Energy Production and Metabolism — MCQs

Energy Production and Metabolism Indian Medical PG Practice Questions and MCQs

Question 291: Pyruvate dehydrogenase requires all cofactors except:

A. Thiamin
B. Pyridoxin (Vitamin B6) (Correct Answer)
C. Riboflavin
D. Niacin

Explanation: ***Pyridoxin (Vitamin B6)*** - **Pyridoxin** (vitamin B6) is a coenzyme for many enzymes involved in **amino acid metabolism**, but it is **not directly required** by the pyruvate dehydrogenase complex. - The pyruvate dehydrogenase complex uses **thiamine pyrophosphate**, **lipoic acid**, **FAD**, **NAD+**, and **Coenzyme A** as cofactors. *Thiamin* - **Thiamin pyrophosphate** (TPP), derived from thiamin (vitamin B1), is a crucial coenzyme for the **E1 subunit** of the pyruvate dehydrogenase complex. - It participates in the **decarboxylation** of pyruvate, releasing CO2. *Riboflavin* - **FAD** (flavin adenine dinucleotide), derived from riboflavin (vitamin B2), is a coenzyme for the **E3 subunit** (dihydrolipoyl dehydrogenase) of the pyruvate dehydrogenase complex. - It is involved in the **regeneration of oxidized lipoamide**. *Niacin* - **NAD+** (nicotinamide adenine dinucleotide), derived from niacin (vitamin B3), is a coenzyme for the **E3 subunit** of the pyruvate dehydrogenase complex. - It acts as an **electron acceptor** during the reoxidation of FADH2.

Question 292: Which of the following enzyme activity decreases in fasting?

A. Hormone sensitive lipase
B. Glycogen phosphorylase
C. Acetyl CoA Carboxylase
D. Phosphofructokinase I (Correct Answer)

Explanation: ***Phosphofructokinase I*** - **Phosphofructokinase I (PFK-1)** activity **decreases** during fasting due to **decreased insulin-to-glucagon ratio**, which reduces **fructose-2,6-bisphosphate (F-2,6-BP)** levels, a powerful allosteric activator of PFK-1. - This reduction in activity slows down **glycolysis**, conserving glucose for critical tissues like the brain and redirecting metabolism toward **gluconeogenesis**. - **PFK-1 is the rate-limiting enzyme of glycolysis**, making its regulation particularly significant in the fasted state. *Hormone sensitive lipase* - **Hormone sensitive lipase (HSL)** activity **increases** during fasting due to elevated **glucagon** and **epinephrine** levels, which stimulate its phosphorylation via **protein kinase A (PKA)**. - This increased activity promotes the breakdown of stored **triglycerides** in adipose tissue, releasing **fatty acids** for β-oxidation and energy production. *Glycogen phosphorylase* - **Glycogen phosphorylase** activity **increases** during fasting, primarily stimulated by **glucagon** and **epinephrine**, leading to the breakdown of **glycogen** stores. - This enzyme is crucial for **glycogenolysis**, providing glucose to maintain blood sugar levels when dietary intake is absent. *Acetyl CoA Carboxylase* - **Acetyl CoA Carboxylase (ACC)** activity also **decreases** during fasting, as it is inhibited by **phosphorylation** mediated by **AMP-activated protein kinase (AMPK)** and **protein kinase A (PKA)**. - This reduction in activity inhibits **fatty acid synthesis**, shifting metabolism towards fatty acid **oxidation** for energy production. - **Note:** While ACC activity does decrease during fasting, **PFK-1** is considered the primary answer as it represents the key regulatory point for **glucose metabolism** (glycolysis vs. gluconeogenesis), which is the central metabolic shift during fasting.

Question 293: Which of the following is not a free radical?

A. Superoxide anion
B. Hydrogen peroxide (H2O2) (Correct Answer)
C. Nitric oxide (NO·)
D. Hydroxyl radical (.OH)

Explanation: ***Hydrogen peroxide (H₂O₂)*** - **Hydrogen peroxide** is a **reactive oxygen species (ROS)** but is not a free radical because it has **no unpaired electrons** in its outermost shell. - While it can be converted into the highly reactive hydroxyl radical via the **Fenton reaction**, it is stable enough to be transported across membranes. *Superoxide anion (O₂⁻)* - The **superoxide anion (O₂⁻)** is a free radical because it has an **unpaired electron** in its outer shell. - It is one of the primary **reactive oxygen species** formed during cellular metabolism and can damage cellular components. *Nitric oxide (NO·)* - **Nitric oxide** is an important **free radical** with a single **unpaired electron** in its molecular structure. - It functions as a vital signaling molecule in vascular biology, regulating blood pressure and neurotransmission, despite being a free radical. *Hydroxyl radical (·OH)* - The **hydroxyl radical (·OH)** is one of the most reactive and damaging **free radicals** in biological systems. - It has a single **unpaired electron**, making it highly unstable and able to react indiscriminately with virtually all types of biomolecules.

