Figure 1.
Potential mechanism of potentiation of the second phase of insulin secretion by fatty acid and synthetic ligand stimulation of GPR40/free fatty acid receptor 1. Signaling through Gaq/11 results in PLC activation, hydrolyzing phosphoinositols, which generates IP3 and diacylglycerol. IP3 leads to increased Ca2+ release from the endoplasmic reticulum aiding granule movement/fusion. Diacylglycerol may directly assist in granule fusion as well as activating PKD1, resulting in F-actin depolymerazation and also assisting in insulin granule movement, which augments insulin release.