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14.) Lipoproteins: structure, components, roles of apoproteins (apo A1, Apo B48 and apo B100, apo CII, apo E), metabolism of chylomicrons, VLDL, HDL. Increased LDL/HDL ratio as a risk factor for atherosclerosis. Deficiency/defects of LPL, apo CII, LDL receptor and apo B100 and their consequences.

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  1. Front
    Lipoproteins
    Back
    Particles that keep hydrophobic lipids soluble in blood and transport mainly triacylglycerols and cholesteryl esters
  2. Front
    General structure of a lipoprotein
    Back
    Hydrophobic core of TAG and cholesteryl esters surrounded by an amphipathic shell of phospholipids, free cholesterol, and apoproteins
  3. Front
    Major lipoproteins to know
    Back
    Chylomicrons, VLDL, LDL, and HDL
  4. Front
    Master map of lipoprotein function
    Back
    Chylomicrons carry dietary TAG, VLDL carries hepatic or endogenous TAG, LDL carries cholesterol to tissues, and HDL removes cholesterol from tissues and returns it to the liver
  5. Front
    Basic organization shared by all lipoproteins
    Back
    Neutral lipid core with an amphipathic surface shell
  6. Front
    Core of lipoproteins
    Back
    Triacylglycerols and cholesteryl esters
  7. Front
    Surface shell of lipoproteins
    Back
    Phospholipids, free cholesterol, and apoproteins
  8. Front
    High-yield lipoprotein structure summary
    Back
    Core is hydrophobic and surface is amphipathic
  9. Front
    Site of chylomicron assembly
    Back
    Intestinal mucosal cells or enterocytes
  10. Front
    Main job of chylomicrons
    Back
    Transport dietary triacylglycerols from intestine to other tissues
  11. Front
    Major integral apoprotein of nascent chylomicrons
    Back
    Apo B48
  12. Front
    Apoproteins acquired by chylomicrons in blood
    Back
    Apo CII and apo E
  13. Front
    Source of apo CII and apo E for chylomicrons
    Back
    HDL
  14. Front
    High-yield summary of chylomicrons
    Back
    Chylomicrons transport dietary TAG and apo B48 is the key structural apoprotein
  15. Front
    Site of VLDL production
    Back
    Liver
  16. Front
    Main lipid carried by VLDL
    Back
    Endogenous triacylglycerol made in the liver
  17. Front
    Main job of VLDL
    Back
    Carry hepatic TAG to peripheral tissues
  18. Front
    Major structural apoprotein of nascent VLDL
    Back
    Apo B100
  19. Front
    Apoproteins acquired by VLDL in plasma
    Back
    Apo CII and apo E
  20. Front
    Source of apo CII and apo E for VLDL
    Back
    HDL
  21. Front
    High-yield summary of VLDL
    Back
    VLDL transports liver TAG and apo B100 is its key structural apoprotein
  22. Front
    How LDL is formed
    Back
    VLDL loses TAG in circulation and becomes IDL and then LDL
  23. Front
    Relative composition of LDL
    Back
    Smaller, denser, and relatively cholesterol-rich
  24. Front
    Apoprotein retained by LDL
    Back
    Apo B100
  25. Front
    How LDL is taken up by tissues and liver
    Back
    Through the LDL receptor
  26. Front
    Ligand recognized by the LDL receptor on LDL
    Back
    Apo B100
  27. Front
    High-yield summary of LDL
    Back
    LDL delivers cholesterol to tissues and apo B100 is the LDL receptor ligand
  28. Front
    How HDL is formed
    Back
    By lipidation of apo A1 synthesized in liver and intestine
  29. Front
    Major apoprotein of HDL
    Back
    Apo A1
  30. Front
    Function of HDL as an apoprotein reservoir
    Back
    Provides apo CII and apo E to chylomicrons and VLDL
  31. Front
    Function of HDL in peripheral tissues
    Back
    Takes up cholesterol from peripheral tissues
  32. Front
    Enzyme that esterifies cholesterol on HDL
    Back
