Free ASCP MLS Biochemistry Mock Test: Part 49 – Lipids, Lipoproteins & Cholesterol Metabolism Practice Exam

This is the key structural difference that defines a phospholipid.

• A triglyceride is composed of a glycerol backbone and three fatty acids.

• A phospholipid is composed of a glycerol backbone, two fatty acids, a phosphate group, and usually a nitrogen-containing base (such as choline or ethanolamine) or another polar head group attached to the phosphate.

This structure gives phospholipids their amphipathic nature (having both hydrophilic and hydrophobic regions), which is essential for their role as the primary building blocks of cellular membranes.

The other options are incorrect:

• b) Three fatty acids: This describes a triglyceride.

• c) Only one fatty acid: This is not a standard structure for major phospholipids or triglycerides.

• d) A carbohydrate chain: This describes glycolipids, not phospholipids.

In lipoprotein electrophoresis, the distance a particle migrates is determined by its size and charge. Chylomicrons are the largest and least charged lipoprotein particles. Due to their massive size and low net charge, they migrate the least and remain closest to the origin (the point of application on the gel).

The other lipoproteins migrate further:

• c) VLDL: Migrates to the pre-beta region.

• b) LDL: Migrates to the beta region.

• a) HDL: Migrates the farthest, to the alpha region.

• The major ketone bodies produced during ketogenesis are:

  1. Acetoacetate

  2. Beta-hydroxybutyrate

  3. Acetone (minor, volatile)

• Pyruvate is a glycolytic intermediate, not a ketone body. It can be converted to acetyl-CoA, which may then enter ketogenesis, but pyruvate itself is not classified as a ketone body.

A triglyceride is formed through a dehydration synthesis reaction between one molecule of glycerol and three molecules of fatty acids. This structure makes triglycerides the main form of stored energy in the body.

The other options describe different types of molecules:

• b) Glycerol and one phosphate group: This describes the backbone of a phosphoglyceride, which is a type of phospholipid (not a triglyceride).

• c) Three glucose molecules: This would form a trisaccharide, a type of carbohydrate.

• d) Two fatty acids and one amino group: This is not a standard structure for a major lipid class.

• Lipids are primarily composed of fatty acids and glycerol (in triglycerides) or other backbones (like sphingosine in sphingolipids).

• Fatty acids: long hydrocarbon chains with a terminal carboxyl group, serving as the building blocks for most lipids.

Other options:

• Amino acids → building blocks of proteins

• Monosaccharides → building blocks of carbohydrates

• Nucleotides → building blocks of nucleic acids (DNA/RNA)

HDL (High-Density Lipoprotein) is responsible for reverse cholesterol transport. This is the process of picking up excess cholesterol from peripheral tissues (including the walls of arteries) and transporting it back to the liver for excretion or re-use.

Other options:

• a) Chylomicrons: Transport dietary lipids from the intestine to peripheral tissues and the liver.

• b) VLDL (Very-Low-Density Lipoprotein): Transport endogenous triglycerides from the liver to peripheral tissues.

• c) LDL (Low-Density Lipoprotein): Delivers cholesterol to peripheral tissues and is the main cholesterol carrier in the blood.

• Prominent chylomicrons in fasting serum indicate type I hyperlipoproteinemia (Familial LPL deficiency).

• Lipoprotein Lipase (LPL) deficiency → impaired hydrolysis of triglycerides in chylomicrons → accumulation of chylomicrons, causing:

  • Lipemic serum

  • Recurrent abdominal pain (from pancreatitis)

  • Eruptive xanthomas in some cases

Other options:

• LDL receptor deficiency → leads to elevated LDL, not chylomicrons (type IIa hyperlipoproteinemia).

• Apo A-I deficiency → affects HDL formation; low HDL, not chylomicrons.

• Hepatic triglyceride lipase deficiency → affects VLDL and HDL metabolism; chylomicrons usually normal.

Lipoprotein lipase (LPL) is often referred to as the “clearance factor” for triglycerides. It is the key enzyme responsible for hydrolyzing (breaking down) the core triglycerides in chylomicrons and VLDL, allowing fatty acids to be taken up by tissues for energy use or storage. This action clears triglyceride-rich lipoproteins from the plasma.

The other options are incorrect:

• a) HDL: Involved in reverse cholesterol transport, not triglyceride clearance.

• b) LDL: Delivers cholesterol to peripheral tissues and is not involved in triglyceride metabolism.

