Metabolism of Triacylglycerols — MCQs

10 questions

A person switches from a high-fat diet to a low-fat diet with a compensatory increase in carbohydrates to maintain the same caloric intake. Which lipoprotein is likely to increase?

Which of the following actions of GH is mediated by IGF-1?

In case of LPL deficiency, which of the following will increase after a fat rich diet?

A patient came to the emergency room with severe abdominal pain. The serum triglyceride level was $1500 \mathrm{mg} / \mathrm{dL}$. What is the most likely defect?

All are activated by insulin except?

Which of the following is not a substrate for glucose formation?

Active metabolite in the synthesis of fatty acids is:

What is the primary mechanism of action of 5-α reductase?

What is the primary receptor for High-Density Lipoprotein (HDL) in cholesterol metabolism?

Q10

Which of the following is a lipotropic factor?

Metabolism of Triacylglycerols Indian Medical PG Practice Questions and MCQs

Question 1: A person switches from a high-fat diet to a low-fat diet with a compensatory increase in carbohydrates to maintain the same caloric intake. Which lipoprotein is likely to increase?

A. Chylomicron
B. IDL
C. HDL
D. VLDL (Correct Answer)

Explanation: ***VLDL*** - A low-fat diet with increased **carbohydrates** can lead to increased hepatic synthesis of triglycerides, which are then packaged into **VLDL** particles for transport from the liver. This is because excess carbohydrates can be converted to fatty acids and then to triglycerides in the liver. - The liver's increased triglyceride production, driven by abundant **glucose** from carbohydrates, directly corresponds to a rise in **VLDL** secretion to export these lipids. *Chylomicron* - **Chylomicrons** primarily transport **dietary fats** (exogenous triglycerides) absorbed from the intestine. - Switching to a low-fat diet would typically lead to a *decrease* in chylomicron production, as less dietary fat is available for absorption. *IDL* - **IDL** (Intermediate-Density Lipoprotein) is a remnant of **VLDL** metabolism, formed after VLDL loses some triglycerides. - While VLDL may increase, leading to *more* IDL formation, IDL itself is not the primary component that *increases* directly due to high carbohydrate intake; rather, the precursor **VLDL** is directly affected. *HDL* - **HDL** (High-Density Lipoprotein) is involved in **reverse cholesterol transport**, picking up excess cholesterol from peripheral tissues and returning it to the liver. - High carbohydrate intake, especially refined carbohydrates, can sometimes lead to a *decrease* in HDL levels, not an increase.

Question 2: Which of the following actions of GH is mediated by IGF-1?

A. Na+ retention
B. decreases insulin
C. Antilipolysis (Correct Answer)
D. Lipolysis

Explanation: ***Antilipolysis*** * **Insulin-like growth factor 1 (IGF-1)**, stimulated by GH, plays a role in reducing **lipolysis** indirectly. * IGF-1 promotes **anabolic processes** and nutrient storage, which can lead to decreased fat breakdown. *Na+ retention* * **Na+ retention** is more directly influenced by hormones like **aldosterone** and **ADH**, not IGF-1. * While GH can exert some influence on fluid and electrolyte balance, this specific action is not primarily mediated by IGF-1. *decreases insulin* * IGF-1 and GH generally tend to **increase insulin sensitivity** in some tissues or antagonize insulin effects indirectly. * IGF-1's primary metabolic role is not to decrease insulin itself directly. *Lipolysis* * **Growth hormone (GH)** directly promotes **lipolysis**, breaking down fat for energy. * However, the question specifically asks for actions mediated by **IGF-1**, which has an opposite, antilipolytic effect.

Question 3: In case of LPL deficiency, which of the following will increase after a fat rich diet?

