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Lipid mobilization" describes the enzymatic breakdown and movement of stored lipids (triglycerides) in adipose tissue into free fatty acids and glycerol, which are then released for use by other tissues as energy substrates. This process, referred to as lipolysis, primarily involves enzymes such as adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL), and monoacylglycerol lipase (MGL). Lipid mobilization is regulated by signaling pathways under the control of hormones (e.g., adrenaline, glucagon), which act via membrane receptors (β-adrenergic receptors) and second messengers (cAMP, protein kinases), ultimately activating neutral lipases to hydrolyze triglycerides. The released fatty acids are transported in the blood bound to albumin to be used by organs such as muscle and liver for β-oxidation and energy production. This process is tightly regulated and altered in metabolic disorders including obesity and diabetes[1][2][3][4][5][6]. Key point: "Lipid mobilization" is a major physiological process, but it is not a molecule, protein, or classic drug target. If seeking a therapeutic target within this process, one would focus on enzymes such as adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL), or receptors like the β-adrenergic receptor that regulate the process[1][2][5]. If you are seeking structured drug target information, a more specific molecular target name (e.g., "adipose triglyceride lipase" or "hormone-sensitive lipase") should be provided.
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