pubmed-article:6197336 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:6197336 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:6197336 | lifeskim:mentions | umls-concept:C0027788 | lld:lifeskim |
pubmed-article:6197336 | lifeskim:mentions | umls-concept:C0001563 | lld:lifeskim |
pubmed-article:6197336 | lifeskim:mentions | umls-concept:C0021547 | lld:lifeskim |
pubmed-article:6197336 | lifeskim:mentions | umls-concept:C0004462 | lld:lifeskim |
pubmed-article:6197336 | lifeskim:mentions | umls-concept:C0439830 | lld:lifeskim |
pubmed-article:6197336 | lifeskim:mentions | umls-concept:C1708528 | lld:lifeskim |
pubmed-article:6197336 | lifeskim:mentions | umls-concept:C0243067 | lld:lifeskim |
pubmed-article:6197336 | lifeskim:mentions | umls-concept:C2348243 | lld:lifeskim |
pubmed-article:6197336 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:6197336 | pubmed:dateCreated | 1984-2-24 | lld:pubmed |
pubmed-article:6197336 | pubmed:abstractText | The effects of orally-administered myo-inositol have been compared with those of an aldose reductase inhibitor on acute neurological defects in experimentally diabetic rats. Three groups of streptozotocin-treated diabetic rats (50 mg/kg, IP) together with three groups of age-matched controls (saline, IP) were compared. One pair of groups (control and diabetic) were untreated for 3 weeks, another pair of groups received daily oral myo-inositol (667 mg/kg) and the third pair received an aldose reductase inhibitor (ICI 105 552; 50 mg . kg-1, day-1, orally). The untreated diabetic group showed statistically significant deficits in accumulation, proximal to 24 h sciatic nerve constrictions, of choline acetyltransferase activity by comparison with untreated controls (2.8 +/- 0.4 versus 5.1 +/- 0.4 nmol acetylcholine . h-1 . nerve-1; p less than 0.001). The untreated diabetic rats also showed a fall in motor nerve conduction velocity of 6.2 +/- 0.7 m/s which was statistically significant (p less than 0.001). Treatment of the diabetic group with myo-inositol prevented the development of both defects of axonal transport and conduction velocity; both measurements were similar to those of the myo-inositol treated control rats. Likewise the diabetic rats which received aldose reductase inhibitor showed prevention of both defects. Nerves from untreated diabetic rats showed marked sorbitol accumulation and a statistically significant reduction in myo-inositol content by comparison with the untreated controls (sorbitol, 1.56 +/- 0.22 versus 0.8 +/- 0.01 and myo-inositol, 1.47 +/- 0.10 versus 2.3 +/- 0.10 nmol/mg; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
pubmed-article:6197336 | pubmed:language | eng | lld:pubmed |
pubmed-article:6197336 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:6197336 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:6197336 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:6197336 | pubmed:month | Nov | lld:pubmed |
pubmed-article:6197336 | pubmed:issn | 0012-186X | lld:pubmed |
pubmed-article:6197336 | pubmed:author | pubmed-author:TomlinsonD... | lld:pubmed |
pubmed-article:6197336 | pubmed:author | pubmed-author:MayerJ HJH | lld:pubmed |
pubmed-article:6197336 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:6197336 | pubmed:volume | 25 | lld:pubmed |
pubmed-article:6197336 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:6197336 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:6197336 | pubmed:pagination | 433-8 | lld:pubmed |
pubmed-article:6197336 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:6197336 | pubmed:year | 1983 | lld:pubmed |
pubmed-article:6197336 | pubmed:articleTitle | Prevention of defects of axonal transport and nerve conduction velocity by oral administration of myo-inositol or an aldose reductase inhibitor in streptozotocin-diabetic rats. | lld:pubmed |
pubmed-article:6197336 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:6197336 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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