• d) Acetyl-CoA: A metabolic intermediate, not an enzyme that clears triglycerides from plasma.

• Triglyceride levels are highly affected by recent food intake because chylomicrons from dietary fat enter the bloodstream postprandially.

• Fasting 12–14 hours ensures:

  • Chylomicrons are cleared

  • Triglyceride measurement reflects the baseline (fasting) metabolic state

• Other tests:

  • Serum sodium → not significantly affected by fasting

  • Total cholesterol → minimally affected by meals

  • LD (Lactate Dehydrogenase) → unaffected by fasting

HMG-CoA reductase is the primary rate-limiting enzyme in the cholesterol biosynthesis pathway. It catalyzes the conversion of HMG-CoA to mevalonate, which is the committed and most highly regulated step in the pathway. This enzyme is the target of statin drugs, which are used to lower cholesterol levels.

The other enzymes have different roles:

• b) Acetyl-CoA carboxylase: This is the rate-limiting enzyme in fatty acid synthesis.

• c) Lipase: This is a general term for enzymes that break down lipids (e.g., triglyceride lipase, lipoprotein lipase).

• d) G6PD (Glucose-6-phosphate dehydrogenase): This is the rate-limiting enzyme in the pentose phosphate pathway.

• Reverse cholesterol transport is the process by which cholesterol is removed from peripheral tissues and transported back to the liver for excretion or recycling.

• HDL (High-Density Lipoprotein) is the main mediator:

  • Collects cholesterol from tissues and atherosclerotic plaques

  • Transfers cholesterol to the liver either directly or via transfer to other lipoproteins

Other lipoproteins:

• Chylomicrons → transport dietary triglycerides

• VLDL → transport endogenous triglycerides from the liver

• LDL → delivers cholesterol to tissues, not away from them

Chylomicrons are the specific lipoprotein particles responsible for transporting dietary lipids (exogenous triglycerides and cholesterol) from the small intestine into the bloodstream and lymphatic system.

The other lipoproteins have different primary transport functions:

• a) LDL (Low-Density Lipoprotein): Transports endogenous cholesterol from the liver to peripheral tissues.

• b) HDL (High-Density Lipoprotein): Transports cholesterol from peripheral tissues back to the liver (reverse cholesterol transport).

• d) VLDL (Very-Low-Density Lipoprotein): Transports endogenous triglycerides synthesized in the liver to peripheral tissues.

Low-Density Lipoprotein (LDL) carries the majority (60-75%) of the total cholesterol in the bloodstream. This is why LDL cholesterol is often referred to as “bad cholesterol,” as high levels are directly associated with an increased risk of atherosclerosis and coronary artery disease.

The other lipoproteins carry a much smaller fraction:

• a) Chylomicrons: Carry primarily dietary triglycerides, not cholesterol.

• b) VLDL: Carries mostly triglycerides; while it contains cholesterol, it is not the major carrier.

• d) HDL: Carries only about 20-30% of total plasma cholesterol.

Bile acids are synthesized in the liver from cholesterol. This is the major pathway for the elimination of cholesterol from the body. The conversion of cholesterol to bile acids involves a series of reactions in the liver, including hydroxylation and side-chain oxidation.

The other options are incorrect:

• a) Glucose: Glucose is a carbohydrate and is not a direct precursor for bile acid synthesis.

• c) Triglycerides: Triglycerides are broken down into fatty acids and glycerol; they are not used to synthesize bile acids.

• d) Phospholipids: Phospholipids are structural components of cell membranes and are not precursors for bile acid synthesis.

• High triglycerides (1200 mg/dL) + chylomicrons present → serum is lipemic.

• Overnight refrigeration:

  • Chylomicrons (very low density) rise to the top → form a thick creamy layer

  • VLDL (less dense than LDL but denser than chylomicrons) remain in the turbid infranatant → cloudy layer

• This pattern is characteristic of type V hyperlipoproteinemia (combined chylomicron + VLDL elevation).

Other options:

• Clear → would indicate normal lipids

• Uniformly cloudy → only VLDL elevation, no chylomicrons

• Creamy layer over clear serum → isolated chylomicronemia (type I)

The first and committed step of cholesterol synthesis occurs in the cytoplasm. This step is the conversion of acetyl-CoA to 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA), which is then reduced to mevalonate by the enzyme HMG-CoA reductase. This enzyme is the key regulated step in the entire cholesterol synthesis pathway.

