Lipid Metabolism — MCQs
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Fatty acids are stored as
Which of the following best describes the properties of acetyl-CoA carboxylase?
Fraternal twin sisters present with episodes of fasting hypoglycemia, hypoketonemia, and muscle weakness occurring only during periods of caloric deprivation. One twin dies at 5 months of age. The surviving twin develops a cardiomyopathy diagnosed at 3 years of age. Carnitine esters are elevated in muscle tissue and serum. Which of the following is the most likely diagnosis?
What is the most important predictor of coronary artery disease?
Which of the following is true about the action of LCAT?
Fatty liver is due to the accumulation of which substance?
Which of the following is a derived lipid?
Which vegetable oil has the highest concentration of linoleic acid?
What is the major regulatory step in cholesterol synthesis?
Which enzyme in the fatty acid synthase complex utilizes pantothenic acid as a coenzyme?
Lipid Metabolism Indian Medical PG Practice Questions and MCQs
Question 51: Fatty acids are stored as
- A. Cholesterol
- B. Triglycerides (Correct Answer)
- C. Sphingomyelin
- D. None of the above
Explanation: ### Explanation **Correct Answer: B. Triglycerides** **Why it is correct:** Fatty acids are stored in the body primarily as **Triglycerides** (Triacylglycerols or TAGs). Chemically, TAGs consist of three fatty acid chains esterified to a single glycerol backbone. They serve as the ideal storage form of energy because they are **highly reduced** (yielding ~9 kcal/g) and **anhydrous** (non-polar/hydrophobic). Unlike glycogen, which binds to water, TAGs are stored in a concentrated, water-free form within the lipid droplets of **adipocytes**, allowing the body to store vast amounts of energy with minimal weight. **Why the other options are incorrect:** * **A. Cholesterol:** While cholesterol is a vital lipid component of cell membranes and a precursor for steroid hormones and bile acids, it is not a storage form for fatty acids. Excess cholesterol is typically esterified into cholesterol esters for transport or membrane structural integrity, not for energy storage. * **C. Sphingomyelin:** This is a structural phospholipid found in cell membranes, particularly in the **myelin sheath** of nerve fibers. It is composed of a sphingosine backbone rather than glycerol and is not used for energy storage. **NEET-PG High-Yield Pearls:** * **Site of Storage:** The primary site is white adipose tissue. * **Hormonal Regulation:** Storage (lipogenesis) is stimulated by **Insulin**, while mobilization (lipolysis) is triggered by **Glucagon and Epinephrine** via Hormone-Sensitive Lipase (HSL). * **Energy Yield:** Oxidation of fatty acids provides more than double the energy per gram compared to carbohydrates or proteins. * **Transport:** Since TAGs are insoluble, they are transported in the blood via lipoproteins (Chylomicrons and VLDL).
Question 52: Which of the following best describes the properties of acetyl-CoA carboxylase?
- A. Required Cofactor - Biotin; Intracellular Location - Mitochondrial; Allosteric Modifier - Citrate; Enzyme That Catalyzes a Covalent Modification - PKA
- B. Required Cofactor - Biotin; Intracellular Location - Cytoplasmic; Allosteric Modifier - Citrate; Enzyme That Catalyzes a Covalent Modification - AMP-activated protein kinase (Correct Answer)
- C. Required Cofactor - Thiamin; Intracellular Location - Mitochondrial; Allosteric Modifier - Acetyl-CoA; Enzyme That Catalyzes a Covalent Modification - PKA
- D. Required Cofactor - Thiamin; Intracellular Location - Cytoplasmic; Allosteric Modifier - Acetyl-CoA; Enzyme That Catalyzes a Covalent Modification - AMP-activated protein kinase
Explanation: **Explanation:** Acetyl-CoA Carboxylase (ACC) is the **rate-limiting enzyme** for de novo fatty acid synthesis (Lipogenesis). Understanding its regulation is crucial for NEET-PG. 1. **Why Option B is Correct:** * **Required Cofactor:** Like most carboxylases (ABC enzymes: Acetyl-CoA, Biotin, Carboxylase), ACC requires **Biotin (Vitamin B7)** to fix $CO_2$. * **Intracellular Location:** Lipogenesis occurs in the **cytosol**; therefore, ACC is a cytoplasmic enzyme. * **Allosteric Modifier:** **Citrate** acts as a feed-forward activator. High mitochondrial citrate levels signal energy surplus, causing citrate to shuttle into the cytoplasm where it polymerizes and activates inactive ACC dimers. * **Covalent Modification:** ACC is inactivated by phosphorylation. While PKA can play a role, the primary physiological "energy sensor" that phosphorylates and inhibits ACC is **AMP-activated protein kinase (AMPK)**. This ensures fatty acid synthesis stops when cellular energy (ATP) is low. 2. **Why Other Options are Incorrect:** * **Options C & D:** These list **Thiamin (B1)** as a cofactor. Thiamin is required for oxidative decarboxylation (e.g., Pyruvate Dehydrogenase), not carboxylation. * **Option A:** Incorrectly identifies the location as mitochondrial. While a minor isoform (ACC2) exists in mitochondria to regulate beta-oxidation, the primary functional context for ACC in metabolic questions is cytoplasmic lipogenesis. Furthermore, AMPK is the more specific covalent regulator compared to PKA in this context. **High-Yield Clinical Pearls for NEET-PG:** * **Inhibitor:** ACC is allosterically inhibited by **Palmitoyl-CoA** (the end product of the pathway). * **Hormonal Control:** **Insulin** activates ACC (via phosphatase), while **Glucagon/Epinephrine** inhibit it. * **Malonyl-CoA:** The product of ACC, Malonyl-CoA, inhibits **Carnitine Palmitoyltransferase-I (CPT-1)**, preventing a futile cycle by stopping fatty acid breakdown while synthesis is active.
