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Papers In Press, published online ahead of print April 27, 2006
Research Service (151), J.A. Haley Veterans' Hospital, Tampa, FL 33612
Corresponding Author: rfarese{at}com1.med.usf.edu
The role of atypical protein kinase C (aPKC) in insulin-stimulated glucose transport in myocytes and adipocytes is controversial. Whereas studies involving the use of adenoviral-mediated expression of kinase-inactive aPKC in L6 myocytes and 3T3/L1 and human adipocytes, and data from knockout of aPKC in adipocytes derived from mouse embryonic stem cells and subsequently derived adipocytes, suggest that aPKCs are required for insulin-stimulated glucose transport, recent findings in studies of aPKC knock down by small interfering RNA (RNAi) in 3T3/L1 adipocytes are conflicting. Moreover, there no reports of aPKC knockdown in myocytes, wherein insulin effects on glucose transport are particularly relevant for understanding whole body glucose disposal. Presently, we exploited the fact that L6 myotubes and 3T3/L1 adipocytes have substantially different (30% non-homology) major aPKCs, viz., PKC-
J. Biol. Chem, 10.1074/jbc.M510803200
Submitted on October 4, 2005
Accepted on April 27, 2006
Repletion of atypical protein kinase C following RNAi-mediated depletion restores insulin-stimulated glucose transport
in L6 myotubes and PKC-
in 3T3/L1 adipocytes, that nevertheless can function interchangeably for glucose transport. Accordingly, in L6 myotubes, RNAi targeting PKC-, but not PKC-, markedly depleted aPKC and concomitantly inhibited insulin-stimulated glucose transport; more importantly, these depleting/inhibitory effects were rescued by adenoviral-mediated expression of PKC-. Conversely, in 3T3/L1 adipocytes, RNAi constructs targeting PKC-{lambda, but not PKC-, markedly depleted aPKC and concomitantly inhibited insulin-stimulated glucose transport; here again, these depleting/inhibitory effects were rescued by adenoviral-mediated expression of PKC- These findings in knockdown and, more convincingly, rescue studies, strongly support the hypothesis that aPKCs are required for insulin-stimulated glucose transport in myocytes and adipocytes.
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