AMPK (AMP-activated protein kinase) acts as a cellular energy sensor. Which combination of effects results from AMPK activation under low energy (high AMP/ATP ratio) conditions?
- A Activates ACC (fatty acid synthesis) and activates mTOR (protein synthesis)
- B Activates glycogen synthase and inhibits glycogenolysis
- C Increases SREBP-1c nuclear translocation to upregulate lipogenic genes
- D Inhibits ACC (reducing malonyl-CoA) and inhibits mTOR, shifting metabolism toward catabolism ✓
Explanation
AMPK is activated when AMP/ADP rises (low cellular energy). It phosphorylates and inactivates acetyl-CoA carboxylase (ACC), reducing malonyl-CoA, which relieves inhibition of carnitine palmitoyltransferase-I (CPT-I) and promotes beta-oxidation. AMPK also phosphorylates and inhibits mTORC1 (via TSC2 and Raptor), suppressing protein synthesis and cell growth. AMPK activates GLUT4 translocation and glycolysis while simultaneously inhibiting anabolic pathways (glycogen synthase, fatty acid synthesis, sterol synthesis). It is the master switch from anabolism to catabolism. SREBP-1c is a downstream target of insulin/mTOR, not AMPK activation.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.