Differential signaling of insulin and IGF-1 receptors to glycogen synthesis in murine hepatocytes

Biochemistry. 1999 Jun 8;38(23):7517-23. doi: 10.1021/bi9830718.

Abstract

We have used SV40-transformed hepatocytes from insulin receptor-deficient mice (-/-) and normal mice (WT) to investigate the different abilities of insulin and IGF-1 receptors to stimulate glycogen synthesis. We report that insulin receptors are more potent than IGF-1 receptors in stimulating glycogen synthesis. Both receptors stimulate glycogen synthesis in a PI 3-kinase-dependent manner, but only the effect of insulin receptors is partially rapamycin-dependent. Insulin and IGF-1 receptors activate Akt to a similar extent, whereas GSK-3 inactivation in response to IGF-1 is considerably lower in both -/- and WT cells, compared to the effect of insulin in WT cells. The findings indicate that (i) the potency of insulin and IGF-1 receptors in stimulating glycogen synthesis correlates with their ability to inactivate GSK-3, (ii) the extent of GSK-3 inactivation does not correlate with the extent of Akt activation mediated by insulin or IGF-1 receptors, indicating that the effect of insulin on GSK-3 requires additional kinases, and (iii) the pathways required for insulin stimulation of glycogen synthesis in mouse hepatocytes are PI 3-kinase-dependent and rapamycin-sensitive.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Androstadienes / pharmacology
  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinases / antagonists & inhibitors
  • Cell Line
  • Enzyme Activation / genetics
  • Glycogen / biosynthesis*
  • Glycogen Synthase / metabolism
  • Glycogen Synthase Kinase 3
  • Liver / cytology
  • Liver / enzymology
  • Liver / metabolism*
  • Mice
  • Mice, Knockout
  • Phosphoinositide-3 Kinase Inhibitors
  • Phosphorylation
  • Protein Kinase Inhibitors
  • Protein Kinases*
  • Protein Serine-Threonine Kinases / metabolism
  • Proto-Oncogene Proteins c-akt
  • Proto-Oncogene Proteins*
  • Receptor, IGF Type 1 / physiology*
  • Receptor, Insulin / deficiency
  • Receptor, Insulin / genetics
  • Receptor, Insulin / physiology*
  • Ribosomal Protein S6 Kinases
  • Signal Transduction / genetics
  • Signal Transduction / physiology*
  • Sirolimus / pharmacology
  • Wortmannin

Substances

  • Androstadienes
  • Phosphoinositide-3 Kinase Inhibitors
  • Protein Kinase Inhibitors
  • Proto-Oncogene Proteins
  • Glycogen
  • Glycogen Synthase
  • Protein Kinases
  • Receptor, IGF Type 1
  • Receptor, Insulin
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • Ribosomal Protein S6 Kinases
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Glycogen Synthase Kinase 3
  • Sirolimus
  • Wortmannin