While some later steps in the complex pathway involve other organelles, the foundational and rate-limiting reactions begin and are primarily carried out in the cytoplasmic compartment of the cell.

Lipoprotein lipase (LPL) is an enzyme anchored to the capillary endothelium in extrahepatic tissues (primarily adipose tissue and muscle). Its primary function is to hydrolyze (break down) the core triglycerides in chylomicrons and VLDL into free fatty acids and glycerol. These breakdown products are then taken up by the local tissues for energy use or storage.

The other options are incorrect:

• b) LDL only: LPL does not act on LDL. LDL is formed from the metabolism of VLDL and is rich in cholesterol, not triglycerides.

• c) HDL only: LPL does not act on HDL. HDL is involved in reverse cholesterol transport.

• d) Free fatty acids: LPL acts on the triglycerides within lipoproteins to produce free fatty acids; it does not act on free fatty acids themselves.

A turbid or milky serum specimen is caused by an increased concentration of light-scattering particles. Chylomicrons and VLDL are large, triglyceride-rich lipoproteins that cause this turbidity by scattering light.

Here’s why the other options are incorrect:

• a) Cholesterol: Elevated cholesterol itself does not cause turbidity. LDL and HDL particles are too small to scatter light significantly, so serum with high cholesterol but normal triglycerides can appear clear.

• b) Albumin: Albumin is a clear, soluble protein and does not contribute to serum turbidity.

• d) Free Fatty Acids: Free fatty acids are bound to albumin in the blood and are in a clear solution; they do not cause turbidity.

Apolipoprotein B-100 (Apo B-100) is a very large, insoluble protein that serves as the primary structural component for lipoproteins assembled in the liver.

• It is synthesized in the liver and is incorporated into VLDL (Very-Low-Density Lipoprotein) when this particle is first assembled and secreted.

• As VLDL is metabolized in the bloodstream (losing triglycerides), it transforms first into IDL (Intermediate-Density Lipoprotein) and then into LDL (Low-Density Lipoprotein). The same single molecule of Apo B-100 remains with the particle throughout this entire process.

Therefore, Apo B-100 is a major component of both VLDL and its metabolic product, LDL.

Why the other options are incorrect:

• a) Chylomicrons: Chylomicrons, which are assembled in the intestine, contain Apo B-48, a shorter form of the protein.

• b) HDL: HDL’s major

Phospholipids are the major structural component of all cell membranes. They form the lipid bilayer that creates a barrier between the inside and outside of the cell and its organelles. Their unique structure—with a hydrophilic (water-attracting) head and hydrophobic (water-repelling) tails—allows them to spontaneously assemble into stable membranes in an aqueous environment.

The other lipids have different primary functions:

• a) Triglycerides: Function primarily as energy storage molecules.

• c) Steroids: Include cholesterol, which helps regulate membrane fluidity, but is not the primary structural component.

• d) Waxes: Serve as protective coatings in plants and animals, not as structural components of cell membranes.

The Friedewald formula is:
LDL Cholesterol = Total Cholesterol – HDL Cholesterol – (Triglycerides / 5)

The term (Triglycerides / 5) is an estimate of VLDL cholesterol. For this estimation to be valid, the measurements for Total Cholesterol and Triglycerides must be performed using the same chemical procedure and be standardized consistently.

The reason is that the formula relies on the proportional relationship between these two values. If different methods with different calibrations or specificities are used for Total Cholesterol and Triglycerides, the ratio between them becomes inaccurate, leading to a significant error in the calculated LDL value.

While HDL cholesterol is a component of the formula, it is measured using a separate, direct method (like a homogeneous assay) and its accuracy is independent of the Total Cholesterol and Triglyceride measurements.

• The Friedewald formula estimates LDL cholesterol as:

LDL-C=Total Cholesterol−HDL-C−Triglycerides5(mg/dL)\text{LDL-C} = \text{Total Cholesterol} – \text{HDL-C} – \frac{\text{Triglycerides}}{5} \quad (\text{mg/dL})LDL-C=Total Cholesterol−HDL-C−5Triglycerides​(mg/dL)

• Assumes VLDL cholesterol ≈ triglycerides ÷ 5.

• Requires measurements of:

  1. Total cholesterol

  2. HDL cholesterol

  3. Triglycerides

Other options (HDL + total protein, HDL + glucose, total cholesterol + calcium) are not used in LDL calculation.

