Figure 2.

Insulin synthesis and secretion is increased in apoA‐I treated pancreatic β cells via a PKA‐FoxO1 dependent mechanism. Interaction between apoA‐I and ABCA1 at the cell surface results in (A) activation of the Gα_s subunit of the heterotrimeric G protein and (B) activation of adenylate cyclase which converts ATP to cAMP. Elevated cAMP levels activate PKA (C), which translocates to the nucleus, where it phosphorylates and excludes FoxO1 (D), resulting in derepression of insulin gene transcription (E). Activated PKA also increases intracellular calcium levels (F), and increases insulin secretion. ABCA1 indicates ATP‐binding cassette transporter A1; apoA‐I, apolipoprotein A‐I; FoxO1, forkhead box protein O1; PKA, protein kinase A.