A clinical test shows high triglycerides and low HDL cholesterol. What metabolic condition might be indicated?
Answer: B
High triglycerides with low HDL is characteristic of metabolic syndrome, often associated with insulin resistance, obesity, and increased cardiovascular risk.
Q.2Hard
In the mobilization of fatty acids from adipose tissue, which hormone plays the primary regulatory role?
Answer: B
Epinephrine and glucagon activate hormone-sensitive lipase via cAMP signaling in adipose tissue, promoting lipolysis and release of free fatty acids during fasting or stress.
Q.3Hard
Which of the following conditions results from deficiency of lipoprotein lipase?
Answer: A
Lipoprotein lipase deficiency causes Type I hyperlipoproteinemia with severe accumulation of chylomicrons and triglycerides (>1000 mg/dL), risk of acute pancreatitis.
Q.4Hard
What is the net ATP yield from complete oxidation of one molecule of a 16-carbon saturated fatty acid (palmitate)?
Answer: B
Palmitate (C16) undergoes 7 cycles of beta-oxidation producing 8 acetyl-CoA molecules, 7 FADH2, and 7 NADH. Total ATP yield is approximately 129 ATP (accounting for initial activation cost).
Q.5Hard
Apolipoproteins serve multiple functions in lipid transport. Which apolipoprotein is most important for HDL maturation and cholesterol efflux?
Answer: B
ApoA-I is the major apolipoprotein of HDL, essential for LCAT activation and cholesterol esterification, promoting reverse cholesterol transport and HDL maturation.
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Q.6Hard
In the synthesis of eicosanoids, what is the first critical step?
Answer: B
Eicosanoid synthesis begins with phospholipase A2-mediated release of arachidonic acid (C20 polyunsaturated fatty acid) from membrane phospholipids, which then serves as substrate for COX and LOX pathways.
Q.7Hard
A 45-year-old patient presents with xanthomas and corneal arcus. Which lipid abnormality is most consistent with these clinical signs?
Answer: B
Xanthomas (lipid deposits in skin and tendons) and corneal arcus (lipid deposition in cornea) are hallmark signs of severe hypercholesterolemia, typically with very high LDL cholesterol levels.
Q.8Hard
Which of the following correctly describes the relationship between LDL particle size and cardiovascular risk?
Answer: A
Small, dense LDL particles (Pattern B) are more atherogenic because they penetrate arterial walls more easily, are more susceptible to oxidation, and have reduced hepatic clearance compared to large, buoyant LDL particles.
Q.9Hard
A patient with Tangier disease shows extremely low HDL levels (<5 mg/dL). This condition results from defective:
Answer: B
Tangier disease results from mutations in ABCA1 gene, which encodes an ATP-binding cassette transporter essential for HDL biogenesis. This leads to severe HDL deficiency and cholesterol accumulation in tissues.
Q.10Hard
In the carnitine shuttle system, carnitine palmitoyltransferase I (CPT-I) is inhibited by:
Answer: B
CPT-I is allosterically inhibited by malonyl-CoA, a key regulatory point linking fatty acid synthesis (high during fed state) with fatty acid oxidation (low during fed state).
Q.11Hard
Which of the following conditions would result in elevated levels of lipoprotein(a) (Lp(a))?
Answer: B
Lp(a) levels are primarily determined by genetic factors (LPA gene polymorphisms) and are elevated in chronic kidney disease due to reduced catabolism. Lp(a) is an independent cardiovascular risk factor.
Q.12Hard
A 50-year-old female with hypothyroidism presents with elevated cholesterol. Which mechanism explains the increased cholesterol in hypothyroidism?
Answer: D
Thyroid hormones upregulate LDL receptors and also inhibit HMG-CoA reductase. In hypothyroidism, all these effects are reversed, leading to increased cholesterol levels through multiple mechanisms.
Q.13Hard
The oxidative stress marker oxidized LDL (oxLDL) primarily activates which receptor to promote foam cell formation?
Answer: B
OxLDL is recognized by scavenger receptors (SR-A and LOX-1) on macrophages, not by the classical LDL receptor. This leads to unregulated cholesterol uptake and foam cell formation in atherosclerosis.
Q.14Hard
In Type III hyperlipoproteinemia (Familial Dysbetalipoproteinemia), the primary defect involves:
Answer: A
Type III hyperlipoproteinemia results from apoE2 homozygosity combined with another genetic or environmental factor. ApoE2 has reduced affinity for lipoprotein receptors, impairing remnant particle clearance.
Q.15Hard
A patient with primary biliary cholangitis shows elevated cholestanol levels. Which enzyme defect is most likely responsible?
Answer: B
Sterol 27-hydroxylase catalyzes the side-chain oxidation of cholesterol to form bile acid precursors. Its deficiency or dysfunction leads to cholestanol accumulation and neuropathy. Elevated cholestanol is a characteristic finding in sterol 27-hydroxylase deficiency.
Q.16Hard
During the fed state, acetyl-CoA carboxylase (ACC) is activated by which mechanism?
Answer: D
In the fed state, high citrate levels allosterically activate ACC, and insulin signaling causes PKB/Akt to phosphorylate and activate ACC. This promotes fatty acid synthesis. Conversely, AMPK phosphorylation inactivates ACC during energy deprivation.
Q.17Hard
A deficiency of apolipoprotein B-48 synthesis would primarily affect which lipid transport pathway?
Answer: B
ApoB-48 is the truncated form of apoB synthesized in intestinal enterocytes and is essential for chylomicron assembly and secretion. Its deficiency causes abetalipoproteinemia, characterized by fat malabsorption and severe deficiency of fat-soluble vitamins.
Q.18Hard
A 35-year-old patient with atherosclerosis has normal LDL cholesterol but elevated lipoprotein(a). Which genetic polymorphism is primarily responsible for high Lp(a) levels?
Answer: B
Lipoprotein(a) levels are predominantly determined by genetic variations in the LPA gene, which encodes apolipoprotein(a). Smaller isoforms are associated with higher plasma Lp(a) levels and increased cardiovascular risk, independent of LDL cholesterol levels.
Q.19Hard
A patient presents with neurodegenerative symptoms, progressive neuropathy, and xanthomas. Plasma cholestanol and cholestane-3-beta,5-alpha,6-beta-triol levels are markedly elevated. Which genetic defect is most likely?
Answer: B
CYP27A1 mutations cause cerebrotendinous xanthomatosis (CTX), characterized by elevated cholestanol and cholestane triol precursors due to impaired side-chain oxidation of cholesterol. This leads to progressive neurological deterioration, cataracts, and diarrhea. Chenodeoxycholic acid therapy is beneficial.
Q.20Hard
Tangier disease is associated with deficiency of which protein?
Answer: B
Tangier disease results from mutations in the ABCA1 gene, which encodes a cholesterol transporter. This leads to severe HDL deficiency and accumulation of cholesterol esters in tissues.
