Glucagon binds its GPCR on hepatocytes. The subsequent activation of PKA phosphorylates phosphofructokinase-2 (PFK-2/FBPase-2 bifunctional enzyme). The NET metabolic effect of this phosphorylation is:

• A Increased fructose-2,6-bisphosphate levels, stimulating glycolysis
• B Activation of PFK-2 kinase activity, increasing fructose-2,6-bisphosphate
• C Inhibition of FBPase-2 activity, preserving fructose-2,6-bisphosphate levels
• D Decreased fructose-2,6-bisphosphate levels, inhibiting glycolysis and stimulating gluconeogenesis ✓

Explanation

PKA phosphorylates the bifunctional PFK-2/FBPase-2 enzyme at Ser32; this phosphorylation INHIBITS the kinase activity and ACTIVATES the phosphatase (FBPase-2) activity of the same enzyme, causing net degradation of fructose-2,6-bisphosphate (F-2,6-BP). Since F-2,6-BP is the most potent allosteric activator of PFK-1 and inhibitor of FBPase-1, its depletion simultaneously inhibits glycolysis and activates gluconeogenesis, appropriate for the fasting glucagon signal.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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