Given that cPLA2 is essential for arachidonic acid release and subsequent PG synthesis, the hyperphagia observed in shPLA2 mice is consistent with PG-mediated appetite suppression, particularly under stimulated conditions—such as hyperglycemia, postprandial insulin signaling, or satiety—where PGE2 is normally upregulated to limit food intake [9,10]. This evidence concerns the gene INS and Hyperglycemia.