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Lipoproteins and Lipid Transport

Tier 2 · #11 of 33 · high yield · topic 3.16 — every high-yield fact from the book chapter, exam-ready.

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  1. Front
    What is the structural arrangement of a lipoprotein particle's surface monolayer?
    Back
    Amphipathic phospholipids with polar heads facing outward (plasma) and fatty-acid tails facing inward toward the hydrophobic core.
  2. Front
    Which two neutral lipids make up the hydrophobic core of a lipoprotein particle?
    Back
    Triacylglycerols (TAG) and cholesteryl esters .
  3. Front
    Which lipoprotein class is the LARGEST and LEAST dense?
    Back
    Chylomicrons .
  4. Front
    Which lipoprotein class is the SMALLEST and most dense?
    Back
    HDL .
  5. Front
    Explain the inverse relationship between a lipoprotein 's lipid content and its density.
    Back
    The more lipid relative to protein, the larger and less dense the particle — fat is lighter than protein .
  6. Front
    The signature apolipoprotein of the chylomicron is ______.
    Back
    ApoB-48 .
  7. Front
    Where is apoB-48 synthesized?
    Back
    Intestinal enterocytes (intestine only).
  8. Front
    Why can apoB-48 NOT bind the LDL receptor ?
    Back
    It is a truncated form of apoB-100 lacking the receptor-binding domain .
  9. Front
    What does the '48' in apoB-48 signify?
    Back
    It represents 48% of the full-length apoB-100 mRNA/message.
  10. Front
    Where is apoB-100 synthesized?
    Back
    The liver only.
  11. Front
    Across which particles does apoB-100 remain throughout its lifespan?
    Back
    VLDL → IDL → LDL (it stays on all of them) .
  12. Front
    Which apolipoprotein is the ligand recognized by the LDL receptor (B/E receptor)?
    Back
    ApoB-100 .
  13. Front
    ApoCII is the obligate activator of which enzyme?
    Back
    Lipoprotein lipase (LPL) .
  14. Front
    Which lipoprotein donates apoCII to chylomicrons and VLDL in circulation?
    Back
    HDL (apoCII is donated by HDL, then returned to it).
  15. Front
    Which apolipoprotein mediates remnant clearance (chylomicron remnants and IDL) by the liver ?
    Back
    ApoE .
  16. Front
    Which apoE genotype causes remnant accumulation and Type III hyperlipoproteinemia ?
    Back
    ApoE2/E2 homozygosity (apoE2 binds the LDL receptor poorly).
  17. Front
    ApoA-I is the main structural/functional protein of which lipoprotein ?
    Back
    HDL .
  18. Front
    Which enzyme is activated by apoA-I ?
    Back
    LCAT (lecithin:cholesterol acyltransferase).
  19. Front
    Into which circulatory compartment is the nascent chylomicron secreted (not portal blood)?
    Back
    The lymphatic system (lacteals), reaching blood via the thoracic duct .
  20. Front
    Why does plasma turn milky white ( lactescent ) after a fatty meal?
    Back
    It contains a suspension of chylomicrons .
  21. Front
    Which two apolipoproteins does a chylomicron acquire from HDL after entering the blood?
    Back
    ApoCII and apoE .
  22. Front
    Where on the body is lipoprotein lipase (LPL) located?
    Back
    The luminal surface of capillary endothelium (in adipose tissue and muscle ), anchored by heparan sulfate proteoglycans.
  23. Front
    What two products does LPL release when it cleaves core triglycerides ?
    Back
    Fatty acids and glycerol .
  24. Front
    Which hormone stimulates LPL activity in adipose tissue ?
    Back
    Insulin .
  25. Front
    Which LPL isoform has the LOWER Km (higher affinity) — muscle or adipose ?
    Back
    The muscle isoform ( low Km ), so muscle scavenges fatty acids even when plasma TAG is low.
  26. Front
    Why does the high-Km adipose LPL isoform ensure fat storage is a post-prandial event?
    Back
    Its low affinity means it only operates efficiently when plasma TAG is high (after a meal) .
  27. Front
    What is a chylomicron remnant enriched in (relative to TAG) after LPL action?
    Back
    Cholesteryl esters .
  28. Front
    Which two apolipoproteins remain on the chylomicron remnant that the liver uses to clear it?
    Back
    ApoE and apoB-48 (the liver clears via apoE recognition ).
  29. Front
    Which receptors clear chylomicron remnants from the blood?
    Back
    Hepatic apoE receptors — the LDL receptor and LRP — by receptor-mediated endocytosis.
  30. Front
    Which mandatory structural apolipoprotein does the liver use to assemble VLDL ?
    Back
    ApoB-100 .
  31. Front
    What is the predominant core lipid of freshly secreted VLDL ?
