• stimulates beta cells of pancreas to produce insulin.
• liver takes up glucose to prod glycogen
• blood glucose goes back to normal

•  epinephrine is released
• muscle receptors stimulate local breakdown of glycogen for energy
• liver breaks down glycogen using G-6-Pase

• alpha cells produce glucagon
• liver breaks down glycogen with G-6-Pase

• epinephrine binds beta-adrenergic receptor in muscle or alpha/beta adrenergic receptor in liver
• beta receptor: PKA is activated; it phosphorylates glycogen phosphorylase kinase
• alpha receptor: PLC releases IP3 which releases Ca2+ (stimulates glyphos kinase)
• glycogen phosphorylase kinase phosphorylates gly phos b to form gly phos a (active)

glucagon receptor is a G protein coupled receptor. same mechanism as beta receptor and epinephrine; only occurs in liver

16 subunits of 4 types: alpha beta gamma delta

gamma: contains PK activity

delta: calmodulin; senses and binds calcium

beta: rapid site of phosphorylation

alpha: slow site of phosphorylation

Calcium not bound, not phosphorylated: not active

calcium bound or phosphorylated: partially active

both calcium and phosphorylated: fully active

calcium-only: short bursts of excercise or rest (glucose is still high so PKA isn't stimulated)

• energy charge regulates activity of Phosphorylase b: ATP keeps it inactive
• high AMP shifts equilibrium to R; phosphorylase is still in "b"/dephosphorylated state, but active
• This is so muscle can rapidly respond to local energy needs

glucose regulates phosphorylase a: goes to T state so it is inactive but still phosphorylated

this inhibits immediate glycogen breakdown when blood glucose is already high

long term down-regulation: PP1 changes a to b

tyrosine kinase receptor.

activated receptor phosphorylates peripheral membrane proteins - insulin receptor substrates (IRS)

signal transduction cascade - downstream protein kinases activated