A. LDL
B. HDL
C. Lipoprotein (a)
D. Chylomicron (Correct Answer)

Explanation: ***Chylomicron*** - **LPL (lipoprotein lipase)** is crucial for the breakdown of **chylomicrons** and VLDL. A deficiency leads to an accumulation of undigested chylomicrons in the bloodstream after a fat-rich meal. - **Chylomicrons** transport dietary triglycerides from the intestines to tissues. Without LPL, these triglycerides remain packaged in chylomicrons. *LDL* - **LDL (low-density lipoprotein)** levels are not directly increased by a short-term fat-rich diet in the context of LPL deficiency. LDL primarily carries cholesterol and is formed from VLDL remnants, a process that is also impaired by LPL deficiency indirectly. - While chronic LPL deficiency can affect overall lipid metabolism, the immediate post-meal increase is not in LDL but in triglyceride-rich lipoproteins. *HDL* - **HDL (high-density lipoprotein)** is involved in reverse cholesterol transport and is generally not directly increased after a fat-rich diet, especially in LPL deficiency. - In fact, severe hypertriglyceridemia, often seen in LPL deficiency, can sometimes lead to lower HDL levels due to altered lipid exchange. *Lipoprotein (a)* - **Lipoprotein (a)**, or Lp(a), is a genetically determined lipoprotein similar to LDL but with an added apolipoprotein (a) and its levels are not acutely affected by dietary fat intake or LPL deficiency. - Lp(a) levels are determined primarily by genetic factors and do not participate in the post-prandial handling of dietary fats.

Question 4: A patient came to the emergency room with severe abdominal pain. The serum triglyceride level was $1500 \mathrm{mg} / \mathrm{dL}$. What is the most likely defect?

A. Apo B-48
B. Apo B-100
C. Apo C-II (Correct Answer)
D. LDL receptor
E. Lipoprotein lipase

Explanation: ***Apo C-II*** - **Apo C-II** is an essential cofactor for **lipoprotein lipase (LPL)**, which is responsible for hydrolyzing triglycerides from chylomicrons and VLDL. - A defect in Apo C-II leads to severely impaired triglyceride clearance, resulting in **chylomicronemia** and extremely high serum triglyceride levels (e.g., 1500 mg/dL), which can cause acute pancreatitis. - Both Apo C-II deficiency and LPL deficiency present similarly, but Apo C-II deficiency is the more specific answer when considering the **"defect"** terminology, as it represents the regulatory cofactor rather than the enzyme itself. *Apo B-48* - **Apo B-48** is a structural protein uniquely found on **chylomicrons**, synthesized in the intestine, and is essential for their formation and secretion. - A defect in Apo B-48 (e.g., in abetalipoproteinemia) would lead to the **absence of chylomicrons**, resulting in very low or undetectable triglyceride levels after a fat-containing meal, not high levels. *Apo B-100* - **Apo B-100** is the primary apolipoprotein of **VLDL, IDL, and LDL**, and it is crucial for VLDL assembly in the liver and for LDL receptor binding. - Defects in Apo B-100 leading to hyperlipidemia typically cause elevated LDL cholesterol (e.g., familial defective Apo B-100), rather than severe hypertriglyceridemia associated with chylomicronemia. *LDL receptor* - The **LDL receptor** is responsible for the uptake of **LDL particles** from the bloodstream, primarily in the liver. - A defect in the LDL receptor (e.g., in familial hypercholesterolemia) primarily causes **elevated LDL cholesterol** levels, but typically does not lead to the extreme hypertriglyceridemia seen in this patient. *Lipoprotein lipase* - **Lipoprotein lipase (LPL)** is the enzyme that hydrolyzes triglycerides in chylomicrons and VLDL particles. - A primary deficiency of LPL itself (Type I familial chylomicronemia) would also cause severe hypertriglyceridemia similar to Apo C-II deficiency. - However, Apo C-II deficiency is the more specific answer as it represents the **cofactor defect** that impairs LPL function, while direct LPL deficiency is a separate genetic entity.

Question 5: All are activated by insulin except?

