Biochemistry - MCQ Practice Questions

HMG-CoA reductase catalyzes the conversion of HMG-CoA to mevalonate and is the rate-limiting step in cholesterol biosynthesis. It is inhibited by statins.

Cholesterol molecules insert between phospholipids in the bilayer, regulating membrane fluidity. At high temperatures, it reduces fluidity; at low temperatures, it increases it.

Lipoproteins are organized with a hydrophobic lipid core (cholesterol esters and triglycerides) surrounded by a hydrophilic shell of proteins, free cholesterol, and phospholipids.

Familial hypercholesterolemia results from mutations in the LDL receptor gene, leading to impaired LDL uptake and elevated plasma LDL cholesterol levels.

During fasting, the liver increases synthesis and secretion of VLDL to transport endogenous triglycerides produced from gluconeogenesis and fatty acid oxidation.

LCAT esterifies free cholesterol on lipoprotein surfaces, forming cholesterol esters that move to the hydrophobic core. This process is essential for lipoprotein maturation.

ApoE acts as a ligand recognized by hepatic receptors (LDL receptor and LDL receptor-related protein), mediating the uptake of chylomicron remnants and VLDL remnants.

Niemann-Pick disease results from deficiency of sphingomyelinase, leading to accumulation of sphingomyelin in lysosomes, particularly affecting the nervous system and liver.

Saturated fatty acids have higher melting points and are typically solid at room temperature due to tight packing. They are more stable and less prone to oxidation than unsaturated fatty acids.

Approximately 70-80% of body cholesterol is synthesized de novo, primarily in the liver. The remaining 20-30% comes from dietary sources.

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.

LDL carries cholesterol into arterial walls and can be oxidized, promoting atherosclerosis. HDL mediates reverse cholesterol transport, removing cholesterol from tissues and delivering it to the liver.

Myelin contains approximately 80% lipid by weight, with cholesterol being the most abundant lipid (27% of total myelin mass), followed by galactocerebroside.

Deficiency of lipoprotein lipase or its cofactor apoC-II results in severe hypertriglyceridemia with elevated chylomicrons and VLDL but relatively normal LDL levels.

Acetoacetate is the first ketone body formed from two molecules of Acetyl-CoA via HMG-CoA synthase. It can be reduced to beta-hydroxybutyrate or decarboxylated to acetone.

Carnitine, via carnitine palmitoyltransferase (CPT), transfers long-chain fatty acyl groups across the inner mitochondrial membrane, enabling their oxidation in the matrix.

Severe hypertriglyceridemia (>1000 mg/dL) significantly increases the risk of acute pancreatitis due to pancreatic inflammation caused by triglyceride-rich lipoproteins.

Prostaglandins are eicosanoids derived from arachidonic acid (20-carbon polyunsaturated fatty acid). They act as paracrine and autocrine signaling molecules.