Lipid Metabolism — MCQs
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Which mineral is required for cholesterol biosynthesis?
A newborn presented with chest retractions, dyspnea, and lethargy. The pediatrician diagnosed the baby with respiratory distress syndrome. This occurs due to the deficiency of:
Rate limiting step in fatty acid synthesis is?
Bile acid has a detergent action due to?
In Retinitis pigmentosa, which fatty acid is found to be decreased in the retina?
Which of the following helps in the transport of fatty acids across the inner mitochondrial membrane?
In a patient with lipoprotein lipase deficiency, which of the following is increased following a fatty meal?
What is the type of cholesterol primarily found in gallstones?
Which apolipoprotein is associated with an increased risk of Alzheimer's disease?
How many molecules of Acetyl CoA are produced from β-oxidation of palmitic acid?
Lipid Metabolism Indian Medical PG Practice Questions and MCQs
Question 661: Which mineral is required for cholesterol biosynthesis?
- A. Fe
- B. Mn
- C. Mg (Correct Answer)
- D. Cu
Explanation: ***Mg*** - **Magnesium (Mg)** is an essential cofactor for multiple enzymes in **cholesterol biosynthesis**, particularly the **ATP-dependent kinases** in the mevalonate pathway. - **Mevalonate kinase** and **phosphomevalonate kinase** require Mg²⁺ as a cofactor for their catalytic activity. - **Squalene synthase**, which catalyzes the formation of squalene from farnesyl pyrophosphate, also requires Mg²⁺. - Deficiency in magnesium can impair these critical steps in **cholesterol synthesis**. *Fe* - **Iron (Fe)** is vital for many enzymatic reactions, particularly in **oxygen transport** (hemoglobin), **electron transport** (cytochromes), and **energy metabolism**. - It does not function as a cofactor in the enzymatic steps of **cholesterol biosynthesis**. *Mn* - **Manganese (Mn)** serves as a cofactor for enzymes involved in **carbohydrate metabolism**, **bone formation**, and **antioxidant defense** (superoxide dismutase). - While important for various metabolic processes, it is not specifically required for **cholesterol synthesis**. *Cu* - **Copper (Cu)** is a component of several enzymes, including **cytochrome c oxidase** and **superoxide dismutase**, involved in electron transport and antioxidant defense. - It does not play a direct role as a cofactor in the key enzymatic steps of **cholesterol synthesis**.
Question 662: A newborn presented with chest retractions, dyspnea, and lethargy. The pediatrician diagnosed the baby with respiratory distress syndrome. This occurs due to the deficiency of:
- A. Dipalmitoyl inositol
- B. Dipalmitoylphosphatidylethanolamine
- C. Lecithin (Correct Answer)
- D. Sphingomyelin
Explanation: ***Lecithin*** - **Respiratory distress syndrome (RDS)** in newborns is primarily caused by a deficiency of pulmonary **surfactant**. - **Lecithin (phosphatidylcholine)**, specifically in its dipalmitoyl form (**dipalmitoylphosphatidylcholine or DPPC**), is the main active component of surfactant, constituting ~40-50% of surfactant lipids. - DPPC is crucial for reducing surface tension in the alveoli and preventing their collapse during expiration. - This is the **primary biochemical deficiency** in neonatal RDS. *Dipalmitoyl inositol* - **Inositol** is a sugar alcohol involved in various cellular processes and is present in surfactant as phosphatidylinositol, but it is not a primary functional component. - Deficiency of this compound does not directly lead to **respiratory distress syndrome**. *Dipalmitoylphosphatidylethanolamine* - **Phosphatidylethanolamine (PE)** is a phospholipid found in cell membranes but is not the primary phospholipid responsible for surfactant function. - Note: This is PE, not PC (phosphatidylcholine). While PE is present in surfactant, its deficiency does not specifically cause **neonatal RDS**. *Sphingomyelin* - **Sphingomyelin** is a sphingolipid found in cell membranes and myelin sheaths, but it is not the critical component of pulmonary surfactant. - The **lecithin-to-sphingomyelin (L/S) ratio** is used to assess fetal lung maturity; an L/S ratio >2 indicates mature lungs capable of producing adequate surfactant.
