From catecholamine stimulus to FFA release: the complete cAMP/PKA/HSL cascade inside an adipocyte, with insulin/PDE3B as the dominant inhibitory input.
A free, animated fat loss signaling pathway you can read here or embed on any website, from Scrollchart.
Fat Loss Signaling Pathway
Fat release from an adipocyte is controlled by a second-messenger cascade centered on cyclic AMP (cAMP). Multiple pro-lipolytic hormones (catecholamines, glucagon, GH) and a single dominant anti-lipolytic hormone (insulin) compete to set the intracellular cAMP level. When cAMP is high, protein kinase A activates hormone-sensitive lipase (HSL) and perilipin, the lipid droplet coat protein, enabling triglyceride hydrolysis.
Catecholamines bind beta-adrenergic receptors (beta-3 dominant in adipose), coupling to Gs protein, which activates adenylyl cyclase to convert ATP to cAMP. PKA phosphorylates perilipin-1 (fragmenting the lipid droplet coat) and HSL (activating it). ATGL performs the first hydrolysis step; HSL the second; MGL the third.
Insulin suppresses the cascade at two points: Akt activates PDE3B, which rapidly degrades cAMP; and Akt also directly phosphorylates and inactivates HSL. Both insulin actions converge to halt lipolysis within minutes of a meal.
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Source & accuracy
This fat loss signaling pathway 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.
The cAMP cascade inside an adipocyte
Catecholamines such as adrenaline and noradrenaline bind beta-adrenergic receptors on the fat cell surface. This activates adenylyl cyclase, which raises cyclic AMP (cAMP). Rising cAMP activates protein kinase A (PKA), which phosphorylates hormone-sensitive lipase (HSL) and the lipid droplet protein perilipin. The activated lipases hydrolyze stored triglyceride into free fatty acids and glycerol, which leave the cell for transport in blood.
Insulin as the dominant brake
The strongest opposing signal is insulin. Insulin activates phosphodiesterase 3B (PDE3B), which breaks down cAMP, collapsing the PKA signal and shutting off HSL. This is why fat mobilization is suppressed after carbohydrate-rich meals when insulin is high, and rises during fasting or exercise when insulin is low.
These steps describe a signaling mechanism, not a guaranteed rate of fat loss in any individual; whole-body fat balance still depends on total energy intake and expenditure. General educational information, not medical advice.
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Reference
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A free, embeddable, animated fat loss signaling pathway for any website.
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