Activation of PI 3-kinase by the hexosamine biosynthesis pathway.

It has been shown that hyperglycaemia-induced defects in glucose transport and insulin action are mediated by increased flux of excess glucose through the hexosamine biosynthesis pathway (HBP). We have previously demonstrated that in rat adipocytes, increased flux through the HBP activates protein kinase C (PKC). The aim of the present study was to explore the mechanism for HBP-mediated activation of PKC.