Biochemistry - MCQ Practice Questions

VLDL triglyceride content increases during increased hepatic triglyceride synthesis (fed state, fatty liver). HDL is the smallest and most dense; chylomicrons have the lowest protein percentage; LDL particle size varies (pattern A = large, pattern B = small and dense).

Severe hypertriglyceridemia with eruptive xanthomas and lipemia retinalis indicates predominantly elevated chylomicrons and/or VLDL. This is seen in Type I (lipoprotein lipase deficiency), Type IV (VLDL overproduction), or Type V hyperlipoproteinemia.

Sterol 7-alpha-hydroxylase catalyzes the first committed step of bile acid synthesis, forming 7-alpha-hydroxycholesterol from cholesterol. This is the rate-limiting step and is regulated by feedback inhibition by bile acids and activation by cholesterol.

Dietary cholesterol intake inversely affects endogenous cholesterol synthesis through feedback inhibition of HMG-CoA reductase. However, saturated and trans fats have a greater impact on LDL cholesterol than dietary cholesterol itself. Genetic factors are the primary determinant of serum cholesterol.

Gaucher disease is caused by deficiency of glucocerebrosidase (beta-glucosidase), leading to accumulation of glucocerebroside in macrophages of the reticuloendothelial system. Type 1 is the non-neuronopathic form with hepatosplenomegaly; Type 2 and 3 involve CNS involvement.

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.

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

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.

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.