The liver is the primary site for de novo fatty acid synthesis (lipogenesis). It possesses all the necessary enzymes, notably acetyl-CoA carboxylase and fatty acid synthase, to convert excess dietary carbohydrates and proteins into fatty acids, which are then used to synthesize triglycerides for storage or export.

The other organs have different primary roles in lipid metabolism:

• a) Kidney: While the kidneys can perform some lipid metabolism, they are not a major site for fatty acid synthesis.

• c) Brain: The brain relies on glucose and ketone bodies for energy and has very limited capacity for fatty acid synthesis.

• d) Muscle: Skeletal muscle primarily uses fatty acids for energy (beta-oxidation) rather than synthesizing them for storage.

A deficiency in lipoprotein lipase (LPL) directly causes hypertriglyceridemia (severely elevated triglyceride levels). This enzyme is essential for breaking down triglycerides in chylomicrons and VLDL. When it is deficient, these triglyceride-rich lipoproteins accumulate in the bloodstream.

The other conditions are not the direct result of LPL deficiency:

• b) Hypoglycemia: This refers to low blood sugar and is not directly caused by LPL deficiency.

• c) Hypercholesterolemia: This refers to high cholesterol, particularly LDL. While lipid profiles can be complex, the primary lipid abnormality in LPL deficiency is high triglycerides, not isolated high cholesterol.

• d) Ketosis: This is a state of elevated ketone bodies, typically caused by accelerated fat breakdown (lipolysis), not a defect in lipoprotein clearance.

Elevated levels of LDL are most directly and causally associated with the development of premature atherosclerosis. This is because LDL particles transport cholesterol into the artery wall, where it can become oxidized and taken up by macrophages, leading to the formation of foam cells and the initiation of atherosclerotic plaques.

The other options are incorrect because:

• a) Chylomicrons: These are primarily associated with hypertriglyceridemia and pancreatitis, not directly with atherosclerosis.

• b) High-Density Lipoproteins (HDL) and d) Apolipoprotein A-I: High levels of HDL and its main protein, Apo A-I, are associated with a decreased risk of atherosclerosis due to their role in reverse cholesterol transport.

HDL (High-Density Lipoprotein) is responsible for reverse cholesterol transport, the process of carrying cholesterol from peripheral tissues (including artery walls) back to the liver. This is a key mechanism for removing excess cholesterol from the body and helps protect against atherosclerosis.

The other lipoproteins have different primary functions:

• a) VLDL (Very-Low-Density Lipoprotein): Carries endogenous triglycerides from the liver to peripheral tissues.

• b) LDL (Low-Density Lipoprotein): Delivers cholesterol to peripheral tissues.

• d) IDL (Intermediate-Density Lipoprotein): A transient remnant in the conversion of VLDL to LDL; it is not primarily involved in reverse cholesterol transport.

• Cholesterol is a vital lipid with multiple roles, including serving as a precursor for:

  1. Bile acids → aid in fat digestion and absorption

  2. Vitamin D → synthesized in skin from 7-dehydrocholesterol

  3. Steroid hormones → cortisol, aldosterone, estrogen, testosterone, and progesterone

Other options:

• Amino acids → derived from protein, not cholesterol

• Glucose → derived from carbohydrates

• Fatty acids → synthesized from acetyl-CoA, not cholesterol

VLDL (Very-Low-Density Lipoprotein) is produced by the liver. Its primary role is to transport endogenous triglycerides (those synthesized in the liver from carbohydrates and other sources) to peripheral tissues (like muscle and adipose) for energy storage or use.

Here is why the other options are incorrect:

• a) Cholesterol from peripheral cells to the liver: This is the function of HDL (reverse cholesterol transport).

• b) Exogenous dietary triglycerides: This is the primary function of Chylomicrons.

• d) Phospholipids to cell membranes: While VLDL contains phospholipids in its shell, this is not its primary function. Phospholipids are a structural component of all lipoproteins.

• In the indirect (precipitation) method, apoB-containing lipoproteins (LDL, VLDL) are precipitated using reagents like heparin–Mn²⁺ or dextran sulfate–Mg²⁺, and cholesterol is measured in the supernatant as HDL-C.

• Most common error: Incomplete precipitation → residual LDL or VLDL remains → falsely elevated HDL cholesterol.

Other options:

• Over-precipitation of HDL → rare; HDL is resistant to precipitation

• Hemolysis → may interfere with some assays but is not the most consistent source of error

• High triglycerides → may affect precipitation efficiency, but the principal error is incomplete removal of apoB lipoproteins

Elevated LDL cholesterol is a primary, major risk factor for the development of atherosclerosis. This is because LDL particles transport cholesterol into the artery wall, where it can become oxidized and taken up by macrophages, leading to the formation of foam cells and the initiation of atherosclerotic plaques.

