Lipid Transport Tournament
Two onboarding diagrams orient you in the lipoprotein cycle. Then eight MCAT-level rounds: apoC-II switching on lipoprotein lipase, how statins really lower LDL, familial hypercholesterolemia, the dietary-fat route from micelle to remnant, the apolipoprotein job list, apoB-48 vs apoB-100, the density-versus-triglyceride table, and reverse cholesterol transport.
Where the Plasma lipoprotein assembly, remodeling, and clearance fits in Transport of small molecules
Triglyceride and cholesterol are hydrophobic, so they cannot simply dissolve in plasma and drift to their destinations - they have to be packaged into particles with a phospholipid shell and an apolipoprotein address label. The highlighted panel is that logistics system: the assembly, remodeling, and clearance cycle of the plasma lipoproteins. Click the highlighted Plasma lipoprotein panel to enter the tournament.
Click the highlighted Plasma lipoprotein assembly, remodeling, and clearance box to continue.
What this tournament tests
Each task maps to a distinct MCAT cognitive demand. The first two orient you in the broader topology; the next eight test the high-yield mechanism, regulation, sequence and quantitative reasoning that consistently appear on test day.
The Bigger Picture
Anchor plasma lipoprotein assembly, remodeling, and clearance inside transport of small molecules on the live Reactome map.
Whole-Pathway Overview
Pan and zoom the curated WikiPathways LDL, HDL, and triglyceride metabolism figure before you start answering.
Fill in the Blank
Recall apoC-II as the cofactor that activates lipoprotein lipase on capillary endothelium.
Fill in the Blank
Trace how statins inhibit HMG-CoA reductase and indirectly upregulate hepatic LDL receptors.
Disruptor
Explain why a heterozygous LDL receptor defect produces tendon xanthomas and a myocardial infarction in a patient's 30s.
Sequence Ordering
Order the dietary-fat journey from mixed micelle to apoB-48 chylomicron to lymphatics to lipoprotein lipase to hepatic remnant clearance.
Match the Pairs
Pair each apolipoprotein and transport protein (apoB-48, apoB-100, apoC-II, apoE, apoA-I, LCAT, PCSK9, CETP) with its precise job.
Numeric Input
Recall that apoB-48 is the N-terminal 48 percent of apoB-100, generated by APOBEC-1 mRNA editing.
Select All That Apply
Identify TRUE statements about the five lipoprotein classes: density versus triglyceride content, exogenous versus endogenous fat, and VLDL to IDL to LDL conversion.
Odd One Out
Separate the reverse cholesterol transport machinery (apoA-I, LCAT, SR-B1) from the forward triglyceride-delivery arm.
Public leaderboard
Your score posts to a global, persistent leaderboard scored by points first, time as tiebreaker.
Lipid transport in 60 seconds
Lipids travel in plasma inside lipoproteins - a hydrophobic core of triglyceride and cholesteryl ester wrapped in phospholipid, free cholesterol, and apolipoproteins. Because protein is dense and triglyceride is not, the five classes line up predictably: as you go chylomicron -> VLDL -> IDL -> LDL -> HDL, density rises and triglyceride content falls.
The delivery arm runs forward. Chylomicrons carry dietary triglyceride from the intestine on apoB-48, reaching blood through the lymphatics; VLDL carries endogenous triglyceride from the liver on apoB-100. Both borrow apoC-II and apoE from HDL, and lipoprotein lipase on capillary endothelium - activated by apoC-II - releases fatty acids into adipose and muscle. The apoE-rich remnants go to the liver, and progressive VLDL lipolysis yields IDL and then cholesterol-rich LDL.
LDL is the main cholesterol delivery particle, cleared when its apoB-100 is grabbed by the LDL receptor and internalized in a clathrin-coated pit. Defects here cause familial hypercholesterolemia. Pharmacology follows the same logic: statins deplete hepatocyte cholesterol so SREBP-2 makes more receptors, ezetimibe blocks intestinal NPC1L1, and PCSK9 inhibitors stop PCSK9 from dragging the receptor to the lysosome so each receptor recycles more often.
Running the other direction, HDL performs reverse cholesterol transport: apoA-I accepts cholesterol effluxed by ABCA1, LCAT esterifies it into the core, and the cargo reaches the liver via SR-B1 or via CETP transfer to apoB particles. Two boundary diseases pin the system down - abetalipoproteinemia (defective microsomal triglyceride transfer protein, so no chylomicrons or VLDL can be built) and Tangier disease (defective ABCA1, so almost no HDL forms).
FAQ
Why do dietary fats enter the lymph instead of the portal vein?
Chylomicrons are far too large to cross the fenestrated but basement-membrane-lined capillary endothelium of the intestinal villus, so they are exocytosed into the much more permeable lymphatic lacteals and reach blood at the thoracic duct. Short- and medium-chain fatty acids are small and water-soluble enough to skip packaging entirely and go straight into the portal vein bound to albumin, which is exactly why medium-chain triglyceride formulas are used when chylomicron assembly or lymphatic drainage fails.
What actually goes wrong in abetalipoproteinemia?
Microsomal triglyceride transfer protein (MTP) is the chaperone that loads lipid onto apoB, so losing it means neither the intestine nor the liver can secrete an apoB-containing particle. Patients have no chylomicrons, VLDL, or LDL: fat accumulates in enterocytes, causing steatorrhea and failure to thrive, and the fat-soluble vitamins are poorly absorbed. Vitamin E deficiency drives the spinocerebellar ataxia and retinitis pigmentosa, and the smear shows acanthocytes.
Is HDL cholesterol simply 'good' cholesterol?
The cholesterol molecule is identical in every particle - what differs is direction of traffic. HDL removes cholesterol from peripheral tissue and returns it to the liver for excretion in bile, so higher HDL cholesterol correlates with lower cardiovascular risk. But correlation is not mechanism: drugs that only raise the HDL number, such as CETP inhibitors, have not reduced events, so what matters is functional cholesterol efflux capacity rather than the measured concentration.
How do I keep apoC-II and apoE straight?
Tie each to its verb. ApoC-II is the Catalytic cofactor that switches on lipoprotein lipase, so losing it blocks triglyceride unloading and gives severe fasting hypertriglyceridemia with pancreatitis. ApoE is the Extraction tag that lets the liver take up chylomicron remnants and IDL, so a defective apoE2/E2 genotype leaves remnants circulating - type III hyperlipoproteinemia, with palmar xanthomas.
Do I need an account to play?
No. The tournament is fully public. You get a randomized handle and your score posts to the public leaderboard at the bottom of this page.
Keep going
Where the cholesterol being shipped is actually made - the mevalonate pathway, HMG-CoA reductase, and how statins act on it.
What tissue does with the fatty acids lipoprotein lipase delivers - carnitine shuttle, beta-oxidation, and acetyl-CoA.
Overview diagram: Reactome Pathway R-HSA-382551, licensed CC BY 4.0.