Yu, HaiyanFujii, Nobuharu LToyoda, TaroAn, DingFarese, Robert VLeitges, MichaelHirshman, Michael FMul, Joram D.Goodyear, Laurie2016-01-042015Yu, Haiyan, Nobuharu L Fujii, Taro Toyoda, Ding An, Robert V Farese, Michael Leitges, Michael F Hirshman, Joram D Mul, and Laurie J Goodyear. 2015. “Contraction stimulates muscle glucose uptake independent of atypical PKC.” Physiological Reports 3 (11): e12565. doi:10.14814/phy2.12565. http://dx.doi.org/10.14814/phy2.12565.2051-817Xhttp://nrs.harvard.edu/urn-3:HUL.InstRepos:23993466Exercise increases skeletal muscle glucose uptake, but the underlying mechanisms are only partially understood. The atypical protein kinase C (PKC) isoforms λ and ζ (PKC-λ/ζ) have been shown to be necessary for insulin-, AICAR-, and metformin-stimulated glucose uptake in skeletal muscle, but not for treadmill exercise-stimulated muscle glucose uptake. To investigate if PKC-λ/ζ activity is required for contraction-stimulated muscle glucose uptake, we used mice with tibialis anterior muscle-specific overexpression of an empty vector (WT), wild-type PKC-ζ (PKC-ζWT), or an enzymatically inactive T410A-PKC-ζ mutant (PKC-ζT410A). We also studied skeletal muscle-specific PKC-λ knockout (MλKO) mice. Basal glucose uptake was similar between WT, PKC-ζWT, and PKC-ζT410A tibialis anterior muscles. In contrast, in situ contraction-stimulated glucose uptake was increased in PKC-ζT410A tibialis anterior muscles compared to WT or PKC-ζWT tibialis anterior muscles. Furthermore, in vitro contraction-stimulated glucose uptake was greater in soleus muscles of MλKO mice than WT controls. Thus, loss of PKC-λ/ζ activity increases contraction-stimulated muscle glucose uptake. These data clearly demonstrate that PKC-λ ζ activity is not necessary for contraction-stimulated glucose uptake.en-USGlucose uptakeatypical PKCMuscle contractionContraction-stimulated glucose uptakeJournal Article2016-01-0410.14814/phy2.12565