The other options are incorrect because:

• a) Elevated HDL cholesterol and d) Elevated Apo A-I: High levels of HDL and its main protein, Apo A-I, are associated with a decreased risk of atherosclerosis due to their role in reverse cholesterol transport.

• c) Low total cholesterol: Low total cholesterol is generally not a risk factor for atherosclerosis. In fact, very low levels may be associated with other health issues, but not an increased risk of heart disease.

Here’s the reasoning:

• Milky appearance: This indicates a high concentration of triglyceride-rich lipoproteins in the blood.

• Thick creamy layer after refrigeration: This layer is caused by chylomicrons, which float to the top due to their low density.

• Turbid infranatant (the liquid below the layer): This turbidity is caused by VLDL, which remains suspended in the serum, giving it a cloudy appearance.

• Density of lipoproteins is inversely related to their lipid content: the more triglyceride-rich, the lower the density.

• Chylomicrons are:

  • Largest in size

  • Richest in triglycerides

  • Lowest in density → float to the top when serum is allowed to stand or is centrifuged

Other lipoproteins:

• VLDL → also triglyceride-rich, but denser than chylomicrons

• LDL → cholesterol-rich, moderate density

• HDL → protein-rich, highest density

Ketone bodies (acetoacetate, beta-hydroxybutyrate, and acetone) are produced in the liver from acetyl-CoA derived from the beta-oxidation of fatty acids. This process occurs primarily during prolonged fasting, starvation, or in uncontrolled diabetes when glucose is not available as an energy source, and the body shifts to breaking down fats for fuel.

The other options are incorrect:

• a) Glucose: Glucose is broken down through glycolysis and the citric acid cycle, not converted into ketone bodies.

• b) Amino acids: While some amino acids can be ketogenic (converted to acetyl-CoA), fatty acids are the primary substrate for ketogenesis.

• d) Cholesterol: Cholesterol is not broken down into ketone bodies; it is excreted in bile or converted into bile acids and steroid hormones.

This option best reflects the unique chemical composition of HDL (High-Density Lipoprotein), which is characterized by:

• High Protein Content (about 50%): HDL is the densest lipoprotein because it has the highest protein-to-lipid ratio. Its main protein is ApoA-I.

• Low Triglyceride Content (about 5%): HDL carries very little triglyceride compared to other lipoproteins.

• Cholesterol/Cholesteryl Ester Content (about 15-20%): A significant portion of HDL’s core is made of cholesteryl esters.

For comparison, the other options describe different lipoproteins:

• a) Triglyceride 60%, Cholesterol 15%: Similar to VLDL composition.

• b) Triglyceride 10%, Cholesterol 45%: Similar to LDL composition.

• d) Triglyceride 85%, Cholesterol 5%: Similar to Chylomicron composition.

• HDL (High-Density Lipoprotein) is often called “good cholesterol.” High levels of HDL are associated with reverse cholesterol transport, meaning it carries cholesterol away from the arteries to the liver for excretion.

• This reduces the risk of atherosclerosis and cardiovascular disease.

Other options:

• Chylomicrons – transport dietary triglycerides; high levels do not protect against atherosclerosis.

• VLDL (Very-Low-Density Lipoprotein) – rich in triglycerides; high levels can contribute to plaque formation.

• LDL (Low-Density Lipoprotein) – “bad cholesterol”; high levels increase atherosclerosis risk.

• Lipoprotein Lipase (LPL) is an enzyme located on the endothelial surface of capillaries in adipose tissue, muscle, and heart.

• Its main function is to hydrolyze triglycerides in chylomicrons and VLDL, releasing free fatty acids for tissue uptake.

• Deficiency of LPL → impaired triglyceride clearance → accumulation of chylomicrons in the blood, causing type I hyperlipoproteinemia.

Other options:

• LCAT → esterifies cholesterol in HDL; deficiency → low HDL, not chylomicron accumulation.

• Hepatic lipase → hydrolyzes triglycerides in IDL and HDL; deficiency → altered HDL/IDL metabolism, not primary chylomicron accumulation.

• Apolipoprotein B-100 → structural protein of VLDL/LDL; deficiency affects LDL formation, not chylomicrons (which have ApoB-48).

