& u for P110 inhibited insulin-stimulated glucose uptake in CHO cells, providing additional support for the role of PI-3 kinase on Glut-4 translocation (36). However, despite excellent studies suggesting potential cellular mechanisms, the specific downstream pathway by which PI-3 kinase activation results in Glut-4 translocation remains unknown. A candidate molecule that has received recent interest is the serine/threonine kinase Akt, also known as protein kinase B, or Rac (50,51). PI-3 kinase appears to be an upstream regulator of Akt, as demonstrated by studies showing that wortmannin, dominant-negative PI-3 kinase mutants, and growth factor point mutations prevent the activation of Akt (50-53), and constitutively active mutants of PI-3 kinase are sufficient to stimulate Akt in cells (54,55).

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