Carbohydrate Metabolism — MCQs
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Which of the following statements BEST describes the net ATP production in glycolysis?
What is the net number of ATP molecules and NADH formed in glycolysis per glucose molecule?
Which of the following GAG is not sulfated?
Increased uric acid levels are seen in which glycogen storage disease ?
ATP is consumed at which of the following steps of glycolysis?
At which step in glycolysis is NADH produced during the oxidation of glyceraldehyde-3-phosphate?
Which of the following is an amino sugar formed from fructose-6-phosphate?
Glucose is converted to glucuronate by which process?
Which one of the following statements concerning gluconeogenesis is correct?
Which enzyme is active when the insulin:glucagon ratio is low?
Carbohydrate Metabolism Indian Medical PG Practice Questions and MCQs
Question 771: Which of the following statements BEST describes the net ATP production in glycolysis?
- A. Glycolysis produces 2 molecules of pyruvate
- B. Glycolysis produces a net gain of 2 ATP per glucose molecule (Correct Answer)
- C. Hexokinase consumes ATP during glycolysis
- D. Aldolase catalyzes the conversion of fructose-1,6-bisphosphate into two three-carbon molecules
Explanation: ***Glycolysis produces a net gain of 2 ATP per glucose molecule*** - In the initial "investment" phase of glycolysis, **2 ATP molecules are consumed** to phosphorylate glucose. - In the subsequent "payoff" phase, **4 ATP molecules are produced** through substrate-level phosphorylation, resulting in a net gain of 2 ATP. *Glycolysis produces 2 molecules of pyruvate* - While glycolysis does produce **2 molecules of pyruvate** from one glucose molecule, this statement describes the end product of the pathway, not the net ATP production. - Pyruvate is a crucial product that can be further metabolized in aerobic or anaerobic conditions, but it does not directly represent the energy yield in terms of ATP. *Hexokinase consumes ATP during glycolysis* - **Hexokinase** is indeed the enzyme that catalyzes the first ATP-consuming step in glycolysis, phosphorylating glucose to glucose-6-phosphate. - However, this statement describes only one aspect of ATP utilization within the pathway and does not account for the total ATP produced or the overall net gain. *Aldolase catalyzes the conversion of fructose-1,6-bisphosphate into two three-carbon molecules* - **Aldolase** is a key enzyme in glycolysis responsible for cleaving **fructose-1,6-bisphosphate** into dihydroxyacetone phosphate and glyceraldehyde-3-phosphate. - This step is part of the preparatory phase of glycolysis but does not directly describe the net ATP production.
Question 772: What is the net number of ATP molecules and NADH formed in glycolysis per glucose molecule?
- A. 4 ATP, 2 NADH
- B. 4 ATP, 4 NADH
- C. 2 ATP, 4 NADH
- D. 2 ATP, 2 NADH (Correct Answer)
Explanation: **2 ATP, 2 NADH** - Glycolysis has a net yield of **2 molecules of ATP** because 4 ATP molecules are produced, but 2 ATP molecules are consumed during the initial energy investment phase. - **2 molecules of NADH** are also produced during the energy generation phase when glyceraldehyde-3-phosphate is oxidized. *4 ATP, 2 NADH* - While 4 ATP molecules are indeed produced during glycolysis, this option does not account for the **2 ATP molecules consumed** in the initial steps, leading to an incorrect net value. - The production of **2 NADH** is correct, but the ATP count is the gross rather than the net. *4 ATP, 4 NADH* - This option overstates the production of both ATP and NADH. While **4 ATP are produced (gross)**, the net is 2 ATP. - Only **2 NADH** molecules are formed per glucose molecule in glycolysis, not 4. *2 ATP, 4 NADH* - This option accurately reflects the **net ATP yield of 2 molecules**. - However, it exaggerates the production of NADH, as only **2 molecules of NADH** are formed during glycolysis, not 4.
Question 773: Which of the following GAG is not sulfated?
