The deliberate and precise activation of the biochemical pathway responsible for the hydrolysis of stored triglycerides into free fatty acids and glycerol within adipocytes, specifically aiming at particular adipose tissue depots. This is a crucial metabolic process for energy mobilization and is often regulated by local and systemic hormonal signals like catecholamines and insulin. Clinical protocols utilizing this concept seek to enhance metabolic flexibility and optimize body composition by selectively mobilizing stored fat for fuel. This precision is key to body composition management.
Origin
This term originates from lipid biochemistry and clinical metabolism, combining the process of lipolysis (fat breakdown) with the clinical goal of targeted stimulation. The emphasis on “targeted” reflects the modern understanding of adipose tissue heterogeneity and the desire to influence specific fat stores for therapeutic effect.
Mechanism
Stimulation is primarily achieved through the binding of lipolytic hormones, such as epinephrine or norepinephrine, to beta-adrenergic receptors on the adipocyte surface. This binding activates adenylyl cyclase, which increases intracellular cyclic AMP (cAMP) levels. Elevated cAMP then activates Protein Kinase A (PKA), which phosphorylates and activates Hormone-Sensitive Lipase (HSL) and perilipin, thereby initiating the breakdown of the stored triglycerides into usable energy substrates.
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