Question 663: Rate limiting step in fatty acid synthesis is?
- A. Production of acetyl CoA
- B. Production of oxaloacetate
- C. Production of malonyl-CoA (Correct Answer)
- D. Production of citrate
Explanation: ***Production of malonyl-CoA*** - The conversion of **acetyl-CoA to malonyl-CoA** is catalyzed by **acetyl-CoA carboxylase (ACC)**, which is the **rate-limiting enzyme** in fatty acid synthesis. - This step is highly regulated by **hormones** (e.g., insulin activates, glucagon inactivates) and **nutrient availability**, controlling the overall flux of fatty acid production. *Production of acetyl CoA* - While **acetyl-CoA** is the precursor for fatty acid synthesis, its production (e.g., from glycolysis via pyruvate dehydrogenase) is not the rate-limiting step for the synthesis pathway itself. - The availability of **acetyl-CoA** influences the pathway, but the committed step occurs later. *Production of oxaloacetate* - **Oxaloacetate** is primarily involved in the **citric acid cycle** and gluconeogenesis, and its production is not directly the rate-limiting step in fatty acid synthesis. - It combines with acetyl-CoA to form citrate, allowing acetyl-CoA to be shuttled out of the mitochondria. *Production of citrate* - **Citrate** is formed when **acetyl-CoA and oxaloacetate** combine in the mitochondria and is then transported to the cytoplasm to provide acetyl-CoA for fatty acid synthesis. - Although the availability of **cytoplasmic citrate** is important as a precursor for cytoplasmic acetyl-CoA and an allosteric activator of ACC, its production is not the rate-limiting step of fatty acid synthesis itself.
Question 664: Bile acid has a detergent action due to?
- A. Amphipathic nature of bile salts (Correct Answer)
- B. Formation of medium chain triglycerides
- C. Formation of soap
- D. Formation of zwitter ion
Explanation: ***Amphipathic nature of bile salts*** - Bile salts are **amphipathic molecules**, meaning they have both **hydrophilic** (water-loving) and **hydrophobic** (fat-loving) regions. - This dual nature allows them to emulsify fats, breaking large fat globules into smaller ones, thereby exhibiting a **detergent action**. *Formation of soap* - While soaps also have a detergent action due to their amphipathic nature, the primary mechanism of bile acid's detergent action in the body is not through the formation of soap as a product. - Soap formation involves a saponification reaction, which is not the main process explaining bile acid's emulsifying role in digestion. *Formation of zwitter ion* - A **zwitterion** is a molecule possessing both positive and negative charges, resulting in an overall neutral charge. - While bile acids can have ionizable groups, their detergent action is primarily attributed to the separation of hydrophilic and hydrophobic domains, not merely the presence of zwitterionic characteristics. *Formation of medium chain triglycerides* - **Medium-chain triglycerides** are a type of fat molecule; their formation is not responsible for the detergent action of bile acids. - Bile acids aid in the digestion and absorption of various dietary fats, including triglycerides, but they do not form them.
Question 665: In Retinitis pigmentosa, which fatty acid is found to be decreased in the retina?
- A. Arachidonic
- B. Palmitic acid
- C. Linoleic acid
- D. Docosahexaenoic acid (Correct Answer)
Explanation: ***Docosahexaenoic acid*** - **Docosahexaenoic acid (DHA)** is a crucial **omega-3 fatty acid** abundantly found in the **photoreceptor outer segments** of the retina. - Its reduced levels are linked to photoreceptor dysfunction and degeneration seen in conditions like **Retinitis Pigmentosa**, influencing membrane fluidity and visual function. - DHA comprises up to **50% of the fatty acids** in photoreceptor membranes and is essential for maintaining retinal structure and function. *Arachidonic acid* - **Arachidonic acid** is an **omega-6 fatty acid** primarily involved in **inflammatory pathways** and cellular signaling. - While present in the retina, its decrease is not typically associated with the pathogenesis of **Retinitis Pigmentosa**. *Linoleic acid* - **Linoleic acid** is an **omega-6 essential fatty acid** and a precursor to **arachidonic acid**, but it is not a direct structural component of photoreceptor membranes. - Its levels are not specifically decreased in **Retinitis Pigmentosa** as a primary factor. *Palmitic acid* - **Palmitic acid** is a **saturated fatty acid** present in retinal membranes but not specifically concentrated in photoreceptors. - Its levels are not characteristically decreased in **Retinitis Pigmentosa**, unlike the omega-3 fatty acid DHA.
