MLT GlobeChemistry: Lipids – page 6
107 Chemistry MCQs on Lipids with answers and explanations.
Apolipoprotein E is important in lipid metabolism because it:
Apo E binds hepatic receptors (LDL receptor and LRP) so remnants are cleared. Apo(a), not apo E, binds apo B-100 in Lp(a).
A patient has cholesterol and triglycerides both near 400 mg/dL, palmar xanthomas and a broad beta band on lipoprotein electrophoresis. The most likely disorder is:
Type III results from defective remnant clearance, usually apo E2/E2, giving remnant accumulation seen as a broad beta band, with palmar xanthomas. Familial hypercholesterolemia raises LDL with normal triglycerides.
A lipemic plasma left overnight at 4 °C shows a creamy top layer over a turbid lower layer. Which lipoproteins are increased?
The creamy layer is chylomicrons and the turbid infranate is VLDL, the pattern of type V hyperlipoproteinemia. Chylomicrons alone leave a clear infranate.
A patient receiving intravenous glycerol-containing fluids has a markedly high triglyceride result by a routine enzymatic method. Why?
Enzymatic methods hydrolyse triglyceride and measure the released glycerol, so free glycerol falsely raises results unless a glycerol-blanked method is used.
The CDC reference method for LDL cholesterol (beta-quantification) is based on:
Ultracentrifugation at density 1.006 g/mL floats off VLDL; the bottom fraction is precipitated to remove LDL and Lp(a), leaving HDL. LDL cholesterol = bottom-fraction cholesterol − HDL cholesterol.
A sample with normal triglycerides shows an extra pre-beta band on lipoprotein electrophoresis. On ultracentrifugation it does not float with VLDL but sinks into the LDL density range. This band is most likely:
Lp(a) has pre-beta mobility but is denser than VLDL, so it is called 'sinking pre-beta'. Beta-VLDL of type III disease floats at density 1.006 and gives a broad beta band.
A child has tendon xanthomas and early atherosclerosis with only moderately raised cholesterol. Plasma sitosterol and other plant sterols are markedly high. The defect is in:
Sitosterolemia results from loss of ABCG5/ABCG8, which normally pump plant sterols from gut cells and liver into the gut lumen and bile. Plant sterols accumulate and cause xanthomas.