Hyperosmotic Stress Inhibits Insulin Receptor Substrate-1 Function by Distinct Mechanisms in 3T3-L1 Adipocytes

This publication has 58 references indexed in Scilit:

• Rapamycin partially prevents insulin resistance induced by chronic insulin treatment
  Biochemical and Biophysical Research Communications, 2002
• Regulation of cell size in growth, development and human disease: PI3K, PKB and S6K
  BioEssays, 2002
• Insulin signalling and the regulation of glucose and lipid metabolism
  Nature, 2001
• FRAP-Dependent Serine Phosphorylation of IRS-1 Inhibits IRS-1 Tyrosine Phosphorylation
  Biochemical and Biophysical Research Communications, 2001
• The osmotic shock-induced glucose transport pathway in 3T3-L1 adipocytes is mediated by Gab-1 and requires Gab-1 associated phosphatidylinositol 3-kinase activity for full activation
  Journal of Biological Chemistry, 2000
• The Small Guanosine Triphosphate-Binding Protein Rab4 Is Involved in Insulin-Induced GLUT4 Translocation and Actin Filament Rearrangement in 3T3-L1 Cells
  Endocrinology, 1997
• Phosphoinositide 3-Kinase Is Required for Insulin-Induced but Not for Growth Hormone- or Hyperosmolarity-Induced Glucose Uptake in 3T3-L1 Adipocytes
  Molecular Endocrinology, 1997
• Potential Role of Protein Kinase B in Glucose Transporter 4 Translocation in Adipocytes
  Endocrinology, 1997
• Phosphatidylinositol 3-kinase is necessary and sufficient for insulin- stimulated stress fiber breakdown
  Endocrinology, 1996
• Detrimental effect of hyperosmolality on insulin-stimulated glucose metabolism in adipose and muscle tissue in vitro
  Biochemical Medicine and Metabolic Biology, 1988