Question 294: Energy source used by brain in later days of starvation is

A. Glucose
B. Ketone bodies (Correct Answer)
C. Glycogen
D. Fatty acids

Explanation: ***Ketone bodies*** - During **prolonged starvation**, the liver produces **ketone bodies** (acetoacetate and β-hydroxybutyrate) from fatty acid breakdown. - The brain adapts to utilize these ketone bodies as a primary energy source, reducing its reliance on **glucose**. *Glucose* - While **glucose** is the primary energy source for the brain under normal conditions, its availability diminishes significantly during prolonged starvation. - The brain attempts to conserve glucose for essential functions by switching to alternative fuels. *Glycogen* - The brain stores very limited amounts of **glycogen**, which are rapidly depleted within minutes of glucose deprivation. - It is not a sustainable or significant energy source during extended periods of starvation. *Fatty acids* - **Fatty acids** cannot directly cross the **blood-brain barrier** to a significant extent, thus they are not a direct fuel source for brain cells. - They are, however, used by the liver to synthesize ketone bodies, which then serve as brain fuel.

Question 295: Most abundant source of fuel in starvation -

A. Liver glycogen
B. Muscle glycogen
C. Adipose tissue (Correct Answer)
D. Blood glucose

Explanation: ***Adipose tissue*** - **Adipose tissue** stores **triglycerides**, which are hydrolyzed into fatty acids and glycerol to serve as the body's primary energy source during prolonged starvation. - The energy reserve in adipose tissue is significantly larger than glycogen stores, providing **sustained fuel** for days or weeks. *Liver glycogen* - **Liver glycogen** is a readily available source of glucose but is rapidly depleted within **12-24 hours** during starvation. - Its primary role is to maintain **blood glucose levels** for glucose-dependent tissues like the brain. *Muscle glycogen* - **Muscle glycogen** is used primarily for **muscle contraction** and cannot be directly released into the bloodstream to maintain blood glucose levels. - While it's a significant energy reserve for working muscles, it does not contribute to systemic fuel needs during starvation. *Blood glucose* - **Blood glucose** is the immediate circulating fuel, but it is tightly regulated and its levels decrease during starvation as glycogen stores are depleted. - It is not an abundant stored source of fuel but rather a transport form of energy.

Question 296: Reducing equivalents produced in glycolysis are transported from cytosol to mitochondria by ?

A. Carnitine
B. Creatine
C. Malate-aspartate shuttle (Correct Answer)
D. Glutamate shuttle

Explanation: ***Malate shuttle*** - The **malate-aspartate shuttle** is a primary mechanism for transporting **NADH reducing equivalents** from the cytosol to the mitochondrial matrix for **oxidative phosphorylation**. - It involves a series of **enzymes and transporters** that indirectly move electrons from NADH by converting **oxaloacetate to malate** in the cytosol, which then enters the mitochondria. *Carnitine* - **Carnitine** is primarily involved in the transport of **long-chain fatty acids** into the mitochondrial matrix for **beta-oxidation**. - It is not directly involved in the shuttle of NADH reducing equivalents generated during glycolysis. *Creatine* - **Creatine** and its phosphorylated form, **phosphocreatine**, are crucial for **energy buffering and transport** in tissues with high and fluctuating energy demands, like muscle and brain. - The creatine-phosphocreatine shuttle facilitates the rapid regeneration of ATP, but it is not involved in transporting glycolytic reducing equivalents. *Glutamate shuttle* - While glutamate and aspartate are components of the **malate-aspartate shuttle**, there isn't a standalone "glutamate shuttle" for transporting glycolytic reducing equivalents. - The **glutamate-aspartate transaminase** is an enzyme within the malate-aspartate shuttle, converting oxaloacetate to aspartate and alpha-ketoglutarate to glutamate from the matrix to the cytosol.

Question 297: What is the immediate source of energy for cellular processes?

A. Cori's cycle
B. HMP
C. ATP (Correct Answer)
D. TCA cycle

Explanation: ***ATP*** - **Adenosine triphosphate (ATP)** is the direct and immediate source of energy for almost all cellular processes, including **muscle contraction**, **active transport**, and **biosynthesis**. - Its high-energy phosphate bonds release energy upon hydrolysis, driving various cellular functions. *Cori's cycle* - The **Cori cycle** involves the interconversion of **lactate** and **glucose** between the muscle and the liver to regenerate glucose stores. - It is an important metabolic pathway for glucose homeostasis during anaerobic conditions, but it does not directly provide immediate energy for cellular processes. *HMP* - The **Hexose Monophosphate Pathway (HMP)**, also known as the **pentose phosphate pathway**, primarily produces **NADPH** and **ribose-5-phosphate**. - While it generates NADPH for reductive biosynthesis and protects against oxidative stress, it is not an immediate source of energy. *TCA cycle* - The **Tricarboxylic Acid (TCA) cycle**, or Krebs cycle, is a central metabolic pathway that oxidizes **acetyl-CoA** to produce **ATP**, **NADH**, and **FADH2**. - While it is a major producer of ATP, it is not the *immediate* source; instead, it generates the precursors that fuel oxidative phosphorylation to produce ATP.

Question 298: Which organelle produces and destroys H2O2?

