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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2010-10-18
pubmed:abstractText
The underlying mechanism of palmitate-induced insulin resistance in skeletal muscle cells is obscure. In this study, we showed that palmitate inhibited the insulin signaling in C2C12 myotubes, accompanied with the enhanced phosphorylation of protein kinase C-theta (PKC?). The inhibitory effects of palmitate on the insulin signaling were diminished in PKC?- and mTOR (mammalian target of rapamycin)-deficient C2C12 myotubes, and C2C12 myotubes pre-treated with rapamycin. In addition, the phosphorylation of mTOR and p70 ribosomal S6 kinase (S6K) enhanced by palmitate was attenuated in PKC?-deficient C2C12 myotubes and in C2C12 myotubes treated with PKC? pseudosubstrate. Taken together, our results suggested that palmitate-induced insulin resistance in C2C12 myotubes is mediated by PKC?/mTOR/S6K pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1439-3646
pubmed:author
pubmed:copyrightInfo
© Georg Thieme Verlag KG Stuttgart · New York.
pubmed:issnType
Electronic
pubmed:volume
118
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
657-61
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Palmitate induced insulin resistance by PKCtheta-dependent activation of mTOR/S6K pathway in C2C12 myotubes.
pubmed:affiliation
Department of Pathophysiology, Yunyang Medical College, Shiyan, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't