Lipolysis, via hormone-sensitive lipase (LHS) and monoglyceride lipase (MGL), allows the hydrolysis of triglycerides into diglycerides and diglycerides into monoglycerides themselves degraded into free fatty acids and glycerol. Adipose tissue-specific triglyceride lipase (TGLA) has recently been discovered and has a role that is redundant to that of LHS. Studies of Cao et al. showed that the activation of LHS by catecholamines could constitute a mechanism of regulation of lipolysis during cancer cachexia. . An alteration of TGLA and LHS would also be responsible for an accumulation of DAG and TAG in the muscle of cancerous mice . A recent study showed that the invalidation of TGLA and LHS in 2 models of cachexia induced by injection of Lewis pulmonary carcinoma cells or B16 melanoma cells induced resistance to the development of cachexia by limiting adipose and muscular loss . Systemic inflammation developed during cancerous cachexia could also induce an increase in insulin resistance via TNFalpha . TNFalpha could inhibit the expression of perilipin A, a protein expressed on the surface of adipocyte lipid droplets , which plays a major role in the integrity of adipose tissue since it limits the access of enzymes involved in lipolysis to the lipid droplet . A decrease in the expression of perilipin A would induce an increase in lipolysis. In addition, a study by Stephens et al. in 2011 concluded that the number and size of intramuscular lipid droplets are increased in the presence of cancer and also increase with weight loss / adipose fat loss in other body compartments .