A. Lipoprotein lipase
B. Pyruvate kinase
C. Acetyl-CoA carboxylase
D. Hormone sensitive lipase (Correct Answer)

Explanation: ***Hormone sensitive lipase*** - **Insulin** is an **anabolic hormone** that promotes energy storage; it **inhibits** hormone-sensitive lipase (HSL) activity which is responsible for **fat breakdown (lipolysis)**. - When insulin levels are high, the body stores fat rather than breaks it down, thus **decreasing** HSL activity. *Lipoprotein lipase* - **Insulin activates lipoprotein lipase (LPL)**, an enzyme that breaks down triglycerides in **chylomicrons** and **VLDL** into fatty acids for storage in adipose tissue. - This activation promotes the uptake of fatty acids into fat cells, aligning with insulin's role in **energy storage**. *Pyruvate kinase* - **Insulin activates pyruvate kinase** in glycolysis, promoting the conversion of **phosphoenolpyruvate to pyruvate**. - This enzyme's activation enhances glucose utilization and energy production following a meal when insulin levels are high. *Acetyl-CoA carboxylase* - **Insulin activates acetyl-CoA carboxylase (ACC)**, the **rate-limiting enzyme in fatty acid synthesis**. - Activation of ACC leads to the production of **malonyl-CoA**, which commits acetyl-CoA to fatty acid synthesis, storing excess energy as fat.

Question 6: Which of the following is not a substrate for glucose formation?

A. Lactate
B. Glycerol
C. Alanine
D. Acetyl coenzyme A (Correct Answer)

Explanation: ***Acetyl coenzyme A*** - **Acetyl CoA** cannot be converted to glucose because the two carbons from the acetyl group are lost as carbon dioxide in the **Krebs cycle**, making a net synthesis of glucose impossible. - The irreversible nature of the **pyruvate dehydrogenase complex** prevents the conversion of Acetyl CoA back to **pyruvate**, which is a crucial step for gluconeogenesis. *Lactate* - **Lactate** is a major substrate for gluconeogenesis, particularly during exercise and fasting, via the **Cori cycle**. - **Lactate dehydrogenase** converts lactate to **pyruvate**, which can then enter the gluconeogenic pathway. *Glycerol* - **Glycerol**, derived from triglyceride breakdown, enters gluconeogenesis by being converted to **glycerol-3-phosphate** and then to **dihydroxyacetone phosphate (DHAP)**. - DHAP is an intermediate in glycolysis and gluconeogenesis, allowing for its conversion to glucose. *Alanine* - **Alanine** is a **glucogenic amino acid** that can be transaminated to **pyruvate**. - **Pyruvate** can then proceed through the gluconeogenic pathway to synthesize glucose, especially during prolonged fasting.

Question 7: Active metabolite in the synthesis of fatty acids is:

A. Malonyl CoA (Correct Answer)
B. Stearate
C. Acetyl CoA
D. Palmitate

Explanation: ***Malonyl CoA*** - **Malonyl CoA** is the immediate **two-carbon donor** in fatty acid synthesis, formed from acetyl CoA and bicarbonate. - It adds **two-carbon units** to the growing fatty acid chain during each cycle of synthesis, making it the primary active metabolic form in this process. *Stearate (an end product of fatty acid synthesis)* - **Stearate** is a **saturated fatty acid end product** (C18:0) of fatty acid synthesis, not an active metabolite that directly participates in the elongation process. - While it is a result of fatty acid synthesis, it does not serve as a building block for further elongation in the manner of malonyl CoA. *Acetyl CoA (a precursor in fatty acid synthesis)* - **Acetyl CoA** is the **initial precursor** for fatty acid synthesis, which is then carboxylated to form malonyl CoA. - It is not the *active* two-carbon donor during the elongation steps of fatty acid synthesis itself, but rather the substrate for malonyl CoA synthesis. *Palmitate (an end product of fatty acid synthesis)* - **Palmitate** is the **primary 16-carbon saturated fatty acid** and is the usual end product of *de novo* fatty acid synthesis in humans. - Like stearate, it is an end product and does not serve as an active metabolic intermediate for chain elongation during the synthesis process itself.

Question 8: What is the primary mechanism of action of 5-α reductase?

