Epinephrine Pathway and Glycogen Breakdown

A complete set of 25 vocabulary flashcards detailing the molecular steps, regulatory enzymes, target tissues, physiological role, and pathway perturbations of the epinephrine-stimulated glycogenolysis cascade.

Epinephrine pathway

A signaling cascade activated during fasting when the body needs glucose, with the overall result of breaking down glycogen into glucose via glycogen phosphorylase.

Muscle and liver

The specific tissues in which epinephrine triggers glycogen breakdown.

G protein-coupled receptor (GPCR)

The type of cell-surface receptor that epinephrine binds to initiate intracellular signaling.

G protein subunits

The three components of the heterotrimeric G protein ($\alpha$, $\beta$, and $\gamma$), among which the $\alpha$ subunit binds GDP or GTP.

$\alpha$ subunit

The G protein subunit that releases GDP and binds GTP upon receptor stimulation, thereby activating adenylyl cyclase in the membrane.

Adenylyl cyclase

A membrane-associated enzyme activated by the GTP-bound $\alpha$ subunit that converts ATP into cAMP and PPi.

Cyclic AMP (cAMP)

A second messenger generated from ATP by adenylyl cyclase that serves to activate protein kinase A (PKA).

Protein kinase A (PKA)

A kinase activated by cAMP that activates phosphorylase kinase to promote glycogen breakdown and inactivates glycogen synthase to halt glycogen synthesis.

Phosphorylase kinase

An intermediate kinase activated by PKA that directly activates glycogen phosphorylase.

Glycogen phosphorylase

The enzyme that catalyzes the breakdown of glycogen one unit at a time, releasing glucose 1-phosphate.

Glucose 1-phosphate

The end product released from glycogen degradation during the epinephrine signaling pathway.

Glycogen synthase

An enzyme responsible for glycogen synthesis that is inactivated by PKA to prevent glycogen rebuilding during breakdown.

Signal amplification

The process occurring at multiple cascade steps where one adenylyl cyclase produces numerous cAMP molecules and each kinase activates numerous targets, enabling a single epinephrine molecule to release a massive amount of glucose.

Phosphodiesterase

The enzyme that terminates the epinephrine signal by degrading the second messenger cAMP into AMP.

Epinephrine receptor antagonist

A pharmacological agent that blocks the epinephrine receptor, preventing G protein activation and subsequent cAMP generation, PKA activity, and glycogen breakdown.

Adenylyl cyclase inhibition

A disruption in which epinephrine binding and G protein activation still occur, but lack of cAMP production leaves PKA, phosphorylase kinase, and glycogen phosphorylase inactive.

Caffeine

A substance that inhibits phosphodiesterase, preventing cAMP breakdown and causing PKA to remain active so that glycogen breakdown is stronger and longer-lasting.

Loss of $\alpha$ subunit GTPase activity

A condition in which the $\alpha$ subunit remains continuously bound to GTP, causing adenylyl cyclase to persistently produce cAMP and preventing glycogen breakdown from shutting off.

PKA cAMP-binding mutation

A defect where upstream receptor signaling, G protein activation, adenylyl cyclase, and cAMP production work, but failure of PKA activation leaves phosphorylase kinase and glycogen phosphorylase off while glycogen synthase remains on.

Phosphorylase kinase deficiency

A pathway impairment where cAMP rises, PKA activates, and glycogen synthase is shut off, but glycogen phosphorylase is never activated, preventing glycogen breakdown.

cAMP memory hook

A learning mnemonic linking cAMP directly to the activation of PKA using the 'A' found in AMP.

cAMP target regulation

The dual downstream regulatory effect wherein cAMP activates protein kinases and glycogen phosphorylases while inhibiting glycogen synthase.

GDP vs. GTP binding states

The molecular switch states of the G protein's $\alpha$ subunit, where being bound to GDP corresponds to the 'off' state and being bound to GTP corresponds to the 'on' state.