Lipid Metabolism Flashcards
Explain the role of lipoproteins in atherogenesis.
• Lipoproteins determine the atherogenicity
o By quantity (concentration) → number of LDL particles drives the disease
o By quality (by size) → LDL size modulates the risk Small dense lipoproteins:
o More particles
o Easier access into vessel wall
o Longer circulatory time
o Easily oxidized
o Predicted by low HDL-C and high TG levels
Components of CM
Density <0.95
Diameter: 75-300
90-96% TAG
Apoplipoproteins: B-48, E, C-II
Components of VLDL
Density: 0.95-1.006
Diameter: 30-80
60% TAG
Apolipoproteins: B-100, E, C-II
Components of IDL
Density: 1.006-1.019
Diameter: 23-35
Apolipoproteins: B-48, B-100, E
Components of LDL
Density: 1.019-1.063
Diameter: 18-25
50% Cholesterol
Apolipoproteins: B-100
Components of HDL
Density: 1.063-1.21
Diameter: 5-12
20% cholesterol
Apolipoproteins: A-I, A-II
Apo C-II
activates LPL
CM, VLDL
Apo B-48
Intestinal marker
CM, IDL
Apo B-100
Liver marker
VLDL, IDL, LDL
Apo E
Target for liver remnant receptor
CM, VLDL, IDL
Apo A-II
HDL marker
HDL
Explain the difference between “lipoproteins” and “lipids”
- Lipids = cholesterol, TAGs
- Lipids are surrogate markers for lipoproteins
- So “dyslipidemias” really represent “dyslipoproteinemia”
Friedewald equation
LDL-C = TC – HDL-C – (TG/5)
o Not accurate when assumptions break down:
• As TG levels increase since assuming TG/5 = VLDL-C
• So can’t use when TG > 400
• LDL-C includes IDL and Lp(a) cholesterol
• Misleadingly low when small LDL particle present
• Problem because LDL is main atherogenic lipoprotein!
Exogenous lipid metabolism
o CMs from gut
• Contain Apo B-48, Apo C, Apo E
• TG core undergoes lipolysis via LPL → CM-Remnant
• CM-Remnant cleared by liver
Endogenous lipid metabolism
o Liver produces VLDL
• Contain Apo B-100, Apo E, Apo C
• Lipolysis of TG core via LPL → IDL
o IDL can be shunted back to liver
o IDL can be further converted to LDL via HTGL
• LDL cleared by liver or deposited into tissues