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Neutral fats, predominantly known as triglycerides, and cholesterol are essential lipid molecules that serve as the primary reservoirs for energy storage and the structural foundations of cellular membranes. Triglycerides are stored in adipose tissue and mobilized as free fatty acids during fasting or exercise to meet metabolic demands, while cholesterol is a vital precursor for the synthesis of bile acids, vitamin D, and steroid hormones like cortisol and estrogen [1, 3, 5]. Pathologically, the excessive accumulation of these lipids in the blood or tissues is a major driver of atherosclerosis, metabolic syndrome, and nonalcoholic fatty liver disease (NAFLD) [8, 13]. Although these molecules are the focus of many medical treatments, they are strictly considered metabolic substrates or clinical biomarkers rather than pharmacological targets [6, 16]. Drugs typically lower these lipid levels indirectly by inhibiting the enzymes or transporters that regulate their synthesis, absorption, and clearance, such as HMG-CoA reductase or NPC1L1 [8, 16]. Consequently, monitoring these lipid profiles remains the primary method for assessing cardiovascular health and therapeutic success in dyslipidemic patients.
Drugs modulate levels of these lipids by targeting regulatory proteins: HMG-CoA reductase inhibitors (Statins) reduce cholesterol synthesis; PPAR-alpha agonists (Fibrates) increase triglyceride metabolism; NPC1L1 inhibitors (Ezetimibe) block intestinal cholesterol absorption; and pancreatic lipase inhibitors (Orlistat) prevent the breakdown and absorption of neutral fats [8, 11, 16].
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