Biochemistry - MCQ Practice Questions

Beta-oxidation is the catabolic pathway that breaks down fatty acids in the mitochondria, producing acetyl-CoA which enters the Krebs cycle for ATP production.

High cholesterol, particularly LDL cholesterol, can accumulate in artery walls forming atherosclerotic plaques, leading to arterial narrowing (atherosclerosis) and increased risk of heart disease.

Familial hypercholesterolemia is caused by mutations in the LDL receptor gene, preventing cells from taking up LDL particles, resulting in elevated blood cholesterol levels.

HMG-CoA reductase catalyzes the conversion of HMG-CoA to mevalonate, the rate-limiting and key regulatory step in cholesterol biosynthesis. It is targeted by statin drugs.

Phospholipids have a glycerol backbone with two fatty acids and a phosphate group, making them amphipathic. This structure is crucial for membrane formation.

Excessive dietary saturated fat increases liver production of VLDL, which carries triglycerides and cholesterol. VLDL is converted to LDL in circulation, raising LDL levels.

Cortisol and other corticosteroids are synthesized from cholesterol in the adrenal cortex through a series of enzymatic reactions involving cytochrome P450 enzymes.

The liver is the primary site of lipogenesis, where excess carbohydrates and amino acids are converted to fatty acids and triglycerides for storage and export via VLDL.

AMPK phosphorylates and inactivates acetyl-CoA carboxylase during energy stress (high AMP/ATP ratio), thereby reducing fatty acid synthesis. Citrate and insulin activate the enzyme.

Familial hypercholesterolemia presents with xanthomas due to defective LDL receptors. Type II hyperlipoproteinemia (IIa) is essentially familial hypercholesterolemia with elevated LDL. Both terms describe the same condition in this clinical context.

HDL has approximately 50% protein content, the highest among all lipoproteins. Chylomicrons and VLDL are triglyceride-rich lipoproteins with lower protein ratios.

Ketone bodies (acetoacetate, beta-hydroxybutyrate, and acetone) are synthesized primarily in the liver mitochondria during periods of high fatty acid oxidation.

ApoB-100 is essential for the structural integrity and secretion of VLDL and LDL particles. It remains with these particles throughout their metabolism.

Niemann-Pick Type C results from mutations in NPC1 or NPC2 genes, which encode lysosomal cholesterol transporters, leading to lysosomal accumulation of cholesterol and sphingolipids.

Insulin activates mTORC1, which promotes protein synthesis and lipogenesis. It also increases acetyl-CoA carboxylase activity, promoting fatty acid synthesis from carbohydrate sources.

LCAT is synthesized primarily in the liver and, to a lesser extent, in other tissues. It plays a crucial role in HDL remodeling by converting free cholesterol to cholesterol esters.

Familial hypercholesterolemia results from defective LDL receptors, leading to severely elevated LDL cholesterol (200-1000 mg/dL). This causes premature atherosclerosis, xanthomas, and corneal arcus. The defect prevents normal clearance of LDL from circulation.

Palmitate (16 carbons) undergoes 7 cycles of beta-oxidation (n/2 - 1), each producing one acetyl-CoA. The final cycle releases 2 acetyl-CoA molecules, totaling 8 acetyl-CoA. Each 2-carbon unit is released as acetyl-CoA.

Niemann-Pick disease Type A is caused by deficiency of acid sphingomyelinase, leading to accumulation of sphingomyelin and cholesterol in lysosomes of various tissues, particularly the CNS, liver, and spleen. It presents with hepatosplenomegaly and neurological deterioration.

The E4/E4 genotype carries the highest genetic risk for late-onset Alzheimer's disease. ApoE4 is less efficient at clearing amyloid-beta and is associated with increased neuroinflammation. E4 carriers show earlier cognitive decline compared to E2 and E3 carriers.