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Very-low-density lipoprotein is a lipoprotein complex produced primarily in the liver that is responsible for transporting endogenously synthesized triglycerides and cholesterol to peripheral tissues via the bloodstream. VLDL particles are assembled in hepatocytes from triglycerides, cholesterol, and apolipoproteins—most notably Apo B-100—with the assistance of microsomal triglyceride transfer protein. Once secreted, VLDL undergoes lipolysis and conversion into intermediate-density lipoproteins and then low-density lipoproteins, a process central for lipid homeostasis. Abnormalities in VLDL production, composition, and clearance are major contributors to atherosclerosis, metabolic syndrome, and other cardiometabolic diseases.
Inhibition of microsomal triglyceride transfer protein (blocks VLDL particle assembly and secretion); Reduction of hepatic triglyceride synthesis (lowers substrate for VLDL assembly); Enhancement of lipoprotein lipase activity (increases VLDL catabolism).
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