Lipolysis
The metabolic breakdown of stored fat (triglycerides) into free fatty acids and glycerol for use as energy. Growth hormone stimulates lipolysis, which is the mechanism by which tesamorelin reduces visceral fat. GLP-1 receptor agonists promote lipolysis indirectly through weight loss and improved insulin sensitivity.
Technical Context
Lipolysis pathway: hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) hydrolyse stored triglycerides in adipocytes → glycerol + free fatty acids (FFAs) released into circulation. Hormonal regulation: stimulated by catecholamines (beta-adrenergic receptor → cAMP → PKA → HSL phosphorylation), glucagon, growth hormone, and cortisol; inhibited by insulin (activates PDE3B, reducing cAMP). Tesamorelin promotes lipolysis specifically in visceral adipose tissue through GH-mediated HSL activation. GLP-1 RAs promote lipolysis indirectly: weight loss reduces insulin levels (less lipolysis inhibition), improved insulin sensitivity shifts the hormonal balance toward fat mobilisation, and reduced caloric intake creates energy deficit requiring fat oxidation. Excessive lipolysis can cause: elevated circulating FFAs (promoting insulin resistance), ketogenesis (risk in insulin-deficient states), and lipotoxicity in non-adipose tissues.