    Back
    Triacylglycerol (TAG) .
  32. Front
    As VLDL loses TAG via LPL it first becomes which denser particle?
    Back
    IDL (intermediate-density lipoprotein).
  33. Front
    What are the two fates of IDL ?
    Back
    ~Half is taken up by the liver via apoE-mediated endocytosis ; the other half is converted to LDL by hepatic lipase .
  34. Front
    Which enzyme removes remaining TAG/phospholipid from IDL to form LDL ?
    Back
    Hepatic lipase .
  35. Front
    Which is the ONLY apolipoprotein remaining on the surface of LDL ?
    Back
    ApoB-100 (LDL has lost all apoCII and apoE).
  36. Front
    What lipid makes up almost the entire core of LDL ?
    Back
    Cholesteryl esters (LDL is a cholesterol -delivery particle).
  37. Front
    By what mechanism is the LDL – receptor complex internalized?
    Back
    Receptor-mediated endocytosis in clathrin-coated pits.
  38. Front
    Inside the endosome, what causes LDL to dissociate from the LDL receptor ?
    Back
    Acid pH (the receptor then recycles to the surface).
  39. Front
    Which lysosomal enzyme hydrolyzes LDL 's cholesteryl esters to release free cholesterol ?
    Back
    Acid lipase .
  40. Front
    How does intracellular free cholesterol affect HMG-CoA reductase ?
    Back
    It suppresses HMG-CoA reductase , shutting down endogenous cholesterol synthesis.
  41. Front
    Which enzyme is activated by free cholesterol to re-esterify it for intracellular storage?
    Back
    ACAT (acyl-CoA:cholesterol acyltransferase).
  42. Front
    What is free cholesterol 's third feedback effect on the cell (regarding the LDL receptor )?
    Back
    It downregulates LDL receptor transcription , preventing further LDL uptake.
  43. Front
    What is the name of the cholesterol return route handled by HDL ?
    Back
    Reverse cholesterol transport (RCT) .
  44. Front
    What is the shape and lipid character of nascent HDL when secreted by liver and intestine ?
    Back
    A disc-like (discoidal) particle rich in phospholipids and apoA-I but nearly devoid of cholesterol .
  45. Front
    Cloze: LCAT esterifies free cholesterol using a fatty acid donated from the sn-2 position of ______.
    Back
    Phosphatidylcholine (lecithin) .
  46. Front
    Why must LCAT esterify free cholesterol in HDL to keep RCT going?
    Back
    The nonpolar cholesteryl ester moves into the HDL core, keeping surface free-cholesterol low and maintaining the gradient that drives continued uptake from cells.
  47. Front
    Which receptor lets the liver extract cholesteryl esters from HDL WITHOUT taking up the whole particle?
    Back
    Scavenger receptor SR-BI (the HDL shell is returned to circulation).
  48. Front
    Which protein transfers cholesteryl esters from HDL to VLDL / LDL in exchange for triglycerides ?
    Back
    CETP (cholesteryl ester transfer protein).
  49. Front
    What is the rate-limiting enzyme for peripheral tissue uptake of circulating triglycerides ?
    Back
    Lipoprotein lipase (LPL) .
  50. Front
    In the FASTED state, how does LPL behavior redirect fatty acids?
    Back
    Adipose LPL activity falls , redirecting fatty acids away from storage and toward muscle and heart .
  51. Front
    Type I hyperlipoproteinemia is caused by deficiency of which enzyme or its activator?
    Back
    LPL itself, or equivalently its obligate activator apoCII (familial LPL deficiency).
  52. Front
    Which lipoproteins are massively elevated in Type I (familial LPL deficiency)?
    Back
    Chylomicrons and VLDL ( severe hypertriglyceridemia ).
  53. Front
    Why is there NO increased coronary artery disease risk in classic Type I hyperlipoproteinemia ?
    Back
    LDL (and HDL ) are paradoxically low because the precursor particles are never fully processed.
  54. Front
    What are the presenting complications of Type I hyperlipoproteinemia ?
    Back
    Recurrent eruptive xanthomas and pancreatitis (from the triglyceride load).
  55. Front
    Type IIa (familial hypercholesterolemia) is caused by a defect in which receptor or which ligand?
    Back
    Defective LDL receptor , or a mutation in its ligand apoB-100 .
  56. Front
    What cells take up excess LDL non-specifically in arterial walls to become foam cells ?
    Back
    Macrophages (the cellular hallmark of atherosclerosis ).
  57. Front
    Why do statins NOT adequately treat HOMOZYGOUS familial hypercholesterolemia ?
    Back
    Statins work by upregulating LDL receptor expression , but homozygotes have no functional LDL receptor allele to upregulate .
  58. Front
    Statins inhibit which enzyme?
