For example, downregulation in Camk2n1−/− EAT of Pla2g5 and Pla2g2a and reduced soluble phospholipase A2 activity supports the amelioration in MetS phenotypes in Camk2n1−/− rats, as Pla2g5 is upregulated in obese adipose tissue and promotes leptin secretion, whereas Pla2g2a is causally related to obesity and MetS.30,36 Moreover, soluble phospholipase A2 has been shown to promote adipogenesis and apoptosis associated with obesity.30 Apoptosis is an unlikely cause of reduced adiposity in Camk2n1−/− rats as proapoptic genes (Baiap2l1/Birc5, Dsg2, and Pcdh7) were downregulated. Here, LEP is linked to metabolic syndrome.