Lipid Metabolism — MCQs

Lipid Metabolism Indian Medical PG Practice Questions and MCQs

Question 721: What is the primary product of fatty acid oxidation (β-oxidation)?

A. Acetyl CoA (Correct Answer)
B. Malonyl CoA
C. Ketone bodies
D. Cholesterol

Explanation: ***Acetyl CoA*** - Beta-oxidation of fatty acids involves a series of reactions that cleave two-carbon units from the fatty acyl chain, forming **acetyl CoA**. - **Acetyl CoA** is the direct product of each cycle of β-oxidation and then enters the **citric acid cycle** to generate ATP or serves as a precursor for other anabolic pathways. *Malonyl CoA* - **Malonyl CoA** is a key intermediate in **fatty acid synthesis**, not degradation. - It's formed from acetyl CoA by acetyl-CoA carboxylase and acts as a substrate for **fatty acid synthase**, and also as a physiological inhibitor of carnitine palmitoyltransferase I (CPT-I), thereby regulating β-oxidation. *Ketone bodies* - **Ketone bodies** (**acetoacetate** and **β-hydroxybutyrate**) are produced from acetyl CoA in the liver during conditions of low glucose availability or prolonged fasting. - They serve as an alternative fuel source for tissues like the brain and muscles, but are secondary products derived from the condensation of acetyl CoA molecules, not the primary direct product of fatty acid breakdown itself. *Cholesterol* - **Cholesterol** is a steroid lipid synthesized from **acetyl CoA** through a complex multi-step pathway (via HMG-CoA reductase pathway). - It is an important structural component of cell membranes and a precursor for steroid hormones and bile acids, but not a direct product of fatty acid catabolism.

Question 722: Which molecule serves as the ultimate source of acetyl groups for fatty acid synthesis?

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

Explanation: ***Acetyl CoA*** - **Acetyl CoA** is the ultimate source of all acetyl groups used in fatty acid synthesis - It serves as the substrate for **acetyl CoA carboxylase**, which converts it to **malonyl CoA** - After transport from mitochondria via **citrate**, acetyl CoA is the precursor for all two-carbon units incorporated into fatty acids - One molecule of acetyl CoA also serves as the primer for fatty acid synthesis *Malonyl CoA* - **Malonyl CoA** is the direct two-carbon donor to the growing fatty acid chain - However, it is derived from **acetyl CoA** through carboxylation by **acetyl CoA carboxylase** - It is an intermediate, not the ultimate source of acetyl groups *Palmitate* - **Palmitate** is a 16-carbon saturated fatty acid that is the end product of de novo fatty acid synthesis - It is the product of fatty acid synthesis, not a donor of acetyl groups *Citrate* - **Citrate** transports acetyl groups from the **mitochondria** to the **cytosol** where fatty acid synthesis occurs - In the cytosol, **ATP citrate lyase** cleaves citrate back into **acetyl CoA** and oxaloacetate - Citrate is a transport vehicle, not the ultimate source of acetyl groups

Question 723: Which hormone inhibits hormone-sensitive lipase?

A. Insulin (Correct Answer)
B. GH
C. ACTH
D. Thyroid hormone

Explanation: ***Insulin*** - **Insulin** is a key anabolic hormone that promotes energy storage and inhibits catabolic processes, including the breakdown of triglycerides. - It directly inhibits **hormone-sensitive lipase (HSL)** activity, thus reducing the release of free fatty acids from adipose tissue. *Thyroid hormone* - **Thyroid hormones** (T3 and T4) generally promote catabolism and increase metabolic rate, including the mobilization of lipids. - They tend to **stimulate rather than inhibit** hormone-sensitive lipase expression and activity. *GH* - **Growth hormone (GH)** has lipolytic effects, meaning it promotes the breakdown of fats to provide energy. - GH typically **stimulates HSL activity** and increases the release of free fatty acids from adipocytes. *ACTH* - **Adrenocorticotropic hormone (ACTH)** primarily stimulates the adrenal cortex to produce cortisol. - **Cortisol** can have lipolytic effects in certain contexts and does not directly inhibit HSL; instead, catecholamines act as direct stimulators of HSL.

Question 724: Which of the following is an ω-6 fatty acid?

