Lipid metabolism and lipoproteins

34 Kerala MSc MLT Entrance practice questions on Lipid metabolism and lipoproteins, part of Biochemistry. The first 25 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

   Fatty acid synthase in the liver obtains most of its NADPH from:

   1. AThe citric acid (TCA) cycle
   2. BGlycolysis in the cytosol
   3. CBeta-oxidation of fatty acids in mitochondria
   4. DThe hexose monophosphate shunt

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   Answer: D · The hexose monophosphate shunt

   Each turn of fatty acid synthase uses two NADPH, so making palmitate needs 14. Most comes from glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase of the HMP shunt, with some from malic enzyme. This is why the shunt is very active in liver, adipose tissue and lactating mammary gland. Glycolysis, the TCA cycle and beta-oxidation produce NADH or FADH2, not NADPH.

   • A: The TCA cycle produces NADH and FADH2.
   • B: Glycolysis produces NADH, not NADPH.
   • C: Beta-oxidation is a catabolic pathway that produces NADH and FADH2.

2. Question 2 · Medium

   A fasting plasma shows a dense pre-beta band, a normal beta band and no band at the origin on agarose lipoprotein electrophoresis. Which Fredrickson type fits?

   1. AType V
   2. BType IV
   3. CType I
   4. DType IIa

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   Answer: B · Type IV

   On agarose at pH 8.6, HDL runs in the alpha position, VLDL in the pre-beta position, LDL in the beta position, and chylomicrons stay at the origin. A dense pre-beta band alone therefore means raised VLDL, which is Fredrickson type IV, the commonest pattern in obesity, diabetes and alcohol excess. Type V adds chylomicrons at the origin, and type I shows chylomicrons alone. Type IIa shows a dense beta band.

   • A: Type V shows chylomicrons at the origin as well as raised pre-beta.
   • C: Type I shows chylomicrons at the origin.
   • D: Type IIa shows a dense beta (LDL) band with normal pre-beta.

3. Question 3 · Hard

   A 35-year-old woman has corneal clouding, a mild normochromic anaemia with target cells, and proteinuria. HDL cholesterol is 6 mg/dL, triglyceride 260 mg/dL, and only 8% of her plasma cholesterol is esterified (usually about 70%). Her tonsils are normal. Which protein is most likely deficient?

   1. ACholesteryl ester transfer protein
   2. BLipoprotein lipase
   3. CLecithin-cholesterol acyltransferase
   4. DATP-binding cassette transporter A1

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   Answer: C · Lecithin-cholesterol acyltransferase

   Almost all cholesteryl ester in plasma is made by LCAT, which transfers a fatty acid from lecithin to cholesterol on HDL. A very low esterified fraction with very low HDL is therefore the key finding of familial LCAT deficiency. Free cholesterol deposits in the cornea, red cell membranes (target cells) and kidney, causing proteinuria. Tangier disease (ABCA1) also lowers HDL but leaves esterification normal and gives orange tonsils.

   • A: CETP deficiency raises HDL rather than lowering it.
   • B: Lipoprotein lipase deficiency causes very high triglyceride and does not stop esterification.
   • D: ABCA1 defects (Tangier disease) give orange tonsils and a normal esterified fraction.

4. Question 4 · Hard

   A 24-year-old man has aching muscles and red-brown urine after a day-long trek on little food. CK is 42,000 U/L (reference below 190), and the urine is positive for blood with no red cells. Short bursts of exercise never trouble him, and an ischaemic forearm test gives normal rises in lactate and ammonia. The most likely diagnosis is:

   1. AMyoadenylate deaminase deficiency
   2. BBecker muscular dystrophy
   3. CMcArdle disease
   4. DCPT II deficiency

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   Answer: D · CPT II deficiency

   Rhabdomyolysis after prolonged exercise with fasting, when muscle depends on fatty acids, is typical of carnitine palmitoyltransferase II deficiency, the commonest inherited fatty acid oxidation disorder in adults. The normal lactate rise shows that glycogen breakdown and glycolysis work, which excludes McArdle disease. The normal ammonia rise excludes myoadenylate deaminase deficiency. A muscular dystrophy would give a persistently raised CK and progressive weakness, not episodes.

