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Hepatic triglyceride secretion refers to the liver’s process of exporting triglycerides into the bloodstream as components of very low-density lipoprotein (VLDL) particles. This process is central to maintaining lipid and energy homeostasis and involves the intracellular synthesis of triglycerides, their packaging with apolipoprotein B100, and the assembly of VLDL particles in the endoplasmic reticulum via the enzyme microsomal triglyceride transfer protein (MTTP). Impairment of this process—due to genetic or pharmacological inhibition—can result in hepatic steatosis, while excessive secretion is implicated in hypertriglyceridemia and cardiovascular risk. While drugs such as mipomersen and lomitapide target the proteins involved in this process, hepatic triglyceride secretion itself is not a molecule and thus not a direct drug target but a physiological outcome regulated by multiple molecular entities.
Inhibition of ApoB100 synthesis (reduces VLDL assembly/export); Inhibition of MTTP activity (blocks VLDL formation and triglyceride secretion)
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