    Back
    HMG-CoA reductase .
  59. Front
    Which lipoprotein abnormality defines Type III hyperlipoproteinemia ?
    Back
    Accumulation of IDL/remnants due to apoE2/E2 homozygosity .
  60. Front
    Which liver enzyme lets the liver phosphorylate free glycerol for TAG synthesis?
    Back
    Glycerol kinase ( glycerol + ATP → glycerol-3-phosphate + ADP).
  61. Front
    Why can't adipocytes phosphorylate free glycerol for TAG synthesis?
    Back
    Adipocytes lack glycerol kinase .
  62. Front
    What is the adipocyte 's ONLY source of glycerol-3-phosphate for TAG synthesis?
    Back
    Glycolysis — specifically reduction of the intermediate dihydroxyacetone phosphate (DHAP) by glycerol-3-phosphate dehydrogenase .
  63. Front
    Why can't adipose tissue re-esterify (store) fatty acids when glucose is scarce?
    Back
    No glucose → no glycolytic flux → no DHAP-derived glycerol-3-phosphate backbone , so fat can't be stored even if fatty acids are present.
  64. Front
    Name the four fat-soluble vitamins .
    Back
    A, D, E, and K .
  65. Front
    Which lipoprotein primarily transports the fat-soluble vitamins in blood right after absorption?
    Back
    Chylomicrons .
  66. Front
    Deficiency of fat-soluble vitamins should prompt suspicion of what class of condition?
    Back
    Fat malabsorption (e.g., cystic fibrosis , chronic pancreatitis , cholestasis , celiac disease ).
  67. Front
    Vitamin A (retinol) is transported in blood bound to which protein?
    Back
    Retinol-binding protein (RBP) .
  68. Front
    Which active form of vitamin A is required for rhodopsin formation / night vision?
    Back
    Retinal (11-cis-retinal combines with opsin to form rhodopsin).
  69. Front
    What are the two classic deficiency findings of vitamin A ?
    Back
    Night blindness and xerophthalmia .
  70. Front
    Vitamin D (cholecalciferol) is synthesized in skin from which precursor upon UV-B exposure?
    Back
    7-dehydrocholesterol .
  71. Front
    What is the storage/measured form of vitamin D produced by the liver ?
    Back
    25-hydroxycholecalciferol (calcidiol).
  72. Front
    What is the active form of vitamin D , and where is it made?
    Back
    1,25-dihydroxycholecalciferol (calcitriol), made in the kidney .
  73. Front
    What are the deficiency states of vitamin D in children vs adults?
    Back
    Rickets in children; osteomalacia in adults.
  74. Front
    What is the primary biochemical function of vitamin E (α-tocopherol) ?
    Back
    It is the major lipid-soluble antioxidant in membranes, quenching free-radical chain reactions (lipid peroxidation) in PUFAs.
  75. Front
    On which lipoproteins is vitamin E primarily transported in plasma?
    Back
    LDL and VLDL .
  76. Front
    What are the deficiency manifestations of vitamin E ?
    Back
    Hemolytic anemia (peroxidized RBC membranes) and neurological symptoms ( spinocerebellar ataxia , peripheral neuropathy ).
  77. Front
    Vitamin K is the cofactor for which enzyme?
    Back
    γ-carboxylase (γ-glutamyl carboxylase).
  78. Front
    Which coagulation factors and proteins require vitamin K -dependent γ-carboxylation?
    Back
    Factors II (prothrombin), VII, IX, and X , plus proteins C and S .
  79. Front
    Why is γ-carboxylation of glutamate residues essential for clotting factor function?
    Back
    It enables calcium binding , which is required for coagulation activity.
  80. Front
    Warfarin (coumarin anticoagulants) works by inhibiting which enzyme?
    Back
    Vitamin K epoxide reductase (blocking vitamin K recycling = functional vitamin K deficiency).
  81. Front
    Why do newborns receive intramuscular vitamin K at birth?
    Back
    The gut is sterile — bacteria have not yet colonized to produce vitamin K2 (menaquinone) .
  82. Front
    Distinguish vitamin K1 vs K2 by source.
    Back
    K1 (phylloquinone) comes from leafy green vegetables ; K2 (menaquinone) is synthesized by gut bacteria.
  83. Front
    Which fatty-acid chain lengths does MCADD impair the β-oxidation of?
    Back
    Medium-chain fatty acids, C6–C12 .
  84. Front
    In MCADD , why are there NO/low ketone bodies during fasting?
    Back
    The β-oxidation block prevents acetyl-CoA production, so there is no substrate for ketogenesis .
  85. Front
    Acetyl-CoA from β-oxidation is an allosteric activator of which gluconeogenic enzyme?