• Lipemic serum contains chylomicrons or VLDL, which may float and form a fat layer when frozen.

• Freezing does not destroy triglycerides, but the lipoproteins can separate.

• Warming to 37°C and thorough mixing:

  • Redistributes the lipoproteins evenly throughout the serum

  • Allows accurate enzymatic measurement of triglycerides

Other options:

• Warm to 15°C and centrifuge → insufficient to melt lipid layer; centrifugation may remove lipoproteins, leading to falsely low results.

• Discarding → unnecessary; triglycerides are stable to freezing.

• Organic solvent extraction → not routine and can interfere with standard assays.

Elevated LDL (Low-Density Lipoprotein) levels are a primary risk factor for the development of atherosclerosis. This is because LDL particles transport cholesterol into the artery wall, where it can become oxidized and taken up by macrophages, leading to the formation of foam cells and atherosclerotic plaques.

The other options are incorrect:

• a) Decreased risk of atherosclerosis: This is associated with high levels of HDL, not LDL.

• c) Decreased cholesterol synthesis: LDL levels are not directly correlated with the rate of cholesterol synthesis in a way that would cause this association.

• d) Increased HDL formation: LDL and HDL levels are regulated by different metabolic pathways; high LDL does not cause increased HDL formation.

Tangier disease is a rare genetic disorder characterized by a severe deficiency or near absence of HDL (High-Density Lipoprotein) in the blood. This is caused by a mutation in the ABCA1 gene, which is essential for the proper formation of HDL particles.

The other options are incorrect:

• b) LDL: Deficiencies or problems with LDL are associated with conditions like familial hypercholesterolemia (LDL receptor defect) or abetalipoproteinemia (Apo B deficiency).

• c) VLDL: VLDL levels are not primarily affected in Tangier disease.

• d) Apo B-100: A deficiency of Apo B-100 causes a different disorder (hypobetalipoproteinemia), not Tangier disease. Tangier disease is linked to a problem with Apo A-I and HDL metabolism due to the ABCA1 defect.

• Routine HDL measurement by precipitation involves:

  • Precipitating apoB-containing lipoproteins (LDL, VLDL, chylomicrons) using reagents like heparin–Mn²⁺ or dextran sulfate–Mg²⁺.

  • Measuring cholesterol in the supernatant, which represents HDL.

• Most common error: Incomplete precipitation of LDL or VLDL → these apoB-containing lipoproteins remain in the supernatant → falsely elevated HDL cholesterol.

Other options:

• Inaccurate protein estimation → not relevant; HDL is measured as cholesterol, not protein.

• Coprecipitation of HDL with LDL → rare; HDL is generally resistant to precipitation.

• Small apoB after precipitation → minimal effect compared to incomplete precipitation.

• Triglycerides (260 mg/dL): This value is elevated. A normal fasting triglyceride level is typically considered to be below 150 mg/dL. However, this specimen was drawn 6 hours postprandial (after a meal). After eating, triglyceride levels rise significantly due to the influx of dietary fats packaged into chylomicrons. An elevated level at this time is an expected physiological response and does not necessarily indicate a metabolic problem.

• Cholesterol (120 mg/dL): This is a normal value. Total cholesterol is less affected by a single meal than triglycerides are. A level below 200 mg/dL is generally considered desirable.

Apolipoprotein A-I (Apo A-I) is the major structural protein of HDL, making up about 70% of its protein content. It also acts as a cofactor for the enzyme lecithin-cholesterol acyltransferase (LCAT), which is essential for the maturation of HDL by esterifying free cholesterol within the particle.

The other options are incorrect because:

• a) Apo B-100: The primary structural protein of LDL, VLDL, and IDL.

• b) Apo B-48: The primary structural protein of chylomicrons.

• d) Apo E: A component of several lipoproteins (chylomicron remnants, VLDL, IDL, HDL) and is important for receptor-mediated clearance.

• Synthesis: They are assembled in the epithelial cells of the small intestine after a meal.

• Function: Their primary job is to carry dietary triglycerides (and cholesterol) from the intestine through the lymphatic system and into the bloodstream to deliver them to peripheral tissues (like muscle and fat) for energy or storage.

For comparison:

• a) VLDL: Transports endogenous triglycerides (those synthesized in the liver).

• b) LDL: Delivers cholesterol to peripheral tissues.

• c) HDL: Removes excess cholesterol from tissues and returns it to the liver.

