PLCD4 and adrenal gland hyperfunction: While the transcript counts of the lipid hydroxylase PLCD4 increased with treatment in the present study, the predicted deactivation of lipid-related canonical pathways such as LXR/RXR signaling and sphingosine-1-phosphate signaling further supports the presence of lipid accumulation mechanisms in the canine VAT in response to hypercortisolemia, as also described in humans [50].