Lipoproteins and lipid metabolism

9 DOH Abu Dhabi (HAAD) lab licensing practice questions on Lipoproteins and lipid metabolism, part of Clinical Chemistry. The first 9 are below; the first 5 with answers and explanations (tap Show answer after you have chosen), the rest in Learn with a free account.

1. Question 1 · Medium

   As VLDL is metabolized, the conversion of IDL to LDL is completed mainly by:

   1. ALCAT
   2. BLipoprotein lipase
   3. CHepatic lipase
   4. DCETP

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   Answer: C · Hepatic lipase

   Lipoprotein lipase on capillary walls, activated by apo C-II, removes most of the triglyceride from VLDL and forms IDL. About half of IDL is taken up by the liver through apo E. The rest is acted on by hepatic lipase, which removes remaining triglyceride and phospholipid; apo E is lost, leaving cholesterol-rich LDL with apo B-100 alone. Low hepatic lipase activity lets IDL and remnants accumulate.

   • A: LCAT esterifies cholesterol on HDL.
   • B: Lipoprotein lipase acts mainly on chylomicrons and VLDL, forming remnants and IDL.
   • D: CETP exchanges lipids between lipoproteins but does not hydrolyze triglyceride.

2. Question 2 · Easy

   In the fasting plasma of a healthy adult, most of the cholesterol is carried in:

   1. ALDL
   2. BIDL
   3. CHDL
   4. DVLDL

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   Answer: A · LDL

   LDL carries about 60 to 70% of plasma cholesterol, mostly as cholesteryl ester. HDL carries about 20 to 30% and VLDL most of the rest, while chylomicrons are absent after a fast. This is why total cholesterol tracks LDL closely and why LDL is the main target of lipid-lowering treatment. LDL delivers cholesterol to tissues through the LDL receptor, which recognizes apo B-100.

   • B: IDL is a short-lived intermediate present at low levels.
   • C: HDL carries only about a quarter of plasma cholesterol.
   • D: VLDL carries mainly triglyceride and a small share of cholesterol.

3. Question 3 · Easy

   The rate-limiting enzyme of cholesterol synthesis, and the target of statins, is:

   1. AAcyl-CoA cholesterol acyltransferase
   2. BLecithin-cholesterol acyltransferase
   3. CHMG-CoA reductase
   4. DHMG-CoA synthase

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   Answer: C · HMG-CoA reductase

   HMG-CoA reductase converts HMG-CoA to mevalonate, the committed step of cholesterol synthesis. Statins inhibit it competitively, which lowers cholesterol inside liver cells. The cell responds by making more LDL receptors through the SREBP-2 pathway, so more LDL is cleared from the blood. This is why statins lower LDL cholesterol by 30 to 50% or more.

   • A: Acyl-CoA cholesterol acyltransferase esterifies cholesterol for storage inside cells.
   • B: Lecithin-cholesterol acyltransferase esterifies cholesterol on HDL in the plasma.
   • D: HMG-CoA synthase makes HMG-CoA, the step before; its mitochondrial form also makes ketones.

4. Question 4 · Easy

   Apolipoprotein B-48 is the main structural protein of:

   1. ALipoprotein(a)
   2. BChylomicrons
   3. CVLDL
   4. DIDL

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   Answer: B · Chylomicrons

   Apo B-48 is made only in the intestine and is needed to assemble chylomicrons from dietary fat. The liver makes the full-length apo B-100, which forms VLDL and stays with it as VLDL becomes IDL and then LDL. Each particle carries one apo B molecule for life, so apo B-48 marks intestinal particles and their remnants. Lipoprotein(a) is built on an LDL particle and also carries apo B-100.

   • A: Lipoprotein(a) is apo B-100 linked to apo(a).
   • C: VLDL is made in the liver and carries apo B-100.
   • D: IDL comes from VLDL and carries apo B-100.

5. Question 5 · Hard

   A 32-year-old man has corneal clouding, a normocytic anemia with target cells and proteinuria. HDL cholesterol is 0.12 mmol/L (5 mg/dL), and only about 10% of his plasma cholesterol is esterified (usual about 70%). Which defect is most likely?

   1. AAbetalipoproteinemia
   2. BTangier disease
   3. CLipoprotein lipase deficiency
   4. DFamilial LCAT deficiency

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   Answer: D · Familial LCAT deficiency

   LCAT, activated by apo A-I, esterifies free cholesterol on HDL using a fatty acid from lecithin. Without it, plasma cholesterol stays unesterified and HDL cannot mature, so HDL is very low. Free cholesterol deposits in the cornea, red cell membranes (target cells and mild hemolysis) and the kidney, where progressive renal disease is the main cause of illness. Partial LCAT deficiency (fish-eye disease) causes corneal clouding without the anemia and kidney disease.

   • A: Abetalipoproteinemia causes very low LDL and triglyceride, fat malabsorption and acanthocytes.
   • B: Tangier disease gives very low HDL with orange tonsils, but esterification in plasma is not this low.
   • C: Lipoprotein lipase deficiency causes very high triglyceride and pancreatitis.

6. Question 6 · Medium

   A raised apolipoprotein C-III concentration increases plasma triglyceride mainly by:

   1. AActivating lipoprotein lipase
   2. BActivating LCAT on HDL
   3. CInhibiting lipoprotein lipase
   4. DBinding the LDL receptor

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7. Question 7 · Easy

   On agarose lipoprotein electrophoresis, in which band does VLDL migrate?

   1. APre-beta
   2. BAlpha
   3. COrigin
   4. DBeta

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8. Question 8 · Medium

   PCSK9 inhibitor drugs lower LDL cholesterol. The normal action of PCSK9 that they block is:

   1. ATransferring cholesteryl ester from HDL to LDL
   2. BActivating HMG-CoA reductase in hepatocytes
   3. CInhibiting lipoprotein lipase on capillaries
   4. DDirecting LDL receptors to lysosomal breakdown

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9. Question 9 · Easy

   Which lipoprotein class has both the highest density and the highest protein content?

   1. ALDL
   2. BHDL
   3. CVLDL
   4. DChylomicrons

   Answer and explanation in LearnFree account