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Hepatic lipid metabolism pathways refer collectively to the complex network of biochemical processes in the liver governing the uptake, synthesis (*de novo* lipogenesis), oxidation (β-oxidation), and export of fatty acids and other lipids[1][4][5]. These interconnected processes maintain systemic energy balance and lipid homeostasis and are regulated by key enzymes (e.g., acetyl-CoA carboxylase, fatty acid synthase), transcription factors (e.g., SREBP1c, ChREBP), and hormones (e.g., insulin, thyroid hormone)[1][4]. Dysregulation of hepatic lipid metabolic pathways is central to the development of fatty liver diseases (including MAFLD/NAFLD), dyslipidemias, and atherosclerosis. While the molecular machinery within these pathways (such as specific enzymes or receptors) can be therapeutic targets, the term "hepatic lipid metabolism pathways" describes a biological process, not a single molecular entity, and is thus not a canonical drug target[4][5].\n\n**Note:** "Hepatic lipid metabolism pathways" refers to a process, not a discrete molecular target. The entry is best categorized as not a canonical therapeutic target (is_target: false), and is_incorrect: true for structured drug target databases. For specific drug development, the focus would shift to individual enzymes, transporters, or receptors within these pathways.
Modulation of lipid synthesis (inhibition of HMG-CoA reductase by statins)\nActivation of peroxisome proliferator-activated receptors (PPARα by fibrates)\nInhibition of de novo lipogenesis (various experimental compounds)\nEnhancement of fatty acid oxidation\nReduced VLDL secretion
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