When blood glucose levels in an organism rise, beta cells in the pancreas release insulin. The insulin then travels through the blood stream to specific muscle and fat cells that have Insulin Receptors (IRs) embedded in their cell membranes.

Insulin binds to an insulin receptor allowing the IR to autophosphorylate. This is accomlished through the addition of multiple phosphate groups.

In addition to autophosphorylation, the insulin receptor is also capable of transferring a phosphorylation signal to another protein called Insulin Receptor Substrate 1 (IRS-1).

Insulin receptor substrate 1 then goes on to phosphorylate a kinase protein called PI3K.

PI3K then passes on the signal by phosphorylating PIP2 molecules and converting them into PIP3 molecules. The PIP2 and 3 molecules are embedded in the cell's plasma membrane.

As the quantity of PIP3 molecules rises, they attract a protein called AKT2.

AKT2 is then phosphorylated by two more proteins, mTOR-RICTOR and PDK1.

The fully activated AKT2 then leaves the cell membrane for the cytosol where it can continue multiple insulin-related signal pathways.