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The term 'Fatty acid source' refers to the diverse physiological and metabolic pathways that supply long-chain fatty acids to cells, including exogenous dietary intake, endogenous de novo lipogenesis, and the mobilization of stored lipids (Argus et al., 2020). It is not a singular molecular target such as a specific receptor or enzyme, but rather a functional classification for the origins of the cellular lipid pool (Oliveira et al., 2024). In therapeutic development, specific components of these sources are targeted, such as Fatty Acid Synthase (FASN) for endogenous production or CD36 for exogenous uptake (Menendez & Lupu, 2007). Dysregulation of fatty acid supply is a critical feature of metabolic diseases like obesity and NAFLD, and many cancers rely on specific fatty acid sources to support rapid proliferation and membrane synthesis (Hurtubise et al., 2016). Drugs like orlistat prevent the utilization of dietary sources, while newer agents like denifanstat target synthetic sources to treat metabolic and oncological conditions (Tonazzi et al., 2017). Because it describes a collective metabolic process rather than a distinct protein entity, 'Fatty acid source' is generally considered an incorrect or overly generic designation for a specific therapeutic target (Argus et al., 2020).
Pharmacological interventions targeting fatty acid sources typically act by inhibiting the enzymatic breakdown and absorption of dietary lipids in the gastrointestinal tract, blocking de novo lipogenesis within cells, or preventing the transport and oxidation of fatty acids in the mitochondria.
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