    LCAT
  33. Front
    Apoprotein that activates LCAT
    Back
    Apo A1
  34. Front
    Main transport role of HDL
    Back
    Reverse cholesterol transport back to the liver
  35. Front
    High-yield summary of HDL
    Back
    HDL is the good cholesterol carrier, apo A1 is its major apoprotein, and apo A1 activates LCAT
  36. Front
    Apo A1
    Back
    Major apoprotein of HDL synthesized in liver and intestine that activates LCAT and is important in reverse cholesterol transport
  37. Front
    Apo B48
    Back
    Structural apoprotein of chylomicrons produced in enterocytes and required for chylomicron assembly
  38. Front
    Apo B100
    Back
    Structural apoprotein of VLDL that remains on IDL and LDL and serves as the ligand for the LDL receptor
  39. Front
    Apo CII
    Back
    Apoprotein transferred from HDL to chylomicrons and VLDL that activates lipoprotein lipase
  40. Front
    Apo E
    Back
    Apoprotein transferred from HDL to chylomicrons and VLDL that is important for receptor-mediated uptake of chylomicron remnants and IDL
  41. Front
    Clean apoprotein associations
    Back
    Apo A1 activates LCAT on HDL, apo B48 is the chylomicron structural protein, apo B100 is the VLDL/IDL/LDL structural protein and LDL receptor ligand, apo CII activates LPL, and apo E mediates remnant and IDL uptake by liver
  42. Front
    First step of chylomicron metabolism
    Back
    Chylomicrons are assembled in enterocytes from dietary lipids
  43. Front
    Route of newly formed chylomicrons
    Back
    They enter the lymphatic system and then the blood
  44. Front
    Apoproteins chylomicrons receive in blood
    Back
    Apo CII and apo E from HDL
  45. Front
    What activates LPL during chylomicron metabolism
    Back
    Apo CII
  46. Front
    What LPL does to chylomicrons
    Back
    Hydrolyzes chylomicron TAG to fatty acids and glycerol
  47. Front
    Fate of fatty acids released from chylomicrons
    Back
    Go to adipose tissue for storage or muscle for energy
  48. Front
    What happens to apo CII after chylomicron TAG removal
    Back
    It returns to HDL
  49. Front
    Fate of chylomicron remnants
    Back
    Taken up by the liver
  50. Front
    Apoprotein required for chylomicron remnant uptake
    Back
    Apo E
  51. Front
    High-yield chylomicron metabolism summary
    Back
    Chylomicron remnant uptake depends on apo E, and TAG hydrolysis depends on apo CII plus LPL
  52. Front
    First step of VLDL metabolism
    Back
    VLDL is secreted by the liver as a nascent particle containing apo B100
  53. Front
    Apoproteins VLDL receives in plasma
    Back
    Apo CII and apo E from HDL
  54. Front
    What LPL does to VLDL
    Back
    Hydrolyzes its TAG in peripheral tissues
  55. Front
    Sequence of VLDL conversion
    Back
    VLDL → IDL → LDL
  56. Front
    What happens to apo CII and apo E during VLDL metabolism
    Back
    They are returned to HDL
  57. Front
    Apoprotein retained by LDL after VLDL metabolism
    Back
    Apo B100
  58. Front
    Alternative fate of IDL
    Back
    Some IDL is taken up by the liver using apo E
  59. Front
    High-yield VLDL metabolism summary
    Back
    VLDL carries liver TAG and LDL is its downstream cholesterol-rich product
  60. Front
    First stage of HDL metabolism
    Back
    HDL begins as lipid-poor or nascent particles based on apo A1
  61. Front
    What nascent HDL does
    Back
    Takes up cholesterol from peripheral tissues
  62. Front
    Role of LCAT in HDL metabolism
    Back
    Esterifies cholesterol on HDL
  63. Front
    Maturation sequence of HDL
    Back
    Nascent HDL → HDL3 → HDL2
  64. Front
    Possible fates of cholesteryl esters in HDL
    Back
    Delivered to the liver or transferred to VLDL in exchange for TAG via CETP
