Triacylglycerols represent the largest energy reservoir of the body. The primary fat storage organ is white adipose tissue (WAT), which grows in response to excess energy intake, eventually leading to obesity, and shrinks in response to starvation. In addition to its function as an energy storage organ, the finely tuned regulation of triacylglycerol synthesis and degradation in WAT is required for control of circulating lipid levels. Defective WAT function may result in dyslipidaemia and fatty acid overload of non-adipose tissues, inducing ectopic triacylglycerol deposition, which is associated with insulin resistance, inflammation and impaired metabolic function of insulin-sensitive tissues [1]. This can occur in obese individuals when the storage capacity of adipose tissue is exceeded and in patients with loss-of-function mutations in genes regulating lipid storage, e.g. mutations in the gene encoding lipid droplet protein perilipin 1, which limits the access of lipases to fat stores ...