Question 53: Fraternal twin sisters present with episodes of fasting hypoglycemia, hypoketonemia, and muscle weakness occurring only during periods of caloric deprivation. One twin dies at 5 months of age. The surviving twin develops a cardiomyopathy diagnosed at 3 years of age. Carnitine esters are elevated in muscle tissue and serum. Which of the following is the most likely diagnosis?
- A. a-L-Iduronidase deficiency
- B. Acid maltase deficiency (a 1,4-glucosidase deficiency)
- C. Carnitine uptake deficiency
- D. Long-chain acyl CoA dehydrogenase (LCAD) deficiency (Correct Answer)
Explanation: ### Explanation **1. Why Option D is Correct:** The clinical presentation of **hypoketonemic hypoglycemia** during fasting is the hallmark of a defect in **Fatty Acid Oxidation (FAO)**. Normally, during fasting, the body breaks down fatty acids to produce acetyl-CoA, which enters the TCA cycle or forms ketone bodies. A defect in this pathway leads to low glucose (due to impaired gluconeogenesis) and low ketones. The presence of **elevated carnitine esters** (acylcarnitines) in the serum and muscle indicates that carnitine is successfully binding to long-chain fatty acids (via CPT-I), but the subsequent oxidation step within the mitochondria is blocked. **Long-chain acyl-CoA dehydrogenase (LCAD)** or **VLCAD** deficiency prevents the first step of the $\beta$-oxidation spiral for long-chain fats, leading to energy failure in the heart (cardiomyopathy) and skeletal muscle. **2. Why Other Options are Incorrect:** * **Option A ($\alpha$-L-Iduronidase deficiency):** This causes Hurler syndrome (a Mucopolysaccharidosis). It presents with coarse facial features, hepatosplenomegaly, and corneal clouding, not fasting hypoglycemia. * **Option B (Acid maltase deficiency):** Also known as Pompe disease (GSD Type II). While it causes cardiomyopathy and muscle weakness, it does **not** cause hypoglycemia or hypoketonemia because glycogenolysis and gluconeogenesis remain intact. * **Option C (Carnitine uptake deficiency):** While this also causes hypoketonemic hypoglycemia, it would result in **low** levels of carnitine esters in the tissue, as fatty acids cannot be conjugated or transported into the mitochondria. **3. NEET-PG High-Yield Pearls:** * **MCAD Deficiency:** The most common FAO disorder; presents similarly but usually lacks the severe cardiomyopathy seen in LCAD/VLCAD. * **Differentiating Feature:** If carnitine levels are low in the blood, think **Uptake/Transporter defect**; if acylcarnitines (esters) are high, think **Dehydrogenase defects**. * **Treatment:** Avoidance of fasting and a diet high in carbohydrates and medium-chain triglycerides (MCTs) for LCAD/VLCAD patients.
Question 54: What is the most important predictor of coronary artery disease?
