REGULATION OF PTP-1 AND INSULIN-RECEPTOR KINASE BY FRACTIONS FROM CINNAMON - IMPLICATIONS FOR CINNAMON REGULATION OF INSULIN SIGNALING

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