A study conducted by Yang et al. showed that mesenteric adipose tissue (MAT) collected from obese diabetic subjects had high gene expression of leptin, PPAR-γ, fatty acid translocase (FAT/CD36), and 11β hydroxysteroid hydrogenase (HSD) suggesting that alteration in the mesenteric depot may play a role in the development of metabolic syndrome [181]. Here, CD36 is linked to metabolic syndrome.