- A. VLDL
- B. LDL
- C. Chylomicron
- D. LDL/HDL ratio (Correct Answer)
Explanation: **Explanation:** The risk of Coronary Artery Disease (CAD) is not determined solely by the concentration of a single lipoprotein, but rather by the balance between pro-atherogenic and anti-atherogenic factors. **Why the LDL/HDL ratio is the correct answer:** While LDL (Low-Density Lipoprotein) is the primary carrier of cholesterol to peripheral tissues and is directly involved in plaque formation, HDL (High-Density Lipoprotein) mediates "Reverse Cholesterol Transport," removing excess cholesterol from arteries. The **LDL/HDL ratio** (also known as the Atherogenic Index) serves as the most potent predictor of CAD because it reflects the clinical "tug-of-war" between cholesterol deposition and clearance. A ratio greater than 3.5 is considered a significant risk factor for ischemic heart disease. **Analysis of Incorrect Options:** * **VLDL (Very Low-Density Lipoprotein):** Primarily transports endogenous triglycerides. While elevated VLDL contributes to metabolic syndrome, it is a less specific predictor of CAD than the ratio. * **LDL:** Often called "bad cholesterol," it is a major risk factor. However, a patient with high LDL may be protected if their HDL is also exceptionally high, making the isolated LDL value less predictive than the ratio. * **Chylomicron:** These transport dietary lipids. They are the least dense lipoproteins and are not typically associated with atherosclerosis; their primary clinical risk (when extremely elevated) is pancreatitis. **High-Yield Clinical Pearls for NEET-PG:** * **Apo B/Apo A-1 ratio:** This is often considered even more accurate than the LDL/HDL ratio in predicting cardiovascular risk. * **Friedewald Formula:** LDL = Total Cholesterol – [HDL + (Triglycerides/5)]. (Note: This is invalid if TG >400 mg/dL). * **Small dense LDL (Type B):** These are more atherogenic than large, buoyant LDL particles.
Question 55: Which of the following is true about the action of LCAT?
- A. Formation of fatty acids
- B. Esterification of cholesterol (Correct Answer)
- C. Hydrolysis of fatty acids
- D. Adds an ester group to fatty acids
Explanation: **Explanation:** **LCAT (Lecithin-Cholesterol Acyltransferase)** is a critical enzyme in lipid metabolism, synthesized by the liver and secreted into the plasma. Its primary function is the **esterification of free cholesterol** into cholesterol esters. 1. **Why Option B is Correct:** LCAT acts on the surface of High-Density Lipoprotein (HDL). It transfers a fatty acid from the C2 position of **Lecithin** (Phosphatidylcholine) to the 3-OH group of **free cholesterol**. This process creates a hydrophobic cholesterol ester, which then moves into the core of the HDL particle. This mechanism is the driving force behind **Reverse Cholesterol Transport**, allowing HDL to "scavenge" cholesterol from peripheral tissues and transport it back to the liver. 2. **Why Other Options are Incorrect:** * **Options A & C:** LCAT is not involved in the synthesis or simple hydrolysis of free fatty acids; its specific role is the transfer of an acyl group. * **Option D:** LCAT adds an ester group to *cholesterol*, not to fatty acids. **High-Yield Clinical Pearls for NEET-PG:** * **Activator:** LCAT is activated by **Apo A-I** (found on HDL). * **Fish-Eye Disease:** A partial LCAT deficiency characterized by corneal opacities but without significant renal disease. * **Classic LCAT Deficiency:** A complete deficiency leading to the "Triad" of **Corneal opacities, Hemolytic anemia, and Proteinuria/Renal failure**. * **Intracellular Counterpart:** While LCAT esterifies cholesterol in the *plasma*, the enzyme **ACAT** (Acyl-CoA: Cholesterol Acyltransferase) performs the same function *inside cells*.
Question 56: Fatty liver is due to the accumulation of which substance?
