Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism Indian Medical PG Practice Questions and MCQs

Question 641: Which of the following enzymes does NOT increase its activity during starvation?

A. Pyruvate carboxylase
B. Pyruvate kinase (Correct Answer)
C. PEP carboxykinase
D. Glucose 6 phosphatase

Explanation: **Explanation:** The metabolic goal during **starvation** is to maintain blood glucose levels via **gluconeogenesis** and glycogenolysis. To ensure a net flux toward glucose production, the body must inhibit the glycolytic pathway while activating the gluconeogenic pathway. **Why Pyruvate Kinase is the correct answer:** Pyruvate kinase (PK) is a key regulatory enzyme of **glycolysis**. During starvation, high levels of **glucagon** increase intracellular cAMP, leading to the phosphorylation and **inhibition** of hepatic Pyruvate Kinase. This inhibition prevents "futile cycling" by ensuring that Phosphoenolpyruvate (PEP) is diverted toward glucose synthesis rather than being converted back to pyruvate. Therefore, PK activity **decreases** during starvation. **Analysis of Incorrect Options:** * **Pyruvate carboxylase (A):** This is the first regulatory enzyme of gluconeogenesis (Pyruvate → Oxaloacetate). It is allosterically activated by **Acetyl-CoA**, which rises during starvation due to increased fatty acid oxidation. * **PEP carboxykinase (C):** This enzyme converts Oxaloacetate to PEP. Its expression is transcriptionally **induced** by glucagon and glucocorticoids during fasting. * **Glucose 6-phosphatase (D):** This is the final enzyme of both gluconeogenesis and glycogenolysis, allowing the liver to release free glucose into the blood. Its activity increases significantly during starvation. **High-Yield NEET-PG Pearls:** * **Reciprocal Regulation:** Glucagon inhibits Glycolysis (via PFK-1 and PK) and stimulates Gluconeogenesis. * **The "Bypass" Enzymes:** Options A, C, and D are the three "bypass" enzymes that overcome the irreversible steps of glycolysis. * **Hormonal Control:** Insulin dephosphorylates (activates) PK, while Glucagon phosphorylates (inhibits) it.

Question 642: Von Gierke's disease occurs due to deficiency of which enzyme?

A. Glucose-6-phosphatase (Correct Answer)
B. Liver phosphorylase
C. Muscle phosphorylase
D. Debranching enzyme

Explanation: **Explanation:** **Von Gierke’s Disease (GSD Type I)** is the most common glycogen storage disease. It is caused by a deficiency of **Glucose-6-phosphatase**, the enzyme responsible for converting Glucose-6-phosphate into free glucose. This enzyme is primarily located in the liver and kidneys. Since this is the final step in both glycogenolysis and gluconeogenesis, its deficiency leads to severe fasting hypoglycemia and massive accumulation of glycogen in the liver. **Analysis of Options:** * **Option A (Correct):** Glucose-6-phosphatase deficiency prevents the liver from releasing glucose into the blood, leading to the classic triad of hepatomegaly, hypoglycemia, and lactic acidosis. * **Option B (Incorrect):** Deficiency of **Liver phosphorylase** causes **Hers disease (GSD Type VI)**, which presents with a milder clinical course than Von Gierke’s. * **Option C (Incorrect):** Deficiency of **Muscle phosphorylase** causes **McArdle disease (GSD Type V)**, characterized by exercise-induced cramps and myoglobinuria, but no hypoglycemia. * **Option D (Incorrect):** Deficiency of the **Debranching enzyme** (α-1,6-glucosidase) causes **Cori disease (GSD Type III)**, where glycogen has abnormally short outer branches (limit dextrins). **High-Yield Clinical Pearls for NEET-PG:** * **Biochemical Hallmarks:** Hyperuricemia (due to increased PPP shunt), Hyperlipidemia (increased VLDL), and Lactic Acidosis. * **Clinical Presentation:** "Doll-like" facies (fat deposition), protuberant abdomen (massive hepatomegaly), and stunted growth. * **Treatment:** Frequent oral glucose/cornstarch and avoidance of fructose/galactose (which cannot be converted to glucose).

