Adrenaline responsiveness
Adrenaline answer↑
Also searched as Adrenaline answer.
Adrenaline and noradrenaline are the body’s instruction to release stored fat. In obesity, fat tissue answers that instruction less and less. Inflammation is one driver: in obese mice, the inflammatory kinases IKK-epsilon and TBK1 switch on the enzyme that breaks down the cell’s cAMP signal, and blocking them restored the response to a beta-3 agonist. Restoring sensitivity lets the existing signal work again.
In depth
Catecholamine resistance — fat tissue’s blunted response to adrenaline and noradrenaline, the hormones that release stored fat.
What drives it
Calms inflamed fat tissue increases it.
Inflammation produces catecholamine resistance in obesity through activation of PDE3B by the kinases IKK-epsilon and TBK1. PMID 24368730
Fat-tissue signal (TNF-α) increases it.
Prolonged TNF-alpha exposure decreases the sensitivity of fat cells to beta-adrenergic stimulation. PMID 24368730
What it drives
It reduces Beta-3 receptor signaling.
Reversing obesity-induced catecholamine resistance in mice restored signaling in response to a beta-3 adrenergic agonist. PMID 24368730
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
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