VeryLowDensityLipoprotein

Very-low-density lipoprotein (VLDL) is one of the major classes of lipoproteins produced by the liver. It transports endogenous triglycerides synthesized in hepatocytes to peripheral tissues, where triglycerides are utilized for energy or stored. In the fasting state, VLDL is the predominant triglyceride-rich lipoprotein in plasma.

Composition and structure: VLDL particles are rich in triglycerides, with smaller amounts of cholesterol esters, phospholipids, and apolipoproteins. Each VLDL particle contains a single molecule of apolipoprotein B-100 (ApoB-100) and carries exchangeable apolipoproteins such as ApoC-II and ApoE, which are donated to HDL during lipolysis.

Formation and metabolism: VLDL is secreted by the liver into the bloodstream. Lipoprotein lipase (LPL) hydrolyzes triglycerides in VLDL, producing fatty acids for tissues and generating VLDL remnants like IDL, which are partially converted to LDL by hepatic lipase and further processing. VLDL remnants are cleared by hepatic receptors or converted to LDL.

Clinical relevance: Elevated VLDL levels are associated with hypertriglyceridemia, metabolic syndrome, and type 2 diabetes and can contribute to pancreatitis at very high triglyceride levels. Clinically, VLDL is often inferred from fasting triglyceride concentration or estimated by the Friedewald equation (VLDL = TG/5 in mg/dL) when TG < 400 mg/dL; direct measurement is available in specialized assays. Apolipoprotein B level reflects the number of atherogenic particles, including VLDL.

Management: Approaches focus on reducing hepatic triglyceride production and enhancing clearance, including lifestyle modification (weight loss, exercise, reduced simple carbohydrates) and pharmacotherapy. Fibrates and omega-3 fatty acids are effective at lowering triglycerides and VLDL. Statins reduce LDL but may modestly reduce VLDL; in severe hypertriglyceridemia, fibrates are preferred, sometimes with omega-3 therapy.