The hypertriglyceridaemia observed in patients with the MetS and T2DM originates from (i) lipolysis of TAG store from adipose tissue that causes elevated FFA flux to the liver and hence, increased hepatic TAG synthesis and (ii) inhibition of lipolysis of chylomicrons and VLDL due to decreased LPL levels [8]. This evidence concerns the gene LPL and hypertriglyceridemia.