Regulation of PTP-1 and insulin receptor kinase by fractions from cinnamon: implications for cinnamon regulation of insulin signalling

Horm Res. 1998 Sep;50(3):177-82. doi: 10.1159/000023270.

Abstract

Bioactive compound(s) extracted from cinnamon potentiate insulin activity, as measured by glucose oxidation in the rat epididymal fat cell assay. Wortmannin, a potent PI 3'-kinase inhibitor, decreases the biological response to insulin and bioactive compound(s) from cinnamon similarly, indicating that cinnamon is affecting an element(s) upstream of PI 3'-kinase. Enzyme studies done in vitro show that the bioactive compound(s) can stimulate autophosphorylation of a truncated form of the insulin receptor and can inhibit PTP-1, a rat homolog of a tyrosine phosphatase (PTP-1B) that inactivates the insulin receptor. No inhibition was found with alkaline phosphate or calcineurin suggesting that the active material is not a general phosphatase inhibitor. It is suggested, then, that a cinnamon compound(s), like insulin, affects protein phosphorylation-dephosphorylation reactions in the intact adipocyte. Bioactive cinnamon compounds may find further use in studies of insulin resistance in adult-onset diabetes.

MeSH terms

  • Androstadienes / pharmacology
  • Animals
  • Cinnamomum zeylanicum / analysis*
  • Drug Synergism
  • Enzyme Inhibitors / pharmacology
  • Insulin / physiology*
  • Phosphoric Monoester Hydrolases / pharmacology
  • Phosphorylation / drug effects
  • Plant Extracts / pharmacology*
  • Protein Tyrosine Phosphatases / antagonists & inhibitors
  • Protein Tyrosine Phosphatases / metabolism*
  • Rats
  • Receptor, Insulin / drug effects
  • Receptor, Insulin / metabolism*
  • Signal Transduction / physiology*
  • Wortmannin

Substances

  • Androstadienes
  • Enzyme Inhibitors
  • Insulin
  • Plant Extracts
  • Receptor, Insulin
  • Phosphoric Monoester Hydrolases
  • Protein Tyrosine Phosphatases
  • Wortmannin