Direct evidence to support α cell–mediated GLP-1 secretion as the mechanism of FATP2-KO–associated hyperinsulinemia included (a) colocalization of FATP2 with human and mouse islet α, but not β, cells, (b) FATP2 mRNA expression in human and mouse α, but not β, cells, (c) inhibition of fatty acid uptake by FATP2 inhibitors in α cells, (d) increased GLP-1+ α cell mass in FATP2-KO db/db mice, (e) an increased Pcsk1/Pcsk2 mRNA ratio in αTC1-6 cells treated with lipofermata, and (f) enhanced GLP-1 secretion and exendin[9-39]–inhibitable GSIS in FATP2 inhibitor–treated human islets. Here, SLC27A2 is linked to hyperinsulinism.