A. Cervonic acid
B. Linoleic acid (Correct Answer)
C. Alpha linolenic acid
D. Elaidic acid

Explanation: ***Linoleic acid*** - **Linoleic acid** (LA), an 18-carbon fatty acid with two double bonds (18:2), is classified as an **ω-6 fatty acid** because its first double bond is located at the sixth carbon atom from the methyl end of the fatty acid chain. - It is an **essential fatty acid** that must be obtained through diet, serving as a precursor for other ω-6 fatty acids like arachidonic acid. *Cervonic acid* - **Cervonic acid** is another name for **docosahexaenoic acid (DHA)**, which is an **ω-3 fatty acid** (22:6). - Its first double bond is located at the third carbon from the methyl end. *Alpha linolenic acid* - **Alpha-linolenic acid** (ALA) is an **ω-3 fatty acid** (18:3). - Its first double bond is located at the third carbon atom from the methyl end. *Elaidic acid* - **Elaidic acid** is a **trans fatty acid** (18:1 trans-9). - It is classified as an **ω-9 fatty acid** due to the position of its double bond, but its trans configuration is the primary distinguishing feature.

Question 725: Chylomicron remnants are associated with ?

A. Apo-C
B. Apo-A
C. Apo-E (Correct Answer)
D. Apo-B100

Explanation: ***Apo-E*** - **Apolipoprotein E (Apo-E)** is a crucial apolipoprotein on the surface of chylomicron remnants, acting as a **ligand for the LDL receptor-related protein 1 (LRP1)** in the liver. - This binding facilitates the **hepatic uptake and clearance** of chylomicron remnants from circulation. *Apo-A* - **Apo-AI** is the primary apolipoprotein of **HDL** and plays a key role in reverse cholesterol transport by activating **lecithin-cholesterol acyltransferase (LCAT)**. - While chylomicrons *acquire* some Apo-AI from HDL, it is not the primary apolipoprotein defining their remnants' hepatic clearance. *Apo-C* - **Apo-CII** is a vital activator of **lipoprotein lipase (LPL)**, which metabolizes triglycerides in chylomicrons and VLDL. - **Apo-CIII** inhibits LPL and hinders receptor-mediated uptake, but **Apo-E** is the key for remnant recognition and uptake, not Apo-C in general. *Apo-B100* - **Apo-B100** is the main structural apolipoprotein of **LDL** and **VLDL**, serving as the ligand for the LDL receptor, mediating their hepatic uptake. - While chylomicrons have **Apo-B48**, which is a truncated form of Apo-B100, Apo-B100 itself is not found on chylomicron remnants.

Question 726: Why is oxidized LDL considered more atherogenic?

A. Is not recognized by LDL receptors
B. Is taken up by scavenger receptors (Correct Answer)
C. Promotes inflammation in arterial walls
D. Accumulates in macrophages

Explanation: ***Is taken up by scavenger receptors*** - **Oxidized LDL (oxLDL)** is taken up by **scavenger receptors (CD36, SR-A)** on macrophages, which have **no feedback regulation**. - Unlike native LDL receptors that downregulate when cells have sufficient cholesterol, **scavenger receptors continue unlimited uptake**, leading to foam cell formation. - This **unregulated uptake mechanism** is the key reason why oxLDL is **more atherogenic** than native LDL. - The result is lipid-laden macrophages forming **fatty streaks**, the initial lesions of **atherosclerosis**. *Is not recognized by LDL receptors* - While true that oxLDL has **reduced affinity** for native LDL receptors due to oxidative modification, this alone doesn't explain increased atherogenicity. - The critical factor is what happens instead—its uptake via an **alternative, unregulated pathway**. *Accumulates in macrophages* - This is a **consequence** of scavenger receptor uptake, not the primary mechanism. - Foam cell formation occurs **because** of unregulated scavenger receptor uptake, making this a downstream effect. *Promotes inflammation in arterial walls* - OxLDL does promote inflammation through multiple mechanisms (cytokine release, endothelial dysfunction). - However, this is a **secondary effect** that occurs after uptake and accumulation—not the primary reason for atherogenicity.

Question 727: Apo-E deficiency is seen in which of the following conditions?

A. Type II hyperlipoproteinemia
B. Type III hyperlipoproteinemia (Correct Answer)
C. Type I hyperlipoproteinemia
D. Type IV hyperlipoproteinemia

Explanation: ***Type III hyperlipoproteinemia*** - This condition, also known as **familial dysbetalipoproteinemia** or **broad beta disease**, is characterized by a deficiency or abnormal function of **apolipoprotein E (apoE)**. - The deficiency in functional apoE impairs the clearance of **chylomicron remnants** and **intermediate-density lipoproteins (IDLs)** from the blood. *Type II hyperlipoproteinemia* - This condition primarily involves elevated **LDL cholesterol** and is often due to defects in the **LDL receptor** or mutations in **apoB-100**, not apoE deficiency. - It does not directly involve the impaired clearance of chylomicron remnants or IDLs. *Type I hyperlipoproteinemia* - Also known as **familial chylomicronemia syndrome**, this condition is characterized by severe elevation of **chylomicrons** and **triglycerides**. - It is caused by a deficiency of **lipoprotein lipase (LPL)** or its cofactor **apoC-II**, not apoE. *Type IV hyperlipoproteinemia* - This condition, also known as **familial hypertriglyceridemia**, is characterized by abnormally high levels of **very-low-density lipoproteins (VLDL)** and **triglycerides**. - It is typically caused by increased VLDL production or impaired VLDL clearance, but not directly due to an apoE deficiency.