Question 643: Arrange the following 4 enzymes of gluconeogenesis in sequence:

A. Fructose 1,6 Bisphosphatase - Phosphoenol pyruvate carboxy kinase - Pyruvate carboxylase - Glucose - 6 - phosphatase
B. Pyruvate carboxylase - Phosphoenol pyruvate carboxy kinase - Fructose 1,6 Bisphosphatase - Glucose - 6 - phosphatase (Correct Answer)
C. Glucose - 6 - phosphatase - Pyruvate carboxylase - Fructose 1,6 Bisphosphatase - Phosphoenol pyruvate carboxy kinase
D. Phosphoenol pyruvate carboxy kinase - Fructose 1,6 Bisphosphatase - Glucose - 6 - phosphatase - Pyruvate carboxylase

Explanation: ### Explanation **Underlying Medical Concept** Gluconeogenesis is the metabolic pathway that generates glucose from non-carbohydrate precursors (like lactate, glycerol, and glucogenic amino acids). While it shares many enzymes with glycolysis, it must bypass three irreversible steps of glycolysis using four specific "bypass enzymes." The sequence follows the flow from the mitochondria (starting with pyruvate) to the cytoplasm/ER (ending with free glucose). **Step-by-Step Sequence:** 1. **Pyruvate Carboxylase (Mitochondria):** Converts Pyruvate to Oxaloacetate (OAA). Requires Biotin and ATP. 2. **Phosphoenolpyruvate Carboxykinase (PEPCK):** Converts OAA to Phosphoenolpyruvate (PEP). Requires GTP. 3. **Fructose 1,6-Bisphosphatase:** Converts Fructose 1,6-bisphosphate to Fructose 6-phosphate. This is the **rate-limiting step**. 4. **Glucose-6-Phosphatase (ER):** Converts Glucose 6-phosphate to free Glucose, which can then enter the bloodstream. **Analysis of Options:** * **Option B (Correct):** Correctly follows the anatomical and chemical flow from the mitochondrial matrix to the final release of glucose. * **Option A:** Incorrectly places Fructose 1,6-bisphosphatase before the PEP-forming enzymes. * **Option C:** Starts with the final step (Glucose-6-phosphatase), representing the reverse order. * **Option D:** Misplaces PEPCK as the starting enzyme, skipping the initial carboxylation of pyruvate. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** Gluconeogenesis occurs primarily in the **Liver** (90%) and **Kidney** (10%). * **Cofactor:** Pyruvate Carboxylase is activated by **Acetyl-CoA**. If Acetyl-CoA levels are high, it signals the cell to stop the TCA cycle and start gluconeogenesis. * **Clinical Correlation:** Deficiency of Glucose-6-Phosphatase leads to **Von Gierke’s Disease (GSD Type I)**, characterized by severe fasting hypoglycemia and hepatomegaly. * **Mnemonic:** **P**yruvate **P**unches **F**ructose **G**ently (**P**yruvate carboxylase $\rightarrow$ **P**EPCK $\rightarrow$ **F**ructose 1,6-BPase $\rightarrow$ **G**lucose-6-Pase).

Question 644: The development of cataracts in patients with Diabetes Mellitus is primarily due to the accumulation of which of the following substances in the lens?

A. Galactitol
B. Fructose
C. Mannitol
D. Sorbitol (Correct Answer)

Explanation: ***Correct Option: Sorbitol*** - In the setting of chronic **hyperglycemia**, excess glucose is converted into **sorbitol** by the enzyme **aldose reductase** via the polyol pathway. - Sorbitol is poorly transported out of the lens cells and its accumulation creates an internal **osmotic gradient**, drawing water into the lens, which leads to cell swelling, lens fiber disruption, and eventual **cataract** formation. - This is the **primary mechanism** of diabetic cataract development. *Incorrect Option: Galactitol* - **Galactitol** (also known as dulcitol) is the specific sugar alcohol that accumulates when there is deficiency of **galactokinase** or **galactose-1-phosphate uridyltransferase**. - Its accumulation is characteristic of **galactosemia**, where high galactose levels lead to its formation via aldose reductase, causing congenital cataracts in that condition, not diabetic cataracts. *Incorrect Option: Fructose* - While **fructose** is produced from sorbitol by sorbitol dehydrogenase in the polyol pathway, it is readily metabolized and does not accumulate in lens tissue. - Fructose itself does not cause osmotic damage or cataract formation in diabetes. *Incorrect Option: Mannitol* - **Mannitol** is a hexahydric sugar alcohol primarily used pharmacologically as an osmotic diuretic for conditions like **cerebral edema**. - It is not an endogenous product of glucose metabolism in the lens and is not associated with diabetic cataract formation.

