Indeed, in mouse models of GDM created by feeding a high-fat diet or genetic deficiency of leptin receptors, inhibition of placental Akt activity was associated with improved glucose tolerance and suppression of mRNA expression of pro-inflammatory cytokines and chemokines in the placentas (45, 46), suggesting that placental Akt plays a role in the pathophysiology of GDM pregnancy. This evidence concerns the gene LEPR and glucose measurement.