Biochemistry - MCQ Practice Questions

Acetyl-CoA carboxylase catalyzes the formation of malonyl-CoA from acetyl-CoA, which is the first committed and rate-limiting step in fatty acid synthesis.

Most fatty acids undergo beta-oxidation in the mitochondrial matrix. However, very long chain fatty acids (>20 carbons) are initially oxidized in peroxisomes.

HDL mediates reverse cholesterol transport, removing excess cholesterol from peripheral tissues and transporting it to the liver for excretion. High HDL levels are protective against cardiovascular disease.

Linoleic acid and alpha-linolenic acid are essential fatty acids that cannot be synthesized by humans and must be obtained from dietary sources.

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.

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.

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.

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).

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.

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.

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.

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.

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.

Phospholipids have both hydrophilic (phosphate group) and hydrophobic (fatty acid chains) regions, making them amphipathic. This property allows them to spontaneously form bilayers in aqueous solutions, serving as the structural foundation of biological membranes.