    Back
    Pyruvate carboxylase (the first committed step of gluconeogenesis).
  86. Front
    Why does MCADD cause severe fasting hypoglycemia (two simultaneous failures)?
    Back
    Loss of acetyl-CoA means no ketone bodies AND no activation of pyruvate carboxylase/gluconeogenesis — so after glycogen is exhausted, the infant can make neither glucose nor ketones .
  87. Front
    What is the key diagnostic clue distinguishing MCADD from normal fasting hypoglycemia ?
    Back
    Hypoglycemia with inappropriately LOW or absent ketones (normal fasting hypoglycemia produces HIGH ketones).
  88. Front
    Name the three fundamental roles of apolipoproteins (as a set).
    Back
    (1) Increase structural stability and hydrophilicity/solubility of the particle; (2) act as enzyme activators ; (3) serve as ligands for cellular receptors .
  89. Front
    Which of the three apolipoprotein roles makes the otherwise-hydrophobic lipoprotein particle water-soluble in plasma?
    Back
    The structural role — apolipoproteins increase the particle's hydrophilicity/solubility.
  90. Front
    Unlike water-soluble vitamins, why can fat-soluble vitamins A, D, E, and K accumulate to TOXIC levels?
    Back
    They are stored in fat and the liver (rather than readily excreted), so excessive intake builds up to toxic concentrations.
  91. Front
    What are the three classic features of vitamin A TOXICITY?
    Back
    Liver damage , teratogenicity , and pseudotumor cerebri .
  92. Front
    Which active form of vitamin A acts as a nuclear hormone-receptor ligand (not the vision form)?
    Back
    Retinoic acid .
  93. Front
    What does retinoic acid regulate as a nuclear hormone-receptor ligand?
    Back
    Gene expression — driving embryonic development and epithelial cell differentiation.
  94. Front
    Match the active vitamin A form to its function: retinal vs retinoic acid .
    Back
    Retinal → rhodopsin/night vision (rod photoreceptors); retinoic acid → nuclear-receptor ligand controlling gene expression, development, and epithelial differentiation.
  95. Front
    Vitamin D is classified as what type of molecule (not a true vitamin)?
    Back
    A prohormone .
  96. Front
    What are the three actions of calcitriol (1,25-dihydroxycholecalciferol)?
    Back
    Increases intestinal calcium AND phosphate absorption , promotes bone mineralization, and (at high levels) mobilizes calcium from bone.
  97. Front
    Through what receptor mechanism does calcitriol act?
    Back
    As a nuclear receptor ligand (regulating gene transcription).
  98. Front
    Cloze: Calcitriol increases intestinal absorption of both calcium and ______.
    Back
    Phosphate .
  99. Front
    α-tocopherol has what distinction among the vitamin E forms?
    Back
    It has the highest biological activity (~88% of ingested vitamin E activity).
  100. Front
    Vitamin E exists in which two chemical families?
    Back
    Tocopherols and tocotrienols .
  101. Front
    What is the clinical deficiency presentation of vitamin K ?
    Back
    Bleeding , with prolonged PT and aPTT.
  102. Front
    A patient on warfarin develops bleeding with prolonged PT and aPTT. What functional deficiency does this reflect?
    Back
    Functional vitamin K deficiency (warfarin blocks vitamin K recycling, impairing γ-carboxylation of factors II, VII, IX, X, C, S).
  103. Front
    In LCAT deficiency , why can HDL not mature?
    Back
    Without LCAT , free cholesterol picked up by HDL is not esterified , so it cannot be trapped in the core — the nascent disc never inflates into a mature spherical HDL .
  104. Front
    What are the two characteristic clinical findings of LCAT deficiency ?
    Back
    Low HDL and corneal opacities .
  105. Front
    What overall process fails in LCAT deficiency (explaining the low HDL )?
    Back
    Reverse cholesterol transport — free cholesterol accumulates and cannot be returned to the liver.
  106. Front
    After LPL releases fatty acids, what is their fate in MUSCLE vs ADIPOSE tissue?
    Back
    In muscle they are oxidized for energy ; in adipose tissue they are re-esterified and stored.
  107. Front
    Why should chylomicrons and their remnants be virtually ABSENT from fasting plasma?
    Back
    They are produced only after a fatty meal and are rapidly cleared; if they persist in fasting plasma, something is wrong with LPL or apoCII .
  108. Front
    Why is high HDL cardioprotective (clinically 'good')?
    Back
    HDL runs reverse cholesterol transport — it extracts cholesterol from peripheral tissues and returns it to the liver for excretion as bile acids or neutral sterols.
  109. Front
    For which three cellular uses does LDL deliver cholesterol to peripheral tissues?
    Back
    Membrane synthesis , steroid hormone production, and bile acid synthesis.

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