Question 645: A patient with a history of strenuous exercise skipped a meal and later consumed alcohol at a party. Alcohol inhibits which of the following biochemical processes, potentially leading to hypoglycemia?

A. Glycogenolysis
B. Ketone Body Formation
C. Gluconeogenesis (Correct Answer)
D. Hexose Monophosphate (HMP) Shunt

Explanation: ***Gluconeogenesis*** - Alcohol metabolism by **alcohol dehydrogenase** and **aldehyde dehydrogenase** generates a massive influx of **NADH**, drastically increasing the hepatic NADH/NAD+ ratio. - This high NADH/NAD+ ratio shifts metabolic intermediates, inhibiting key enzymes (e.g., **lactate dehydrogenase** and **malate dehydrogenase**) required to convert precursors like lactate and amino acids into glucose, leading to failure of new glucose synthesis and subsequent hypoglycemia. *Glycogenolysis* - This process, the breakdown of stored **glycogen** into glucose, is not directly inhibited by the increased NADH ratio produced during alcohol metabolism. - In fact, the initial phase of alcohol-induced hypoglycemia relies on the depletion of pre-existing glycogen stores, which is accelerated by factors like strenuous exercise or fasting. *Hexose Monophosphate (HMP) Shunt* - The primary function of the HMP shunt is to produce **NADPH** (for reductive biosynthesis and antioxidant defense) and five-carbon sugars (**ribose-5-phosphate**) for nucleotide synthesis. - Inhibition of the HMP shunt alters cell redox status and nucleotide production but does not directly impair blood glucose maintenance or cause acute hypoglycemia. *Ketone Body Formation* - Alcohol metabolism actually tends to **inhibit** ketone body formation because the high NADH ratio inhibits **beta-oxidation** of fatty acids in the liver, which is required to produce the Acetyl-CoA necessary for ketogenesis. - While ketone formation is inhibited, this is a consequence of high NADH, and the hypoglycemia itself results from the inability to synthesize glucose via gluconeogenesis, not the absence of ketones.

Question 646: A patient with a long-standing history of diabetes presents with cataracts. Which of the following metabolic products is primarily responsible for cataract formation in this condition?

A. Galactitol
B. Mannitol
C. Sorbitol (Correct Answer)
D. Fructose

Explanation: ***Sorbitol*** - When blood glucose is elevated in diabetes, the enzyme **aldose reductase** converts excess glucose into **sorbitol** (a polyol) in tissues like the lens, which do not require insulin for glucose uptake. - Sorbitol is poorly permeable across cell membranes. Its accumulation creates a significant **osmotic gradient** within the lens fibers, causing water influx and subsequent lens swelling and opacification (cataract formation). *Mannitol* - **Mannitol** is a polyol often used as an osmotic diuretic in clinical settings to reduce cerebral edema or intraocular pressure. - Although chemically similar to sorbitol, mannitol accumulation is not the primary mechanism of **cataract formation** specifically linked to chronic hyperglycemia. *Galactitol* - **Galactitol** is NOT responsible for cataract formation in diabetes, but is specifically responsible for cataracts in individuals with **galactosemia** (inability to metabolize galactose). - It is formed from **galactose** via aldose reductase, making it the incorrect metabolite in a patient with diabetes-related cataracts. *Fructose* - **Fructose** is formed when sorbitol is further metabolized by the enzyme **sorbitol dehydrogenase**. - While present in the polyol pathway, **sorbitol** itself is the product whose high intracellular concentration and osmotic activity is the direct cause of the diabetic cataract.

Question 647: A 68-year-old female patient has had a diabetic cataract for 3 months. Accumulation of which of the following substances is responsible for this?

