI content and improved MNCV. Skeletal muscleMI level was also decreased in SMIT knockout mice and continuous MI feedingbrought MI content back to normal. Gastrocnemius mass was reduced in SMITknockout mice and was increased by continuous MI feeding. Functionally,homozygous SMIT knockout mice not receiving MI supplement after weaningshowed a reduction in the length of time that they could hang onto the wire,indicating neuromuscular problem. Depletion of nerve MI may impairphosphatidylinositols synthesis and turnover, and eventually impair proteinkinase C (PKC) and Na+/K+ATPase activity leading to neuropathy. There was asignificant decrease in sciatic nerve PKC activity in SMIT knockout micesuggesting MI depletion in sciatic nerve impaired PKC signaling cascadecausing peripheral neuropathy. The present data suggest that MI is important inmaintaining normal neuromuscular function.-
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd.en_HK
dc.relation.ispartofJournal of Neurochemistryen_HK
dc.rightsJournal of Neurochemistry. Copyright © Blackwell Publishing Ltd.en_HK
dc.subjectenergy-
dc.subjecthormones-
dc.subjections-
dc.subjectlipids-
dc.subjectneuromuscular functions-
dc.subjectothers-
dc.subjectsignal transduction-
dc.subjecttransporters-
dc.titleMyo-inositol is important for neuromuscular functionsen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3042&volume=88 &issue=Suppl 1&spage=85&epage=&date=2004&atitle=Myo-inositol+is+important+for+neuromuscular+functionsen_HK
dc.identifier.emailChau, JFL: flchau@graduate.hku.hken_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_subscribed_fulltext-
dc.identifier.doi10.1046/j.1474-1644.2003.2314p33_01.x-
dc.identifier.hkuros91223en_HK

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