- A. Triglycerides (Correct Answer)
- B. Lipoproteins
- C. LDL
- D. VLDL
Explanation: **Explanation:** **Fatty liver (Steatosis)** is defined as the abnormal accumulation of **Triglycerides (TGs)** within the hepatocytes. Under normal physiological conditions, the liver synthesizes TGs from fatty acids and glycerol. These TGs are then packaged into Very Low-Density Lipoproteins (VLDL) and secreted into the bloodstream. Fatty liver occurs when there is an imbalance between the synthesis/uptake of TGs and their secretion or oxidation. * **Why Triglycerides are correct:** TGs are the primary storage form of lipids. In conditions like chronic alcoholism, obesity, or diabetes, there is either an increased influx of free fatty acids to the liver or impaired fatty acid oxidation, leading to the buildup of neutral fat (TGs) in large vacuoles within the cytoplasm. **Why the other options are incorrect:** * **VLDL:** This is the transport vehicle for TGs. A *deficiency* in VLDL assembly or secretion (often due to lack of Apolipoprotein B-100 or choline) actually causes fatty liver because TGs cannot leave the hepatocyte. * **Lipoproteins:** This is a general category. While lipoproteins are involved in lipid transport, they do not accumulate to cause steatosis; rather, their synthesis failure is a causative factor. * **LDL:** LDL is a product of VLDL metabolism in the peripheral circulation and is primarily involved in transporting cholesterol to tissues, not in the intrahepatic accumulation seen in fatty liver. **High-Yield Facts for NEET-PG:** * **Lipotropic factors:** Substances like **Choline, Methionine, and Betaine** are required for VLDL synthesis. Their deficiency leads to fatty liver. * **Alcoholic Fatty Liver:** Increased NADH/NAD+ ratio inhibits fatty acid oxidation and promotes TG synthesis. * **Non-Alcoholic Fatty Liver Disease (NAFLD):** Strongly associated with insulin resistance and metabolic syndrome. * **Histology:** Characterized by "Signet ring" appearance of hepatocytes where the nucleus is pushed to the periphery by the TG droplet.
Question 57: Which of the following is a derived lipid?
- A. Fatty acids (Correct Answer)
- B. Glycolipid
- C. Phospholipid
- D. Triglyceride
Explanation: ### Explanation Lipids are broadly classified into three categories based on their chemical composition: Simple, Compound, and Derived lipids. **1. Why Fatty Acids are the Correct Answer:** **Derived lipids** are substances produced from the hydrolysis of simple and compound lipids. They possess the characteristics of lipids but do not fit the structural definition of esters. **Fatty acids** are the primary building blocks obtained when triglycerides or phospholipids are broken down. Other examples of derived lipids include glycerol, steroids (cholesterol), fat-soluble vitamins (A, D, E, K), and ketone bodies. **2. Analysis of Incorrect Options:** * **Triglycerides (Option D):** These are **Simple Lipids**. They are esters of fatty acids with glycerol. They serve as the primary storage form of energy in adipose tissue. * **Phospholipids (Option C) & Glycolipids (Option B):** These are **Compound (Complex) Lipids**. They contain fatty acids and an alcohol plus an additional group. Phospholipids contain a phosphoric acid residue (e.g., Lecithin), while glycolipids contain a carbohydrate moiety (e.g., Cerebrosides, Gangliosides). **3. NEET-PG High-Yield Clinical Pearls:** * **Amphipathic Nature:** Phospholipids and fatty acids are amphipathic (possessing both hydrophilic and hydrophobic parts), which is crucial for forming the lipid bilayer of cell membranes. * **Essential Fatty Acids:** Linoleic acid and Linolenic acid cannot be synthesized by the body and must be obtained from the diet. * **Clinical Correlation:** Deficiency of the enzyme *Sphingomyelinase* leads to **Niemann-Pick disease**, while deficiency of *Glucocerebrosidase* leads to **Gaucher’s disease**—both involving the metabolism of complex lipids.
Question 58: Which vegetable oil has the highest concentration of linoleic acid?
- A. Groundnut oil
- B. Safflower oil (Correct Answer)
- C. Mustard oil
- D. Coconut oil
Explanation: **Explanation:** **Linoleic acid (18:2; ω-6)** is an essential polyunsaturated fatty acid (PUFA) that cannot be synthesized by the human body and must be obtained through diet. It serves as the precursor for arachidonic acid, which is vital for the synthesis of eicosanoids (prostaglandins and leukotrienes). **Why Safflower oil is correct:** Safflower oil contains the highest concentration of linoleic acid among common vegetable oils, typically ranging from **70% to 75%**. In medical biochemistry and nutrition, it is considered the gold standard source for ω-6 PUFAs. **Analysis of Incorrect Options:** * **Groundnut oil:** Contains moderate amounts of linoleic acid (approx. 30%), but is primarily rich in monounsaturated fatty acids (MUFA) like oleic acid. * **Mustard oil:** Characterized by a high content of **erucic acid** (a long-chain MUFA) and a balanced ratio of ω-3 and ω-6, but its linoleic acid content is relatively low (approx. 15%). * **Coconut oil:** Predominantly composed of **saturated fatty acids** (over 90%), mainly lauric acid. It contains negligible amounts of linoleic acid (approx. 2%). **High-Yield Clinical Pearls for NEET-PG:** * **Essential Fatty Acids (EFA):** Linoleic acid (ω-6) and α-Linolenic acid (ω-3) are the two EFAs for humans. * **EFA Deficiency:** Characterized by **Phrynoderma** (follicular hyperkeratosis), scaly skin, and poor wound healing. * **PUFA Hierarchy:** Safflower oil (75%) > Corn oil (55-60%) > Soya bean oil (50%) > Groundnut oil (30%). * **Cardiovascular Health:** Replacing saturated fats with PUFA-rich oils like safflower oil helps lower LDL cholesterol levels.