Hormone-sensitive lipase (HSL) is the key enzyme responsible for the hydrolysis (breakdown) of stored triglycerides in adipose tissue. It releases free fatty acids and glycerol into the bloodstream for use as energy by other tissues. Its activity is tightly regulated by hormones like epinephrine, norepinephrine, and insulin.

The other enzymes have different roles:

• a) Lipoprotein lipase: Located on the capillary endothelium, it hydrolyzes triglycerides in circulating lipoproteins (chylomicrons and VLDL) entering the adipose tissue for storage.

• c) Pancreatic lipase: Functions in the small intestine to digest dietary triglycerides.

• d) Lecithin-cholesterol acyltransferase (LCAT): Functions in HDL metabolism in the bloodstream, esterifying free cholesterol.

LDL (Low-Density Lipoprotein) is often referred to as “bad cholesterol” because high levels of LDL are directly associated with an increased risk of atherosclerosis and coronary artery disease. This is because LDL particles transport cholesterol from the liver to peripheral tissues, including the artery walls, where it can accumulate and form plaques.

For comparison:

• a) HDL (High-Density Lipoprotein): Known as “good cholesterol” because it removes cholesterol from arteries and carries it back to the liver.

• c) VLDL (Very-Low-Density Lipoprotein): Carries mainly triglycerides; while it contributes to cardiovascular risk, it is not typically called “bad cholesterol.”

• d) Chylomicron: Transports dietary fats; it is not typically labeled as “bad cholesterol.”

Carnitine is essential for the transport of long-chain fatty acids from the cytosol into the mitochondrial matrix, where beta-oxidation (the process of breaking down fatty acids for energy) occurs. This transport is facilitated by the carnitine shuttle system, which involves the enzymes carnitine palmitoyltransferase I (CPT I) and II (CPT II).

The other options are incorrect:

• b) Synthesis of triglycerides: Carnitine is not involved in triglyceride synthesis; this occurs in the endoplasmic reticulum.

• c) Cholesterol esterification: This process is mediated by the enzyme ACAT (acyl-CoA cholesterol acyltransferase) in cells and LCAT (lecithin-cholesterol acyltransferase) in HDL metabolism.

• d) Lipoprotein assembly: Lipoprotein assembly involves microsomal triglyceride transfer protein (MTP) and apolipoproteins, not carnitine.

HDL (High-Density Lipoprotein) has the highest protein content of all the lipoproteins, typically around 50% by weight. This high protein-to-lipid ratio is what gives HDL its name and its high density compared to other lipoproteins.

For comparison, the other lipoproteins have much lower protein content:

• b) LDL: Approximately 25% protein

• c) VLDL: Approximately 10% protein

• d) Chylomicron: Only 1-2% protein

• Homogeneous (direct) HDL assays are widely used in high-volume clinical laboratories because they:

  • Do not require prior precipitation of other lipoproteins

  • Are automated and suitable for large numbers of samples

  • Provide rapid and accurate HDL cholesterol measurement

Other methods:

• Ultracentrifugation → accurate but time-consuming and labor-intensive, not practical for routine high-volume testing

• Agarose gel electrophoresis → used for research, not routine clinical labs

• Column chromatography → accurate but slow and complex; rarely used for routine HDL measurement

Lipolysis is the specific biochemical process for the breakdown of lipids, primarily triglycerides, into their component parts: glycerol and free fatty acids. This process is crucial for releasing stored energy.

The other options describe different processes:

• a) Lipogenesis: This is the process of synthesizing or creating new lipids.

• c) Lipoxidation: This refers to the oxidation of lipids, often leading to rancidity or cellular damage.

• d) Lipoprotein synthesis: This is the process of creating lipoproteins (like VLDL) to transport lipids in the bloodstream.

LCAT is the enzyme that esterifies cholesterol. It circulates in the blood bound to HDL particles and catalyzes the transfer of a fatty acid from the *sn-2* position of phosphatidylcholine (lecithin) to the 3-OH group of free cholesterol, forming a cholesteryl ester. This reaction is crucial for the maturation of HDL and the reverse cholesterol transport pathway.

The other enzymes have different functions:

• a) Lipase: Hydrolyzes triglycerides (e.g., lipoprotein lipase, hormone-sensitive lipase).

• c) Acetyl-CoA carboxylase: Catalyzes the first committed step in fatty acid synthesis.

• d) HMG-CoA reductase: The rate-limiting enzyme in cholesterol synthesis.

• Enzymatic triglyceride assays work by hydrolyzing triglycerides into glycerol and free fatty acids using lipase.

