Lipolysis Cascade: From Stimulus to Free Fatty Acids
Catecholamines bind beta-adrenergic receptors, cAMP rises via Adenylyl Cyclase, PKA activates HSL and ATGL, triglycerides break to FFA and glycerol.
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Lipolysis Cascade: From Stimulus to Free Fatty Acids
Lipolysis is the hydrolysis of stored triglycerides into free fatty acids (FFAs) and glycerol. It is the central process of fat mobilization and the prerequisite step before fat can be transported and oxidized. The rate-limiting enzymes are hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL).
The cascade is initiated by sympathetic nervous system activation, which drives catecholamine release from the adrenal medulla. Peak catecholamine action occurs within 0-3 minutes of maximal stimulus.
Adrenaline and noradrenaline bind beta-adrenergic receptors (mainly beta-3 in adipose tissue), which couple to Gs protein and activate adenylyl cyclase. cAMP accumulates and activates protein kinase A (PKA).
PKA phosphorylates two key targets: perilipin-1 (the lipid droplet coat protein) and HSL itself. Phospho-perilipin fragments, exposing the triglyceride surface to HSL and ATGL. ATGL performs the first hydrolysis step (TG to DAG); HSL performs the second (DAG to MAG); MAG lipase completes the third (MAG to glycerol + FFA).
Three FFAs and one glycerol molecule exit each adipocyte. FFAs enter circulation bound to albumin; glycerol travels to the liver for gluconeogenesis.
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Source & accuracy
This lipolysis cascade: from stimulus to free fatty acids is an editorial illustration built to represent the concept accurately. Where it shows figures, they are typical or representative values chosen to make the relationship clear, not a single underlying dataset. The diagram and its explainer are reviewed and maintained centrally, and updated over time as understanding improves.
From receptor to second messenger
Lipolysis begins when catecholamines such as adrenaline and noradrenaline bind beta-adrenergic receptors on the adipocyte surface. This activates the G-protein-coupled enzyme adenylyl cyclase, which converts ATP into cyclic AMP (cAMP). Rising cAMP is the second messenger that carries the signal forward into the cell.
Activating the lipases that release fat
cAMP activates protein kinase A (PKA). PKA phosphorylates the lipid droplet coat protein perilipin and the lipases, allowing adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) to access the stored triglyceride. They hydrolyze it stepwise into free fatty acids and glycerol, which exit the cell, the fatty acids bound to albumin for transport in the blood.
This is a signaling cascade, not a direct measure of fat loss; net loss still requires that the released fatty acids be oxidized and that overall energy balance be negative. General educational information, not medical advice.
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