Cardiovascular atlas ↗Fat is absorbed
Enterocytes receive fatty acids and cholesterol after digestion and micellar transport.
CARDIOVASCULAR / LIPOPROTEINS
Lipids need vehicles.
Particles are the traffic.
Triglycerides and cholesterol do not circulate freely in water-rich plasma. Lipoproteins package this cargo, exchange it, deliver it, remodel it, and clear it. Particle concentration, cargo, origin, and residence time are related but distinct measurements.
16-STAGE TRANSPORT MAP
Two delivery routes.
One circulation.
The intestinal ApoB-48 pathway and hepatic ApoB-100 pathway transport triglyceride-rich cargo. HDL-associated ApoA-I participates in exchange and cholesterol efflux, but HDL-C concentration alone is not a complete measure of function.
Chylomicrons assemble
ApoB-48 and microsomal transfer processes package dietary triglyceride and cholesterol.
Lymph reaches blood
Nascent chylomicrons enter lymph before joining systemic venous circulation.
LPL unloads triglyceride
Lipoprotein lipase releases fatty acids for muscle use or adipose storage; regulation changes with tissue and metabolic state.
Remnants return to liver
Cholesterol-enriched chylomicron remnants undergo receptor-mediated hepatic clearance.
Liver secretes VLDL
VLDL exports endogenous triglyceride and cholesterol on one ApoB-100 scaffold per particle.
VLDL is lipolyzed
LPL-mediated triglyceride removal produces smaller remnant particles while fatty acids enter tissues.
IDL is a branch point
IDL/remnants may be cleared by liver or remodeled further toward LDL.
LDL carries cholesterol
LDL is relatively cholesterol-rich and circulates longer than triglyceride-rich precursors.
LDL receptors clear particles
Hepatic LDL-receptor activity removes ApoB-100 particles; intracellular cholesterol and PCSK9 help regulate receptor availability.
Lp(a) adds distinct cargo
Lp(a) is an LDL-like ApoB particle linked to apolipoprotein(a); concentration is largely inherited and adds a distinct risk pathway.
ApoA-I accepts lipid
Nascent ApoA-I interacts with transporters such as ABCA1 to acquire phospholipid and cholesterol from cells.
HDL particles mature
LCAT esterifies cholesterol and HDL particles remodel as they circulate.
Cargo is exchanged
CETP can exchange cholesteryl ester and triglyceride between HDL and ApoB particles; lipases continue remodeling.
Cholesterol reaches liver
HDL-associated cholesterol can reach liver directly or indirectly after transfer to ApoB particles.
Bile route closes the loop
Hepatic cholesterol may be reused, converted to bile acids, or secreted into bile; much is reabsorbed through enterohepatic cycling.
WHAT LABS MEASURE
Cargo, particles,
and inherited context.
These markers overlap but cannot be substituted mechanically. Interpretation depends on fasting context, triglycerides, metabolic state, treatment, and clinical history.
Estimated cholesterol cargo
LDL-C describes cholesterol carried within the LDL fraction; it is not a direct LDL particle count.
Atherogenic cholesterol cargo
Total cholesterol minus HDL-C approximates cholesterol across ApoB-containing particle classes.
Atherogenic particle number
Each VLDL, IDL, LDL, remnant, and Lp(a) particle contains one ApoB molecule, making ApoB useful when cargo and particle count are discordant.
Dynamic traffic signal
Reflect triglyceride-rich lipoprotein traffic and vary with meals, alcohol, metabolic state, genetics, and illness.
HDL cholesterol cargo
HDL-C is associated with risk but does not directly measure all HDL functions or prove that raising it pharmacologically lowers events.
Predominantly inherited particle
Current guidance supports measuring Lp(a) at least once because routine lipid panels do not reveal it.
Current framework: 2026 AHA/ACC Dyslipidemia Guideline ↗ · Endotext: cholesterol-lowering drugs ↗
These pathways explain transport; they do not turn one laboratory value into a diagnosis, treatment recommendation, or personal event forecast.