Linked Life Data

12015381

Source:http://linkedlifedata.com/resource/pubmed/id/12015381

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2002-5-16
pubmed:abstractText
The hypothesis that the accumulation of electron transport system (ETS) abnormalities and sarcopenia are linked was investigated. Vastus lateralis, soleus, and adductor longus muscles were studied in 5-, 18-, and 36-mo-old male Fischer 344 x Brown Norway F(1) hybrid rats. A significant decrease in soleus and vastus lateralis muscle mass was observed with age. Adductor longus was resistant to muscle mass loss. Multiple serial sections were analyzed for the activities of cytochrome-c oxidase (COX) and succinate dehydrogenase (SDH). The number of fibers exhibiting a COX(-)/SDH(++) phenotype increased with age in both vastus lateralis and soleus muscles. No ETS-abnormal fibers were identified in adductor longus at any age. Cross-sectional area of ETS-abnormal fibers decreased in the abnormal region (region displaying COX(-)/SDH(++) phenotype), whereas control fibers did not. The vastus lateralis muscle, which undergoes a high degree of sarcopenia, exhibited more ETS abnormalities and associated fiber loss than the soleus and adductor longus muscles, which are more resistant to sarcopenia, suggesting a direct association between ETS abnormalities and fiber loss.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
8750-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
92
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2617-24
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Mitochondrial abnormalities are more frequent in muscles undergoing sarcopenia.
pubmed:affiliation
Department of Animal Health and Biomedical Sciences, University of Wisconsin, Madison, Wisconsin 53706, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.