Question 59: What is the major regulatory step in cholesterol synthesis?
- A. Cyclization of squalene to lanosterol
- B. 3-hydroxy-3-methylglutaryl-CoA synthase
- C. 3-hydroxy-3-methylglutaryl-CoA lyase
- D. 3-hydroxy-3-methylglutaryl-CoA reductase (Correct Answer)
Explanation: **Explanation:** The synthesis of cholesterol is a complex multi-step process occurring primarily in the liver. The conversion of **HMG-CoA to Mevalonate** is the **committed, rate-limiting, and major regulatory step** of this pathway. **1. Why Option D is Correct:** The enzyme **HMG-CoA Reductase** catalyzes the reduction of HMG-CoA to mevalonate using two molecules of NADPH. It is the primary site for feedback inhibition by cholesterol and is regulated by hormonal control (insulin activates it, while glucagon inhibits it via phosphorylation). Because it is the slowest step, it determines the overall flux of the pathway. **2. Why the Other Options are Incorrect:** * **Option A:** The cyclization of squalene to lanosterol is a later stage in the pathway. While important for forming the steroid nucleus, it is not the primary regulatory checkpoint. * **Option B:** **HMG-CoA Synthase** exists in two isoforms. The *cytosolic* form is involved in cholesterol synthesis, but it is not the rate-limiting step. (Note: The *mitochondrial* form is involved in ketogenesis). * **Option C:** **HMG-CoA Lyase** is an enzyme exclusively involved in **ketogenesis** (breaking down HMG-CoA into acetyl-CoA and acetoacetate) and leucine catabolism. It plays no role in cholesterol synthesis. **Clinical Pearls for NEET-PG:** * **Statins:** Drugs like Atorvastatin and Rosuvastatin are **competitive inhibitors** of HMG-CoA Reductase, used to treat hypercholesterolemia. * **Subcellular Location:** Cholesterol synthesis begins in the **cytosol** and finishes in the **endoplasmic reticulum**. * **SREBP:** The Sterol Regulatory Element-Binding Protein is the transcription factor that regulates the expression of the HMG-CoA Reductase gene.
Question 60: Which enzyme in the fatty acid synthase complex utilizes pantothenic acid as a coenzyme?
- A. Acetyl transacylase
- B. Thioesterase
- C. Enoyl reductase
- D. Acyl carrier protein (Correct Answer)
Explanation: **Explanation:** The **Acyl Carrier Protein (ACP)** is a crucial component of the Fatty Acid Synthase (FAS) multienzyme complex. It functions as the "arm" that carries the growing fatty acid chain between the different catalytic sites of the complex. 1. **Why ACP is correct:** ACP contains a prosthetic group called **4'-phosphopantetheine**, which is derived from **Pantothenic acid (Vitamin B5)**. This group contains a reactive sulfhydryl (-SH) group that forms a high-energy thioester bond with the acyl groups, allowing them to be shuttled through the various stages of fatty acid synthesis. 2. **Why other options are incorrect:** * **Acetyl transacylase:** This enzyme transfers the initial acetyl group from CoA to the ACP. While it interacts with ACP, the enzyme itself does not utilize pantothenic acid as its own coenzyme. * **Thioesterase:** This is the final enzyme in the FAS complex that releases the finished palmitate chain by hydrolyzing the thioester bond. It does not require a B5 derivative. * **Enoyl reductase:** This enzyme performs the final reduction step in each cycle. It utilizes **NADPH** (derived from Vitamin B3/Niacin) as a coenzyme, not pantothenic acid. **High-Yield Clinical Pearls for NEET-PG:** * **Vitamin B5 (Pantothenic acid)** is a constituent of both **Coenzyme A (CoA)** and **ACP**. * The FAS complex is a **homodimer**; each monomer has 7 enzyme activities and one ACP. * **NADPH** is the essential reducing agent for fatty acid synthesis, primarily sourced from the **HMP Shunt**. * The "swinging arm" mechanism of 4'-phosphopantetheine is functionally analogous to the lipoamide arm in the Pyruvate Dehydrogenase complex.
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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