  65. Front
    Liver uptake receptor for HDL cholesteryl esters
    Back
    SR-B1
  66. Front
    High-yield HDL metabolism summary
    Back
    HDL performs reverse cholesterol transport and is therefore protective against atherosclerosis
  67. Front
    Why LDL/HDL ratio matters in atherosclerosis
    Back
    LDL drives cholesterol delivery into tissues and plaque formation, whereas HDL removes cholesterol from tissues and returns it to the liver
  68. Front
    Primary cause of atherosclerosis
    Back
    LDL cholesterol
  69. Front
    How oxidized LDL promotes atherosclerosis
    Back
    Modified or oxidized LDL is taken up by macrophage scavenger receptors
  70. Front
    What happens to macrophages after taking up oxidized LDL
    Back
    They accumulate cholesteryl esters and become foam cells
  71. Front
    Role of foam cells in atherosclerosis
    Back
    Foam cells contribute to atherosclerotic plaque
  72. Front
    Why HDL is protective against atherosclerosis
    Back
    It promotes reverse cholesterol transport from peripheral tissues to the liver
  73. Front
    High-yield LDL/HDL risk sentence
    Back
    High LDL and low HDL increase atherosclerosis risk because LDL drives plaque formation while HDL promotes reverse cholesterol transport
  74. Front
    Mechanism of LPL deficiency
    Back
    LPL cannot hydrolyze TAG in chylomicrons and VLDL
  75. Front
    Mechanism of apo CII deficiency
    Back
    LPL cannot be activated normally
  76. Front
    Shared consequence of LPL deficiency and apo CII deficiency
    Back
    TAG-rich lipoproteins cannot be cleared normally
  77. Front
    Main plasma abnormality in LPL or apo CII deficiency
    Back
    Dramatic accumulation of chylomicrons in plasma even in the fasted state
  78. Front
    Type of hyperlipoproteinemia caused by LPL or apo CII deficiency
    Back
    Type I hyperlipoproteinemia or familial chylomicronemia
  79. Front
    Main lipid abnormality in familial chylomicronemia
    Back
    Severe hypertriglyceridemia
  80. Front
    Major clinical risk in familial chylomicronemia
    Back
    Acute pancreatitis
  81. Front
    High-yield disease summary for LPL and apo CII deficiency
    Back
    LPL deficiency and apo CII deficiency both cause familial chylomicronemia with severe hypertriglyceridemia
  82. Front
    Normal role of LDL receptors
    Back
    Mediate uptake of LDL by recognizing apo B100
  83. Front
    Effect of LDL receptor defect
    Back
    LDL cannot be cleared efficiently
  84. Front
    Type of hyperlipoproteinemia caused by LDL receptor defect
    Back
    Type IIa hyperlipoproteinemia or familial hypercholesterolemia
  85. Front
    Main lipid abnormality in familial hypercholesterolemia
    Back
    Markedly increased LDL cholesterol
  86. Front
    Major clinical consequence of familial hypercholesterolemia
    Back
    Premature atherosclerosis
  87. Front
    High-yield LDL receptor defect summary
    Back
    LDL receptor defect causes familial hypercholesterolemia with high LDL and early atherosclerosis
  88. Front
    Role of apo B100 in LDL metabolism
    Back
    Apo B100 is the ligand for the LDL receptor
  89. Front
    Effect of apo B100 defect on LDL binding
    Back
    LDL binds poorly to the LDL receptor
  90. Front
    Effect of apo B100 defect on LDL clearance
    Back
    LDL clearance falls
  91. Front
    Clinical consequence of apo B100 defect
    Back
    Elevated circulating LDL with increased risk of hypercholesterolemia and atherosclerosis
  92. Front
    High-yield apo B100 defect summary
    Back
    Defective apo B100 behaves like impaired LDL receptor recognition
  93. Front
    Clean disease comparison for LPL deficiency
    Back
    Cannot hydrolyze chylomicron or VLDL TAG, causing severe hypertriglyceridemia, familial chylomicronemia, and pancreatitis risk
