In a patient with a glucagonoma, which metabolic consequence is MOST directly attributable to chronic glucagon excess?
- A Hypoglycaemia from insulin counter-regulatory failure
- B Hyperglycaemia from stimulation of hepatic glycogenolysis and gluconeogenesis ✓
- C Metabolic acidosis from glucagon-stimulated fatty acid synthesis
- D Hypokalaemia from glucagon-stimulated renal K+ excretion
Explanation
Glucagon acts on Gs-coupled glucagon receptors in hepatocytes, raising cAMP and activating PKA, which phosphorylates glycogen phosphorylase (activating it) and glycogen synthase (inactivating it). Simultaneously, glucagon upregulates gluconeogenic enzymes (PEPCK, FBP-1) and inhibits pyruvate kinase. Net result is increased hepatic glucose output causing hyperglycaemia — the defining metabolic feature of glucagonoma along with the 4 D's (diabetes, dermatitis, deep vein thrombosis, depression). Glucagonoma characteristically causes diabetes mellitus, NOT hypoglycaemia.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.