Question 728: What is the characteristic nitrogenous product of lecithin hydrolysis?

A. Fatty acids
B. Choline (Correct Answer)
C. Glucose
D. Phosphoric acid

Explanation: ***Choline*** - Lecithin is a type of **phospholipid** called **phosphatidylcholine**, meaning its head group contains choline. - Therefore, during hydrolysis, the **choline** component is released as the characteristic nitrogenous product. *Glucose* - **Glucose** is a simple sugar and a carbohydrate, not a component of lecithin. - It is a primary source of **energy** for cells but is not released during lipid hydrolysis. *Fatty acids* - While **fatty acids** are indeed components of lecithin (two fatty acid chains are attached to the glycerol backbone), they are not nitrogenous. - Fatty acids are **hydrophobic hydrocarbon chains** that make up a significant part of the lipid structure. *Phosphoric acid* - **Phosphoric acid** (or phosphate) is also a component of lecithin, connecting the glycerol backbone to the choline group. - However, it is an **inorganic acid** and does not contain nitrogen.

Question 729: Lipogenesis is stimulated by?

A. Insulin (Correct Answer)
B. Glucagon
C. Epinephrine
D. Corticosteroids

Explanation: ***Insulin*** - **Insulin** is a key anabolic hormone that promotes the synthesis and storage of fat (lipogenesis) by increasing the uptake of glucose into adipose tissue and stimulating enzymes involved in fatty acid synthesis. - It enhances the conversion of excess carbohydrates into **triglycerides** for storage. *Glucagon* - **Glucagon** is a catabolic hormone that primarily promotes the breakdown of glycogen (glycogenolysis) and fat (lipolysis) to release glucose and fatty acids into the bloodstream, especially during fasting. - It generally **inhibits** lipogenesis and stimulates **gluconeogenesis**. *Epinephrine* - **Epinephrine** (adrenaline) is a stress hormone that promotes the breakdown of fat (lipolysis) to provide energy during acute stress or exercise. - It would **inhibit** lipogenesis, as its primary role is to mobilize energy stores. *Corticosteroids* - While **corticosteroids** can influence fat metabolism, their effect on lipogenesis is complex and often indirect. High levels can lead to fat redistribution (e.g., central obesity) rather than direct stimulation of overall lipogenesis. - Corticosteroids generally promote **lipolysis** in the extremities and can contribute to insulin resistance, which would hinder lipogenesis in some tissues.

Question 730: Which of the following enzymes uses citrate in fatty acid synthesis?

A. Aconitase
B. ATP citrate lyase (Correct Answer)
C. Malic enzyme
D. Citrate synthase

Explanation: ***ATP citrate lyase*** - This enzyme is crucial for fatty acid synthesis, as it cleaves **citrate** in the cytoplasm to generate **acetyl-CoA** and oxaloacetate. - The acetyl-CoA produced is then used as the primary building block for **fatty acid synthesis**. *Aconitase* - This enzyme isomerizes **citrate** to isocitrate within the **Krebs cycle** (TCA cycle) in the mitochondria. - It does not directly participate in the cytosolic pathway of fatty acid synthesis. *Citrate synthase* - This enzyme synthesizes **citrate** from acetyl-CoA and oxaloacetate, initiating the **Krebs cycle** in the mitochondrial matrix. - It is involved in citrate formation, not its utilization for fatty acid synthesis in the cytoplasm. *Malic enzyme* - This enzyme converts **malate** to pyruvate, generating **NADPH** in the cytoplasm. - While NADPH is essential for fatty acid synthesis, malic enzyme does not directly use citrate.

Practice by Chapter

Lipid Classification and Chemistry

Practice Questions

Fatty Acid Oxidation

Practice Questions

Ketone Body Metabolism

Practice Questions

Fatty Acid Synthesis

Practice Questions

Metabolism of Triacylglycerols

Practice Questions

Phospholipid Metabolism

Practice Questions

Cholesterol Metabolism and Biosynthesis

Practice Questions

Bile Acids and Bile Salts

Practice Questions

Lipoprotein Metabolism and Transport

Practice Questions

Dyslipidemias and Atherosclerosis

Practice Questions

Prostaglandins and Eicosanoids

Practice Questions

Fatty Liver and Lipotropic Factors

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free