A. Peroxisome (Correct Answer)
B. Lysosome
C. Golgi body
D. Ribosome

Explanation: ***Peroxisome*** - **Peroxisomes** are organelles that both produce and break down **hydrogen peroxide (H2O2)** during metabolic processes. - They contain **oxidases** (such as D-amino acid oxidase and urate oxidase) that produce H2O2 as a byproduct during oxidation reactions. - They also contain the enzyme **catalase** that converts H2O2 into water and oxygen, protecting the cell from oxidative damage. - This dual function makes peroxisomes unique in H2O2 metabolism. *Lysosome* - **Lysosomes** are responsible for breaking down waste materials and cellular debris through **hydrolytic enzymes**. - They are primarily involved in **cellular digestion** and waste removal, not H2O2 metabolism. *Golgi body* - The **Golgi apparatus** modifies, sorts, and packages proteins and lipids for secretion or delivery to other organelles. - It is crucial for **protein trafficking** and glycosylation, but does not produce or destroy H2O2. *Ribosome* - **Ribosomes** are responsible for **protein synthesis** (translation) based on genetic information carried by mRNA. - They are involved in the assembly of amino acids into proteins, not the metabolism of hydrogen peroxide.

Question 299: What is the theoretical maximum number of ATPs generated from the Krebs cycle per glucose molecule?

A. 24 ATPs
B. 20 ATPs (Correct Answer)
C. 12 ATPs
D. 30 ATPs

Explanation: ***20 ATPs*** - Each **glucose molecule** yields two molecules of **acetyl-CoA** which enter the Krebs cycle. - Each turn of the **Krebs cycle** generates **3 NADH, 1 FADH2, and 1 GTP** (equivalent to 1 ATP). - Using modern **P/O ratios**: 3 NADH × 2.5 = 7.5 ATP, 1 FADH2 × 1.5 = 1.5 ATP, 1 GTP = 1 ATP, totaling **10 ATP per acetyl-CoA**. - Since two acetyl-CoA molecules are produced per glucose, the total is **2 × 10 = 20 ATPs** from the Krebs cycle alone. *24 ATPs* - This value is based on **older P/O ratios** (3 ATP per NADH, 2 ATP per FADH2), which have been revised in modern biochemistry. - While historically taught, current understanding of the **electron transport chain** efficiency yields lower ATP values per NADH and FADH2. *12 ATPs* - This represents the ATP yield from **one turn** of the **Krebs cycle** (or one acetyl-CoA molecule) using older P/O ratios, not a complete glucose molecule. - A single glucose molecule produces **two acetyl-CoA** molecules, each initiating a separate turn of the cycle. *30 ATPs* - This value typically reflects the theoretical maximum **total ATP** generated from **complete oxidation** of **one glucose molecule**, including contributions from **glycolysis** and the **electron transport chain**. - The Krebs cycle alone contributes only a portion of this total; 30 ATPs includes ATP from all stages of glucose metabolism.

Question 300: What is the mechanism of action of Atractyloside?

A. Inhibitor of oxidative phosphorylation (Correct Answer)
B. Uncoupler of oxidative phosphorylation
C. Inhibitor of complex III of the electron transport chain
D. Inhibitor of complex I of the electron transport chain

Explanation: ***Inhibitor of oxidative phosphorylation*** - **Atractyloside** is a potent **inhibitor of oxidative phosphorylation** by binding to and blocking the adenine nucleotide translocase (ANT) protein. - By inhibiting **ANT**, Atractyloside prevents the exchange of **ADP into the mitochondrial matrix** and ATP out, thereby halting ATP synthesis. *Uncoupler of oxidative phosphorylation* - **Uncouplers** dissipate the **proton gradient** across the inner mitochondrial membrane, allowing electron transport to continue without ATP synthesis. - Examples of uncouplers include **dinitrophenol (DNP)** and **thermogenin**, which act by increasing membrane permeability to protons. *Inhibitor of complex III of the electron transport chain* - Inhibitors of **Complex III** (cytochrome bc1 complex) block the transfer of electrons from **ubiquinone (CoQ)** to cytochrome c. - Examples include **antimycin A** and myxothiazol, which lead to an accumulation of reduced ubiquinone and a halt in electron flow. *Inhibitor of complex I of the electron transport chain* - **Complex I inhibitors** block the transfer of electrons from **NADH to ubiquinone (CoQ)** in the electron transport chain. - **Rotenone** and **amytal** are well-known inhibitors that prevent the pumping of protons and reduce ATP synthesis downstream.

Practice by Chapter

Bioenergetics and Thermodynamics

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ATP as Energy Currency

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Tricarboxylic Acid Cycle

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Electron Transport Chain

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Oxidative Phosphorylation

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Mitochondrial Diseases

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Uncouplers and Inhibitors of Oxidative Phosphorylation

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Shuttle Systems: Malate-Aspartate and Glycerol-Phosphate

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Energy Yield from Nutrients

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Metabolic Rate and Basal Metabolism

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Brown Adipose Tissue and Thermogenesis

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Oxygen Toxicity and Free Radicals

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