A. Reduction of C4-C5 double bond (Correct Answer)
B. Breakage of amide bond
C. Breakage of C-N bond
D. Breakage of N-N bond

Explanation: ***Reduction of C4-C5 double bond*** - 5-α reductase is a **NADPH-dependent reductase enzyme** that catalyzes the **reduction (saturation) of the C4-C5 double bond** in the A-ring of testosterone to form **dihydrotestosterone (DHT)**. - This reduction involves **adding two hydrogen atoms** across the double bond, converting it to a single bond with **5-α stereochemistry**. - DHT is a more potent androgen crucial for **prostate development, external genitalia formation, and male pattern baldness**, making 5-α reductase inhibitors (like finasteride) clinically important for treating benign prostatic hyperplasia and androgenetic alopecia. *Breakage of amide bond* - Breaking **amide bonds (C-N bonds with a carbonyl)** is the function of **proteases and amidases**, not reductases. - This process involves **hydrolysis** and is fundamental to protein degradation and peptide metabolism. *Breakage of C-N bond* - **Carbon-nitrogen bond cleavage** occurs in reactions like **deamination** (catalyzed by deaminases) or metabolism of nitrogenous compounds. - Reductases perform **electron transfer reactions**, not bond cleavage reactions. *Breakage of N-N bond* - **Nitrogen-nitrogen bond** cleavage is rare in human biochemistry and may occur in hydrazine metabolism or by specialized enzymes. - Steroid hormones do not contain N-N bonds, making this mechanism irrelevant to 5-α reductase function.

Question 9: What is the primary receptor for High-Density Lipoprotein (HDL) in cholesterol metabolism?

A. SR-BI (Correct Answer)
B. LDLR
C. HDLR
D. SR-82

Explanation: ***SR-BI*** - **Scavenger Receptor class B type 1 (SR-BI)** is the primary receptor responsible for selective uptake of **cholesteryl esters** from HDL into cells, particularly the liver and steroidogenic tissues. - Unlike other lipoprotein receptors, SR-BI mediates the **selective transfer** of cholesterol without internalizing the entire HDL particle. *LDLR* - The **Low-Density Lipoprotein Receptor (LDLR)** is the primary receptor for **LDL** and very low-density lipoprotein (VLDL) remnants, mediating their endocytosis and degradation. - While it plays a crucial role in cholesterol metabolism, its main function is related to the uptake of **LDL cholesterol**, not HDL. *HDLR* - **HDLR** is not a recognized receptor in cholesterol metabolism. - This term may be a distracter created by combining HDL with the common receptor nomenclature. *SR-82* - **SR-82** is not a recognized receptor involved in cholesterol metabolism. - Similar to HDLR, this is a distracter term.

Question 10: Which of the following is a lipotropic factor?

A. Sphingomyelin
B. Histidine
C. Bilirubin
D. Methionine (Correct Answer)

Explanation: ***Methionine*** - **Methionine** is an essential amino acid that serves as a precursor for **choline** and **creatine**, both of which play crucial roles in lipid metabolism and transport. - Lipotropic factors prevent or reverse the accumulation of **fat in the liver** by promoting the synthesis of **lipoproteins**, which package and transport fats from the liver to other tissues. *Sphingomyelin* - **Sphingomyelin** is a type of **sphingolipid**, a component of cell membranes and myelin sheaths, but it does not directly act as a lipotropic factor to prevent fatty liver. - While it's involved in cellular signaling and membrane structure, it does not directly facilitate the metabolism or transport of **hepatic triglycerides** in the same way as lipotropic agents. *Histidine* - **Histidine** is an essential amino acid involved in protein synthesis and the production of **histamine**, but it is not considered a primary lipotropic factor. - Its main roles are in **immune response** and **neurotransmission**, not in preventing fat accumulation in the liver. *Bilirubin* - **Bilirubin** is a waste product from the breakdown of **heme**, primarily from red blood cells. It is excreted by the liver. - It is known for its **antioxidant properties** but does not play a direct role as a lipotropic factor in lipid metabolism or in preventing **fatty liver**.

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