- A. Keratan sulfate
- B. Dermatan sulfate
- C. Chondroitin sulfate
- D. Hyaluronic acid (Correct Answer)
Explanation: ***Hyaluronic acid*** - **Hyaluronic acid** is unique among glycosaminoglycans (GAGs) because it is the only one that is **not sulfated**. - It also distinguishes itself by being the only GAG that does **not form proteoglycans** and is not synthesized in the Golgi apparatus. *Chondroitin sulfate* - **Chondroitin sulfate** is a sulfated glycosaminoglycan that is a major component of the **extracellular matrix**, particularly in cartilage. - Its sulfate groups contribute to its **negative charge**, allowing it to attract water and provide resistance to compression. *Dermatan sulfate* - **Dermatan sulfate** is another sulfated GAG, found predominantly in the skin, blood vessels, and heart valves. - It contains **sulfate groups**, which are crucial for its interactions with various proteins and its role in tissue structure. *Keratan sulfate* - **Keratan sulfate** is a sulfated GAG found in the cornea, cartilage, and bone. - It is distinct from other GAGs due to its **lack of uronic acid** and the presence of sulfate groups.
Question 774: Increased uric acid levels are seen in which glycogen storage disease ?
- A. Type I (Von Gierke's disease) (Correct Answer)
- B. Type II (Pompe disease)
- C. Type IV (Andersen disease)
- D. Type III (Cori disease)
Explanation: ***Type I (Von Gierke's disease)*** - In **Von Gierke's disease**, the deficiency of **glucose-6-phosphatase** leads to accumulation of glucose-6-phosphate in hepatocytes. - **Hyperuricemia** occurs due to: 1. **Increased purine degradation** - Metabolic stress leads to accelerated ATP breakdown and increased uric acid production 2. **Decreased renal excretion** - Lactic acidosis (from G6P → pyruvate → lactate) competitively inhibits uric acid secretion in renal tubules 3. **Enhanced purine synthesis** - Increased availability of ribose-5-phosphate from pentose phosphate pathway - Classic triad: **Hepatomegaly, hypoglycemia, and lactic acidosis with hyperuricemia** *Type II (Pompe disease)* - Caused by a deficiency of **acid alpha-glucosidase** (acid maltase), leading to glycogen accumulation in **lysosomes**. - Primarily affects the **heart**, **muscles**, and **liver**, but does not cause hyperuricemia. *Type IV (Andersen disease)* - Results from a deficiency of **glycogen branching enzyme**, leading to the formation of abnormal glycogen with long, unbranched chains. - Primarily affects the **liver** and **spleen**, causing cirrhosis and hepatic failure, but not hyperuricemia. *Type III (Cori disease)* - Caused by a deficiency of **glycogen debranching enzyme** (amylo-1,6-glucosidase), leading to abnormal accumulation of glycogen with short outer branches. - Presents with hepatomegaly, hypoglycemia, and muscle weakness, but **hyperuricemia is not a characteristic feature**.
Question 775: ATP is consumed at which of the following steps of glycolysis?
- A. Pyruvate kinase
- B. Isomerase
- C. Hexokinase (Correct Answer)
- D. Enolase
Explanation: ***Hexokinase*** - This enzyme catalyzes the **first step of glycolysis**, the phosphorylation of glucose to **glucose-6-phosphate**, which requires the consumption of one molecule of **ATP**. - ATP is hydrolyzed to **ADP**, providing the necessary phosphate group and energy for this irreversible reaction. - Note: Hexokinase is one of **two ATP-consuming steps** in glycolysis (the other being phosphofructokinase in step 3). *Pyruvate kinase* - This enzyme catalyzes the **final step of glycolysis**, converting **phosphoenolpyruvate (PEP)** to pyruvate. - This reaction involves the **production of ATP** from ADP, not its consumption, as it's one of the substrate-level phosphorylation steps. *Isomerase* - Isomerase enzymes, like phosphoglucose isomerase, convert one isomer to another (e.g., glucose-6-phosphate to fructose-6-phosphate). - These reactions generally involve an **internal rearrangement of atoms** and do not directly consume or produce ATP. *Enolase* - Enolase catalyzes the reversible conversion of **2-phosphoglycerate to phosphoenolpyruvate (PEP)**, releasing a molecule of water. - This step occurs before the ATP-generating step catalyzed by pyruvate kinase and **does not consume or produce ATP**.
Question 776: At which step in glycolysis is NADH produced during the oxidation of glyceraldehyde-3-phosphate?