  94. Front
    Clean disease comparison for apo CII deficiency
    Back
    LPL is not activated, producing a picture similar to LPL deficiency with severe chylomicron accumulation and hypertriglyceridemia
  95. Front
    Clean disease comparison for LDL receptor defect
    Back
    Poor LDL clearance causes familial hypercholesterolemia with high LDL and premature atherosclerosis
  96. Front
    Clean disease comparison for apo B100 defect
    Back
    Poor LDL receptor binding impairs LDL uptake and increases hypercholesterolemia and atherosclerosis risk
  97. Front
    Super high-yield distinction for chylomicrons and VLDL
    Back
    Chylomicrons transport dietary TAG, whereas VLDL transports hepatic TAG
  98. Front
    Super high-yield distinction for apo B48 and apo B100
    Back
    Chylomicrons use apo B48, whereas VLDL and LDL use apo B100
  99. Front
    Super high-yield fact about apo CII
    Back
    Apo CII activates LPL
  100. Front
    Super high-yield fact about apo E
    Back
    Apo E mediates hepatic uptake of chylomicron remnants and IDL
  101. Front
    Super high-yield fact about apo A1
    Back
    Apo A1 activates LCAT on HDL
  102. Front
    Super high-yield fact about LDL receptor
    Back
    The LDL receptor recognizes apo B100 on LDL
  103. Front
    Super high-yield fact about HDL as apoprotein donor
    Back
    HDL supplies apo CII and apo E to chylomicrons and VLDL
  104. Front
    Super high-yield fact about HDL and atherosclerosis
    Back
    HDL performs reverse cholesterol transport, so low HDL is a risk factor for atherosclerosis
  105. Front
    Super high-yield fact about LDL cholesterol
    Back
    LDL-C is the primary cause of atherosclerosis
  106. Front
    Super high-yield fact about familial chylomicronemia
    Back
    LPL or apo CII deficiency causes familial chylomicronemia
  107. Front
    Super high-yield fact about familial hypercholesterolemia
    Back
    LDL receptor defect causes familial hypercholesterolemia
  108. Front
    Cheat-sheet lipoprotein structure
    Back
    Core contains TAG and cholesteryl esters, whereas shell contains phospholipids, free cholesterol, and apoproteins
  109. Front
    Cheat-sheet main lipoprotein particles
    Back
    Chylomicrons carry dietary TAG and use apo B48, VLDL carries liver TAG and uses apo B100, LDL delivers cholesterol and uses apo B100, and HDL performs reverse cholesterol transport with apo A1
  110. Front
    Cheat-sheet apoproteins
    Back
    Apo A1 activates LCAT, apo B48 is the chylomicron structural protein, apo B100 is the VLDL/LDL structural protein and LDL receptor ligand, apo CII activates LPL, and apo E mediates remnant and IDL uptake by liver
  111. Front
    Cheat-sheet chylomicron metabolism
    Back
    Chylomicrons are formed in intestine, receive apo CII and apo E from HDL, have TAG hydrolyzed by LPL, and remnants are taken up by liver via apo E
  112. Front
    Cheat-sheet VLDL metabolism
    Back
    VLDL is formed in liver, receives apo CII and apo E from HDL, has TAG removed by LPL, and becomes IDL then LDL
  113. Front
    Cheat-sheet HDL metabolism
    Back
    HDL forms from apo A1, gives apo CII and apo E, collects cholesterol from tissues, apo A1 activates LCAT, and HDL returns cholesterol to the liver
  114. Front
    Cheat-sheet disease association for LPL or apo CII deficiency
    Back
    Familial chylomicronemia with severe hypertriglyceridemia and pancreatitis
  115. Front
    Cheat-sheet disease association for LDL receptor defect
    Back
    Familial hypercholesterolemia with high LDL
  116. Front
    Cheat-sheet disease association for apo B100 defect
    Back
    Poor LDL receptor binding with high LDL

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