   • A: Myoadenylate deaminase deficiency gives no rise in ammonia on the forearm test.
   • B: Becker dystrophy causes progressive weakness with a CK raised between episodes.
   • C: McArdle disease gives no lactate rise and symptoms early in intense exercise.

5. Question 5 · Easy

   Long-chain fatty acids cross the inner mitochondrial membrane for beta-oxidation bound to which carrier?

   1. ACoenzyme A
   2. BGlycerol 3-phosphate
   3. CCarnitine
   4. DAcyl carrier protein

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   Answer: C · Carnitine

   Fatty acyl-CoA formed in the cytosol cannot cross the inner mitochondrial membrane. Carnitine palmitoyltransferase I converts it to acylcarnitine, a translocase carries it across, and CPT II turns it back into acyl-CoA in the matrix. Defects in this shuttle cause hypoketotic hypoglycaemia or muscle breakdown. Short and medium-chain fatty acids enter without carnitine.

   • A: Acyl-CoA cannot cross the inner membrane itself; it is converted to acylcarnitine.
   • B: Glycerol 3-phosphate is used to make triglycerides, not to carry fatty acids.
   • D: Acyl carrier protein is part of fatty acid synthase in the cytosol.

6. Question 6 · Medium

   Statins reduce hepatic cholesterol synthesis. How does this mainly lower plasma LDL cholesterol?

   1. AIt blocks absorption of cholesterol from the gut
   2. BIt activates lipoprotein lipase in capillaries
   3. CIt increases loss of bile acids in the faeces
   4. DIt increases the number of hepatic LDL receptors

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7. Question 7 · Medium

   In X-linked adrenoleukodystrophy, very long-chain fatty acids such as C26:0 accumulate in plasma. Which pathway is defective?

   1. AAlpha-oxidation of phytanic acid
   2. BOmega-oxidation in microsomes
   3. CPeroxisomal beta-oxidation
   4. DMitochondrial beta-oxidation

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8. Question 8 · Medium

   After a carbohydrate-rich meal, beta-oxidation of fatty acids slows because malonyl-CoA inhibits:

   1. ABeta-ketoacyl-CoA thiolase
   2. BLipoprotein lipase
   3. CMedium-chain acyl-CoA dehydrogenase
   4. DCarnitine palmitoyltransferase I

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9. Question 9 · Hard

   Using 2.5 ATP per NADH, 1.5 per FADH2 and 10 per acetyl-CoA oxidised in the TCA cycle, what is the net ATP yield from complete oxidation of one molecule of stearic acid (C18:0)?

   1. A122
   2. B120
   3. C124
   4. D110

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10. Question 10 · Easy

    Citrate activates, and long-chain acyl-CoA inhibits, the enzyme that controls the rate of fatty acid synthesis. This enzyme is:

    1. AFatty acid synthase complex
    2. BAcetyl-CoA carboxylase
    3. CCarnitine palmitoyltransferase I
    4. DHMG-CoA synthase

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11. Question 11 · Medium

    Cholesteryl ester transfer protein (CETP) in plasma moves cholesteryl esters:

    1. AFrom HDL to VLDL and LDL in exchange for triglyceride
    2. BFrom cells to lipid-poor apo A-I
    3. CFrom chylomicrons directly into hepatocytes
    4. DFrom LDL to HDL in exchange for free cholesterol

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12. Question 12 · Easy

    Triglyceride made in the liver is secreted into the blood mainly in which lipoprotein?

    1. AVLDL
    2. BChylomicrons
    3. CLDL
    4. DIDL

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13. Question 13 · Easy

    Lipoprotein lipase on capillary endothelium must be activated by which apolipoprotein before it can hydrolyse chylomicron triglyceride?

    1. AApo C-II
    2. BApo A-II
    3. CApo C-III
    4. DApo B-48

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14. Question 14 · Hard

    A 38-year-old man has thickened Achilles tendons and arcus cornealis. Fasting results: total cholesterol 380 mg/dL, LDL 300 mg/dL, HDL 45 mg/dL, triglyceride 140 mg/dL; TSH, glucose and urine protein are normal. His father had a myocardial infarction at 44. Which defect is most likely?