Question 666: Which of the following helps in the transport of fatty acids across the inner mitochondrial membrane?
- A. Acyl carrier protein
- B. Carnitine (Correct Answer)
- C. Lecithin-cholesterol acyltransferase
- D. Carnitine and albumin
Explanation: ***Carnitine*** - **Carnitine** plays a crucial role in transporting long-chain fatty acids from the **cytosol** into the **mitochondrial matrix** for beta-oxidation. - It acts as a shuttling molecule, forming **acylcarnitine** which can cross the inner mitochondrial membrane via the **carnitine-acylcarnitine translocase**. *Acyl carrier protein* - **Acyl carrier protein (ACP)** is primarily involved in **fatty acid synthesis** in the cytoplasm, not in the transport of fatty acids into mitochondria for degradation. - It carries acyl groups during the elongation reactions of fatty acid synthesis. *Lecithin-cholesterol acyltransferase* - **Lecithin-cholesterol acyltransferase (LCAT)** is an enzyme found in plasma that catalyzes the formation of **cholesterol esters**, which are then transported by lipoproteins. - It is involved in **cholesterol metabolism** and reverse cholesterol transport, not in the mitochondrial transport of fatty acids. *Carnitine and albumin* - While **carnitine** is essential for mitochondrial fatty acid transport, **albumin** transports fatty acids in the blood plasma, from adipose tissue to other tissues. - Albumin does not transport fatty acids across the inner mitochondrial membrane; its role is extra-mitochondrial and related to systemic transport.
Question 667: In a patient with lipoprotein lipase deficiency, which of the following is increased following a fatty meal?
- A. Chylomicrons (Correct Answer)
- B. High-Density Lipoprotein (HDL)
- C. Very Low-Density Lipoprotein (VLDL)
- D. Low-Density Lipoprotein (LDL)
Explanation: ***Chylomicrons*** - **Lipoprotein lipase (LPL)** is essential for the breakdown of **triglycerides** within chylomicrons, which are absorbed after a fatty meal. - In LPL deficiency, **chylomicron clearance** from the bloodstream is impaired, leading to their accumulation and elevated levels. *High-Density Lipoprotein (HDL)* - HDL particles are primarily involved in **reverse cholesterol transport** and are not directly affected by LPL deficiency in terms of their synthesis or initial concentration post-meal. - While LPL activity can influence HDL metabolism, a deficiency would not directly cause an acute increase in HDL levels following a fatty meal. *Very Low-Density Lipoprotein (VLDL)* - VLDL is synthesized in the liver to transport **endogenous triglycerides**, rather than dietary triglycerides. - While prolonged LPL deficiency can indirectly affect VLDL metabolism, it is not the primary lipoprotein that acutely accumulates in response to a fatty meal in this condition. *Low-Density Lipoprotein (LDL)* - LDL is formed from the catabolism of VLDL and **intermediate-density lipoprotein (IDL)**. - In LPL deficiency, the initial step of **triglyceride hydrolysis** for chylomicrons is impaired, making it unlikely for LDL to increase immediately after a fatty meal.
Question 668: What is the type of cholesterol primarily found in gallstones?
- A. Amorphous cholesterol monohydrate.
- B. Amorphous cholesterol dihydrate.
- C. Crystalline cholesterol dihydrate.