- A. Pyruvate kinase
- B. Enolase
- C. PFK-1
- D. Glyceraldehyde-3-phosphate dehydrogenase (Correct Answer)
Explanation: ***Glyceraldehyde-3-phosphate dehydrogenase*** - This enzyme catalyzes the oxidation and **phosphorylation** of glyceraldehyde-3-phosphate, producing **1,3-bisphosphoglycerate**. - During this reaction, **NAD+ is reduced to NADH**, which is a crucial step for energy production. *Pyruvate kinase* - This enzyme catalyzes the final step of glycolysis, transferring a phosphate group from **phosphoenolpyruvate** to ADP, forming ATP and pyruvate. - This step involves **substrate-level phosphorylation** for ATP production, not NADH. *Enolase* - This enzyme catalyzes the dehydration of **2-phosphoglycerate** to form **phosphoenolpyruvate (PEP)**. - This reaction involves the removal of a water molecule and does not produce NADH. *PFK-1* - **Phosphofructokinase-1 (PFK-1)** catalyzes the phosphorylation of fructose-6-phosphate to **fructose-1,6-bisphosphate**. - This is an ATP-consuming and a crucial regulatory step in glycolysis, but it does not involve NADH production.
Question 777: Which of the following is an amino sugar formed from fructose-6-phosphate?
- A. N-acetylglucosamine-6-phosphate
- B. Glucosamine-6-phosphate (Correct Answer)
- C. Galactosamine-6-phosphate
- D. UDP-N-acetylglucosamine
Explanation: ***Glucosamine-6-phosphate*** - This amino sugar is directly synthesized from **fructose-6-phosphate** via a transamidation reaction, where an amino group replaces a hydroxyl group. - It is a key intermediate in the biosynthesis of other **amino sugars** and **glycosaminoglycans**. *N-acetylglucosamine-6-phosphate* - This is formed from **glucosamine-6-phosphate** by the addition of an **acetyl group**, making it a subsequent product, not the initial amino sugar from fructose-6-phosphate. - The N-acetylation step is crucial for its role in cellular signaling and structural components. *Galactosamine-6-phosphate* - While an amino sugar, **galactosamine-6-phosphate** is derived from UDP-N-acetylglucosamine, not directly from fructose-6-phosphate. - Its formation involves an **epimerization** step of an existing N-acetylglucosamine structure. *UDP-N-acetylglucosamine* - This is an **activated form** of N-acetylglucosamine, formed by the addition of UTP to N-acetylglucosamine-1-phosphate. - It serves as a precursor for the synthesis of complex **carbohydrates** and glycoproteins, far downstream from fructose-6-phosphate.
Question 778: Glucose is converted to glucuronate by which process?
- A. Oxidation of aldehyde group
- B. Oxidation of both
- C. Oxidation of the terminal alcohol group (Correct Answer)
- D. None of the options
Explanation: ***Oxidation of the terminal alcohol group*** - **Glucuronate** is formed by the **oxidation of the C-6 carbon** (the terminal primary alcohol group) of glucose. - This process is crucial for the detoxification of various substances in the body, as glucuronate is a key component in **glucuronidation reactions**. *Oxidation of aldehyde group* - Oxidation of the **aldehyde group (C-1)** of glucose typically forms **gluconic acid**, not glucuronate. - Gluconate is derived from the oxidation of the first carbon, while glucuronate is derived from the oxidation of the last carbon. *Oxidation of both* - If both the aldehyde group (C-1) and the terminal alcohol group (C-6) of glucose were oxidized, it would result in the formation of **glucaric acid** (saccharic acid), not glucuronate. - Glucaric acid has two carboxyl groups, one at each end of the molecule. *None of the options* - This option is incorrect because the specific biochemical pathway for glucuronate formation involves the oxidation of the terminal alcohol group. - The conversion of glucose to glucuronate is a well-established metabolic process.
Question 779: Which one of the following statements concerning gluconeogenesis is correct?
- A. It occurs primarily in the liver.
- B. It is stimulated by elevated levels of acetyl CoA.
- C. It is important in maintaining blood glucose during the normal overnight fast. (Correct Answer)
- D. It is primarily inhibited by insulin.