    1. AAbsent lipoprotein lipase activity
    2. BIncreased apo A-I production
    3. CApo E2/E2 remnant accumulation
    4. DReduced LDL receptor function

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15. Question 15 · Hard

    A 52-year-old woman with weight gain, constipation and tiredness has total cholesterol 320 mg/dL, LDL 230 mg/dL and triglyceride 180 mg/dL. CK is 310 U/L (reference up to 170). Her doctor plans to start a statin. Which test should be checked first?

    1. ASerum TSH
    2. BApo E genotype
    3. CSerum lipase
    4. DLipoprotein(a)

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16. Question 16 · Medium

    A 19-year-old with fat malabsorption since infancy has acanthocytes on the smear, progressive ataxia and a serum cholesterol of 45 mg/dL. No apo B-containing lipoproteins are detected. Which defect is most likely?

    1. ALDL receptor
    2. BMicrosomal triglyceride transfer protein
    3. CLipoprotein lipase
    4. DATP-binding cassette transporter A1

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17. Question 17 · Hard

    A report from a referral laboratory gives serum triglyceride as 3.4 mmol/L. The clinician wants it in mg/dL. What is the value?

    1. A34 mg/dL
    2. B61 mg/dL
    3. C301 mg/dL
    4. D131 mg/dL

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18. Question 18 · Hard

    A 2-year-old with a 24-hour history of vomiting has a seizure. Blood glucose 32 mg/dL, urine ketones negative, ammonia mildly raised, and plasma acylcarnitine profile shows a marked rise in octanoylcarnitine (C8). Which treatment advice follows from the diagnosis?

    1. ARestrict dietary protein to lower ammonia
    2. BAvoid lactose and galactose for life
    3. CAvoid prolonged fasting and give glucose during illness
    4. DGive a high-fat ketogenic diet

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19. Question 19 · Medium

    A 12-hour fast is requested before a full lipid profile mainly because a recent meal:

    1. ADoubles the total cholesterol value
    2. BRaises triglyceride through chylomicrons
    3. CLowers HDL cholesterol for two days
    4. DInactivates the cholesterol esterase reagent

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20. Question 20 · Medium

    A plasma sample kept upright at 4 °C overnight shows a creamy layer on top over a turbid lower layer. Which lipoprotein pattern does this suggest?

    1. AExcess LDL alone, as in type IIa
    2. BExcess VLDL alone, as in type IV
    3. CChylomicrons with excess VLDL, as in type V
    4. DChylomicrons alone, as in type I

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21. Question 21 · Medium

    A child presents with fasting hypoglycaemia after a day of vomiting, with low urine ketones and C6-C10 dicarboxylic acids in urine. Which enzyme is most likely deficient?

    1. AGlucose-6-phosphatase
    2. BMedium-chain acyl-CoA dehydrogenase
    3. CHMG-CoA reductase
    4. DPyruvate carboxylase

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22. Question 22 · Easy

    Which apolipoprotein is made only in the intestine and marks a lipoprotein particle as a chylomicron or its remnant?

    1. AApo B-100
    2. BApo B-48
    3. CApo E
    4. DApo A-I

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23. Question 23 · Medium

    Lipoprotein(a) is a cardiovascular risk factor that is little affected by diet. Its distinctive structure is:

    1. AA chylomicron remnant carrying excess apo E
    2. BA small dense HDL rich in apo A-II
    3. CA VLDL particle that has lost all apo C
    4. DAn LDL-like particle with apo(a) bonded to apo B-100

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24. Question 24 · Medium

    Adrenaline release during fasting or stress increases the breakdown of stored triglyceride in adipose tissue mainly by:

    1. APhosphorylating hormone-sensitive lipase through protein kinase A
    2. BRaising lipoprotein lipase on adipose capillaries
    3. CInhibiting carnitine palmitoyltransferase I
    4. DStimulating acetyl-CoA carboxylase in adipocytes

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25. Question 25 · Hard

    A 6-year-old has recurrent abdominal pain and eruptive xanthomas on the buttocks. Fasting triglyceride is 2,400 mg/dL and cholesterol 260 mg/dL. Overnight refrigerated plasma shows a thick creamy layer over a clear infranatant. Post-heparin lipolytic activity is very low. What is the most likely diagnosis?

    1. ALipoprotein lipase deficiency
    2. BFamilial hypercholesterolaemia
    3. CFamilial hypertriglyceridaemia
    4. DFamilial dysbetalipoproteinaemia

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