- D. Crystalline cholesterol monohydrate. (Correct Answer)
Explanation: ***Crystalline cholesterol monohydrate*** - The predominant type of cholesterol found in gallstones is **crystalline cholesterol monohydrate** [1], which reflects the solid form of cholesterol precipitating in bile. - It is often associated with **cholesterol gallstones**, occurring when bile contains excessive cholesterol or insufficient bile salts. *Crystalline Cholesterol dihydrate* - Crystalline cholesterol dihydrate is less commonly associated with gallstones and generally forms in different circumstances, not typical of cholesterol stones. - This type does not represent the main component of gallstones, which primarily consist of monohydrate forms. *Amorphous cholesterol dihydrate* - Amorphous cholesterol dihydrate is not a recognized form typically found in gallstones, as gallstone pathology focuses on crystallized forms. - Amorphous substances are less stable than crystalline forms, making this option unlikely in the context of gallstones. *Amorphous cholesterol monohydrate* - Amorphous cholesterol monohydrate is not the major component found in gallstones; gallstones are more likely to be crystalline in structure. - This form lacks the stable crystalline structure needed to precipitate and form gallstones effectively. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 882.
Question 669: Which apolipoprotein is associated with an increased risk of Alzheimer's disease?
- A. APOE4 (Correct Answer)
- B. APOE3
- C. APOE2
- D. APOB
Explanation: ***APOE4*** - The **APOE4 allele** is the strongest genetic risk factor for **late-onset Alzheimer's disease (AD)**, significantly increasing the risk and lowering the age of onset. - Individuals with one copy of APOE4 have a 2-3 times higher risk, while those with two copies have an 8-12 times higher risk of developing AD compared to those with APOE3. *APOE3* - **APOE3** is the most common allele and is considered a **neutral risk factor** for Alzheimer's disease, serving as the reference for risk comparison. - It plays a normal role in **lipid metabolism** and **cholesterol transport** in the brain. *APOE2* - The **APOE2 allele** is associated with a **reduced risk** of Alzheimer's disease. - It is believed to be **protective** against AD, possibly by **improving amyloid-beta clearance** or reducing neuroinflammation. *APOB* - **Apolipoprotein B (APOB)** is primarily involved in the assembly and secretion of **chylomicrons** and **very-low-density lipoproteins (VLDL)** in the liver and intestine. - While important for lipid metabolism, it is **not directly implicated** as a genetic risk factor for Alzheimer's disease in the same way APOE variants are.
Question 670: How many molecules of Acetyl CoA are produced from β-oxidation of palmitic acid?
- A. 3 acetyl CoA
- B. 16 Acetyl CoA
- C. 6 acetyl CoA
- D. 8 acetyl CoA (Correct Answer)
Explanation: ***8 acetyl CoA*** - Palmitic acid is a **16-carbon saturated fatty acid (C16:0)**. During β-oxidation, each cycle cleaves two carbons as **acetyl CoA**. - The formula for acetyl CoA produced is **n/2**, where n = number of carbons. For palmitic acid: 16/2 = **8 acetyl CoA molecules**. - Alternatively: Palmitic acid undergoes **7 cycles of β-oxidation** [(n/2) - 1 = 7], each producing 1 acetyl CoA (7 total), plus the final 2-carbon fragment forming the 8th acetyl CoA. *3 acetyl CoA* - This number is too low for a 16-carbon fatty acid. **Short-chain fatty acids** would produce fewer acetyl CoA molecules. - This value corresponds to β-oxidation of a **6-carbon fatty acid** (hexanoic acid), not palmitic acid. *6 acetyl CoA* - This number is also too low for a 16-carbon fatty acid. - This quantity would be produced from a **12-carbon fatty acid** (lauric acid), not palmitic acid. *16 Acetyl CoA* - This number is too high and would incorrectly imply that each carbon forms an acetyl CoA independently. - Sixteen acetyl CoA molecules would be produced from a **32-carbon fatty acid**, which is extremely rare in biological systems.
Practice by Chapter
Lipid Classification and Chemistry
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Fatty Acid Oxidation
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Ketone Body Metabolism
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Fatty Acid Synthesis
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Metabolism of Triacylglycerols
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Phospholipid Metabolism
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Cholesterol Metabolism and Biosynthesis
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Bile Acids and Bile Salts
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Lipoprotein Metabolism and Transport
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Dyslipidemias and Atherosclerosis
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Prostaglandins and Eicosanoids
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Fatty Liver and Lipotropic Factors
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