Effects of adenoviral gene transfer of wild-type, constitutively active, and kinase-defective protein kinase C-lambda on insulin-stimulated glucose transport in L6 myotubes

Endocrinology. 2000 Nov;141(11):4120-7. doi: 10.1210/endo.141.11.7766.


We used adenoviral gene transfer methods to evaluate the role of atypical protein kinase Cs (PKCs) during insulin stimulation of glucose transport in L6 myotubes. Expression of wild-type PKC-lambda potentiated maximal and half-maximal effects of insulin on 2-deoxyglucose uptake, but did not alter basal uptake. Expression of constitutively active PKC-lambda enhanced basal 2-deoxyglucose uptake to virtually the same extent as that observed during insulin treatment. In contrast, expression of kinase-defective PKC-lambda completely blocked insulin-stimulated, but not basal, 2-deoxyglucose uptake. Similar to alterations in glucose transport, constitutively active PKC-lambda mimicked, and kinase-defective PKC-lambda completely inhibited, insulin effects on GLUT4 glucose transporter translocation to the plasma membrane. Expression of kinase-defective PKC-lambda, in addition to inhibition of atypical PKC enzyme activity, was attended by paradoxical increases in GLUT4 and GLUT1 glucose transporter levels and insulin-stimulated protein kinase B enzyme activity. Our findings suggest that in L6 myotubes, 1) atypical PKCs are required and sufficient for insulin-stimulated GLUT4 translocation and glucose transport; and 2) activation of protein kinase B in the absence of activation of atypical PKCs is insufficient for insulin-induced activation of glucose transport.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenoviridae / genetics*
  • Animals
  • Biological Transport / drug effects
  • Cell Line
  • Cell Membrane / metabolism
  • Gene Expression
  • Gene Transfer, Horizontal*
  • Glucose / metabolism*
  • Glucose Transporter Type 1
  • Glucose Transporter Type 4
  • Insulin / pharmacology*
  • Isoenzymes / genetics
  • Isoenzymes / metabolism
  • Monosaccharide Transport Proteins / metabolism
  • Muscle Proteins*
  • Muscle, Skeletal / metabolism*
  • Mutation
  • Protein Kinase C / genetics*
  • Protein Kinase C / metabolism
  • Protein-Serine-Threonine Kinases*
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-akt
  • Rats


  • Glucose Transporter Type 1
  • Glucose Transporter Type 4
  • Insulin
  • Isoenzymes
  • Monosaccharide Transport Proteins
  • Muscle Proteins
  • Proto-Oncogene Proteins
  • Slc2a1 protein, rat
  • Slc2a4 protein, rat
  • Protein-Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • Protein Kinase C
  • Glucose