• The glycerol is then quantified, often through subsequent reactions producing a colorimetric or fluorometric signal proportional to the triglyceride concentration.

• Key point: the assay measures total glycerol, which reflects the triglyceride content in the sample.

Other options:

• Fatty acids → released in the reaction but not directly measured.

• Phospholipids → not involved in standard triglyceride assays.

• Pre-beta lipoprotein → a fraction of HDL; unrelated to triglyceride measurement.

Glucagon is a primary hormone that stimulates lipolysis (the breakdown of triglycerides into free fatty acids and glycerol in adipose tissue). It acts during fasting states to mobilize energy stores.

The other hormones have different effects:

• a) Insulin: Strongly inhibits lipolysis and promotes fat storage. This is the opposite effect.

• c) Thyroxine: Can have a permissive role in lipolysis but is not a primary stimulator like glucagon.

• d) Oxytocin: Involved in uterine contractions and milk ejection, not lipid metabolism.

• In the endogenous lipid pathway, the liver synthesizes triglycerides (from carbohydrates and fats) and packages them into Very-Low-Density Lipoproteins (VLDL).

• VLDL function:

  • Transport endogenous triglycerides to peripheral tissues

  • As VLDL delivers triglycerides, it is converted to IDL and eventually to LDL, which is richer in cholesterol

Other options:

• Chylomicrons → transport dietary (exogenous) triglycerides from the intestine

• IDL → intermediate formed from VLDL metabolism

• LDL → primarily carries cholesterol to tissues

In a non-fasting patient, the most significantly and directly elevated lipid result is triglycerides. This is because chylomicrons, which are rich in dietary triglycerides, are present in the bloodstream after eating. These chylomicrons can cause a sharp, temporary increase in the measured serum triglyceride level.

Why the other options are incorrect:

• a) Total Cholesterol: While total cholesterol includes cholesterol from chylomicrons and other lipoproteins, it does not fluctuate as dramatically or as quickly after a meal as triglycerides do.

• c) HDL Cholesterol: HDL levels are relatively stable and are not significantly affected by short-term fasting or non-fasting status.

• d) LDL Cholesterol (calculated): The Friedewald formula (LDL = Total Cholesterol – HDL – Triglycerides/5) becomes inaccurate in non-fasting samples because the elevated triglycerides lead to an underestimation, not a direct elevation, of calculated LDL.

• HDL (High-Density Lipoprotein) mediates reverse cholesterol transport:

  • Collects cholesterol from peripheral tissues and arterial walls

  • Delivers it to the liver for excretion in bile or recycling

• This process is protective against atherosclerosis

Other options:

• Deliver triglycerides to cells → function of VLDL and chylomicrons

• Carry cholesterol to tissues → function of LDL

• Transport fatty acids to mitochondria → occurs via albumin, not HDL

• Lipids serve multiple vital roles in the body:

  1. Energy storage → triglycerides store large amounts of energy efficiently.

  2. Structural components → phospholipids and cholesterol form cell membranes, maintaining integrity and fluidity.

  3. Other roles → act as signaling molecules and insulation, but the primary functions are energy storage and membrane structure.

Other options:

• Regulate enzyme activity → some lipids play signaling roles, but this is secondary.

• Produce urea → unrelated; urea is a product of amino acid metabolism.

• Tangier disease is a rare genetic disorder caused by mutations in the ABCA1 transporter, which is essential for forming and secreting HDL particles.

• As a result, patients have:

  • Severely low or absent HDL cholesterol

  • Accumulation of cholesterol in tissues → orange tonsils, hepatosplenomegaly, peripheral neuropathy.

• Other lipoproteins (LDL, VLDL, chylomicrons) may be normal or mildly affected, but the primary defect is in HDL.

• Familial hypercholesterolemia (FH) is a genetic disorder, usually due to mutations in the LDL receptor, leading to impaired clearance of LDL from the blood.

• This results in markedly elevated LDL cholesterol, while other lipoproteins (like HDL and triglycerides) are usually normal.

• Hallmark features include:

  • Premature atherosclerosis

  • Xanthomas (especially tendon xanthomas)

  • Arcus corneae

Other options:

• Chylomicrons → elevated in familial hypertriglyceridemia or type I hyperlipoproteinemia.

• HDL → low HDL may occur in some dyslipidemias, but not the primary finding in FH.

• Apolipoprotein A₁ → main protein of HDL; not elevated in FH.