Linked Life Data

3024950

Source:http://linkedlifedata.com/resource/pubmed/id/3024950

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1987-2-10
pubmed:abstractText
Slowing of nerve conduction, a hallmark of both experimental and human diabetic neuropathy, is improved or corrected by aldose reductase inhibitors such as sorbinil. Animal experiments suggest that a myo-inositol-related defect in nerve sodium-potassium adenosine triphosphatase (ATPase) is responsible for the acute reversible slowing of nerve conduction in diabetes mellitus. This myo-inositol-related defect is at present viewed as a cyclic metabolic defect. Aldose reductase inhibitors have been shown to restore to normal both the myo-inositol content and the sodium-potassium ATPase activity of nerve. This suggests that the acute effects of aldose-reductase inhibitors on nerve conduction in both diabetic animals and human patients may be modified by the correction of an underlying myo-inositol-related defect of nerve sodium-potassium ATPase. Furthermore, this myo-inositol-related defect may contribute to other biochemical, functional and structural abnormalities of diabetic peripheral neuropathy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0012-6667
pubmed:author
pubmed:issnType
Print
pubmed:volume
32 Suppl 2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6-14
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1986
pubmed:articleTitle
Sorbitol, myo-inositol and sodium-potassium ATPase in diabetic peripheral nerve.
pubmed:publicationType
Journal Article, Review