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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2009-3-4
pubmed:abstractText
IL-6 is a biologically active substance which appears to be involved in regulating skeletal muscle lipid oxidation. Ablation of IL-6 (IL-6(-/-)) may therefore be expected to increase intracellular lipid accumulation, possibly via a concurrent increase in fatty acid transporters such as FAT/CD36 and FABPpm. This however may only occur in oxidative muscles which utilize fatty acids at a greater rate than glycolytic muscles. In the present study we examined the fatty acid transporter protein expression as well as the lipid content and profiles of free fatty acids (FFA), diacylglycerols (DGs) and triacylglycerols (TGs) in skeletal muscles of IL-6 deficient mice at 4 and 12 months of age. FAT/CD36 and FABPpm protein content was increased in red muscles in IL-6(-/-) mice compared to WT mice at 4 (RG) and 12 months (soleus and RG). Along with this, FFA, DG and TG concentrations were also increased in these red IL-6(-/-) muscles. In addition, the IL-6(-/-) genotype increased the saturated FA acid composition of the intramuscular TG fraction. In contrast, in white gastrocnemius muscle the IL-6(-/-) genotype has no effect on the expression of fatty acid transporters as well as the lipid content and composition at either 4 mo or 12 months of age. IL-6 ablation increases fatty acid transporter expression and intramuscular lipid accumulation, particularly the saturated fatty acids. These effects however were confined to oxidative muscles, as glycolytic muscles were not affected.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1899-1505
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
59 Suppl 7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
105-17
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
IL-6 deficiency increases fatty acid transporters and intramuscular lipid content in red but not white skeletal muscle.
pubmed:affiliation
Department of Physiology, Medical University of Bialystok, Bialystok, Poland. adrian@amb.edu.pl
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't