Explanation: ***It is important in maintaining blood glucose during the normal overnight fast.*** - **This is the BEST answer** as it emphasizes the **primary physiological role** of gluconeogenesis in human metabolism. - During the **overnight fast** (8-12 hours), hepatic glycogen stores become depleted, making gluconeogenesis the **critical mechanism** to maintain blood glucose for glucose-dependent tissues like the **brain** (requires ~120g glucose/day) and **red blood cells**. - Without gluconeogenesis, blood glucose would drop dangerously during fasting, leading to hypoglycemia and neurological dysfunction. *It occurs primarily in the liver.* - This statement is **technically correct** - the liver accounts for approximately **90%** of total gluconeogenesis under normal conditions. - However, the **kidney cortex** also contributes significantly (10% normally, up to 40% during prolonged fasting), and the **intestine** plays a minor role. - While true, this is more of a **anatomical fact** rather than highlighting the critical physiological importance of the pathway, making it a less comprehensive answer than Option 1. *It is stimulated by elevated levels of acetyl CoA.* - This statement is **biochemically correct** - **Acetyl-CoA** is an important **allosteric activator** of **pyruvate carboxylase**, the first committed enzyme of gluconeogenesis. - However, this represents just **one regulatory mechanism** at the enzymatic level, not the overall physiological significance. - Primary regulation occurs through **hormones** (glucagon, cortisol, epinephrine) that coordinate the entire pathway, making this a narrower answer than Option 1. *It is primarily inhibited by insulin.* - This statement is also **correct** - **Insulin** is the primary hormonal **inhibitor** of gluconeogenesis. - Insulin suppresses gluconeogenesis by inhibiting key enzymes (PEPCK, glucose-6-phosphatase) and decreasing transcription of gluconeogenic genes. - However, this describes **inhibition** rather than the positive physiological role, making it less representative of gluconeogenesis's essential function than Option 1. **Note:** All four statements are technically correct, but Option 1 best captures the **essential physiological importance** of gluconeogenesis in human metabolism, which is why it is the preferred answer for this question.
Question 780: Which enzyme is active when the insulin:glucagon ratio is low?
- A. Fructokinase
- B. Lactate dehydrogenase
- C. Acetyl-CoA carboxylase
- D. Glucose-6-phosphatase (Correct Answer)
Explanation: ***Glucose-6-phosphatase*** - A low **insulin:glucagon ratio** occurs during **fasting, starvation, or stress** (catabolic state). - In this metabolic state, **glucose-6-phosphatase** is **highly active** in the **liver** (and kidneys), catalyzing the final step of both **gluconeogenesis** and **glycogenolysis**. - It converts **glucose-6-phosphate** to **free glucose**, which is released into the bloodstream to maintain **blood glucose levels**. - This enzyme is stimulated by **glucagon** and inhibited by **insulin**. *Fructokinase* - This enzyme phosphorylates **fructose** to **fructose-1-phosphate** in the liver. - It is regulated by **fructose availability**, not by the **insulin:glucagon ratio**. - During a low insulin:glucagon state, **gluconeogenic** and **glycogenolytic** pathways are favored, not fructose metabolism. *Lactate dehydrogenase* - **LDH** interconverts **pyruvate** and **lactate** and functions in both **glycolysis** and **gluconeogenesis**. - While it plays a role in various metabolic states, it is **not specifically activated** by a low insulin:glucagon ratio. - It operates constitutively based on substrate availability rather than hormonal regulation. *Acetyl-CoA carboxylase* - This is the **rate-limiting enzyme** of **fatty acid synthesis** (lipogenesis). - It is **activated by insulin** (fed state) and **inhibited by glucagon** (fasted state). - When the insulin:glucagon ratio is **low**, this enzyme is **phosphorylated and INACTIVE**, shutting down fatty acid synthesis.
Practice by Chapter
Carbohydrate Chemistry and Classification
Practice Questions
Glycolysis: Reactions and Regulation
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Gluconeogenesis: Reactions and Regulation
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Glycogen Metabolism: Synthesis and Breakdown
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Glycogen Storage Diseases
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Pentose Phosphate Pathway
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Metabolism of Fructose and Galactose
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Disorders of Fructose and Galactose Metabolism
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Blood Glucose Regulation
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Diabetes Mellitus: Biochemical Aspects
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Glycosylation and Glycoproteins
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Lactose Intolerance and Galactosemia
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