Insulin signalling activates PI3K, which phosphorylates PIP2 to PIP3. PIP3 recruits PDK1, which activates Akt (PKB). The PRINCIPAL metabolic consequence of this Akt activation in adipose tissue is:

• A Phosphorylation and inactivation of hormone-sensitive lipase (HSL) ✓
• B Activation of adenylyl cyclase and elevation of cAMP
• C Phosphorylation and nuclear export of FOXO1, inducing gluconeogenic genes
• D Direct activation of glycogen phosphorylase b to a conversion

Explanation

Akt phosphorylates and inactivates hormone-sensitive lipase (HSL) directly, suppressing lipolysis in adipose tissue; it also activates phosphodiesterase that hydrolyzes cAMP, further reducing PKA-mediated HSL phosphorylation. Akt does not activate adenylyl cyclase (that is the Gs-cAMP pathway). Akt phosphorylates FOXO1 for nuclear EXPORT, which suppresses (not induces) gluconeogenic gene transcription. Glycogen phosphorylase activation is a glucagon/epinephrine effect via phosphorylase kinase.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.