A. Fructose
B. Lactose + Glucose
C. Sorbitol + Fructose (Correct Answer)
D. Glucose

Explanation: ***Sorbitol + Fructose*** This option correctly identifies the products of the **polyol pathway**, which is significantly activated in lens fibers during **hyperglycemia**. **Sorbitol** is the key substance that accumulates due to high **aldose reductase** activity and low sorbitol dehydrogenase activity, leading to an **osmotic gradient** and water accumulation, causing lens swelling and opacification (cataract). *Glucose* Although high blood **glucose** initiates the process by serving as the substrate for aldose reductase, glucose itself is not the primary substance responsible for the osmotic damage in the lens. In normal lens metabolism, glucose is primarily metabolized via **glycolysis**; only when levels are excessive is the polyol pathway significantly utilized. *Fructose* Fructose is the breakdown product of **sorbitol** (catalyzed by sorbitol dehydrogenase), but its concentration is typically much lower than sorbitol in the lens. **Sorbitol** accumulation is the primary driver of the powerful osmotic effect that leads to water influx into the lens fiber cells and subsequent cataract formation. *Lactose + Glucose* Accumulation of **lactose** is not associated with diabetic cataract; this combination is irrelevant to the pathogenesis of hyperglycemia-induced lens damage. **Galactosemic cataract**, a different type of osmotic cataract, is caused by the accumulation of **galactitol** (a polyol derived from galactose, not glucose).

Question 648: Which of the following cell pathways occurs exclusively in cell cytoplasm?

A. TCA cycle
B. Glycolysis (Correct Answer)
C. Urea cycle
D. Beta oxidation

Explanation: ***Glycolysis***- Glycolysis is the metabolic pathway converting **glucose** to **pyruvate** and occurs entirely within the **cytoplasm** (cytosol) [1].- This pathway is crucial for producing ATP both in the presence (aerobic) and absence (anaerobic) of oxygen [3].*Beta oxidation*- **Beta oxidation**, the breakdown of fatty acids, occurs primarily within the **mitochondrial matrix**.- Long-chain fatty acid activation occurs in the cytosol, but the subsequent oxidative steps are confined to the **mitochondria**.*TCA cycle*- The **TCA cycle** (Krebs cycle) is located exclusively within the **mitochondrial matrix** in eukaryotic cells.- It is responsible for the complete oxidation of acetyl-CoA, producing electron carriers like **NADH** and **FADH2**.*Urea cycle*- The **urea cycle** occurs across **two distinct cellular compartments**: reactions take place in both the **mitochondrial matrix** and the **cytosol** [2].- Specifically, the synthesis of **carbamoyl phosphate** and citrulline occurs in the mitochondria [2].

Question 649: Cancer cells take up excess glucose because?

A. Lactate is produced even in the presence of Oxygen (Correct Answer)
B. High NADH/NAD ratio
C. High GLUT2
D. Absence of Oxygen

Explanation: ***Lactate is produced even in the presence of Oxygen*** - This phenomenon is known as the **Warburg effect** (or aerobic glycolysis). Cancer cells preferentially ferment glucose to lactate, even when adequate **oxygen** is available, bypassing efficient oxidative phosphorylation. - This inefficient use of glucose allows rapid generation of metabolic intermediates (e.g., carbon backbones) required for the synthesis of **lipids**, proteins, and nucleic acids needed for rapid cell proliferation. *High NADH/NAD ratio* - A **high NADH/NAD+ ratio** signals abundance of reducing equivalents, which would typically inhibit glycolysis and favor oxidative phosphorylation. - Rapid glycolysis, as seen in cancer (Warburg effect), requires the constant regeneration of **NAD+** from NADH via lactate dehydrogenase for the pathway to continue. *High GLUT2* - While cancer cells increase glucose uptake by overexpressing glucose transporters, the typically overexpressed transporter in many solid tumors is **GLUT1**, not GLUT2. - **GLUT2** is primarily found in the liver, kidney, and pancreatic beta cells and is less commonly the primary high-affinity transporter driving the intense uptake seen in malignant cells. *Absence of Oxygen* - The characteristic metabolic change in cancer is that glucose uptake and lactate production occur despite the **presence of oxygen** (aerobic glycolysis). - If oxygen were truly absent (anaerobic conditions), all cell types would produce lactate; hence, the defining feature of cancer is the metabolic shift occurring in an **oxygenated environment**.

Question 650: What is the cycle shown below called?

A. Embden-Meyerhof pathway
B. Pentose phosphate pathway
C. Cori cycle (Correct Answer)
D. Pyruvate decarboxylation

Explanation: ***Cori cycle*** - The diagram illustrates the **Cori cycle**, showing **lactate produced in the muscle** during anaerobic glycolysis being transported to the liver. - In the liver, this **lactate is converted back to glucose** via gluconeogenesis, which can then be returned to the muscle. *Embden-Meyerhof pathway* - The **Embden-Meyerhof pathway** is an older name for **glycolysis**, which is only one part of the cycle shown in the diagram (specifically, the conversion of glucose to lactate in the muscle). - It does not encompass the entire pathway of lactate transport to the liver and its conversion to glucose. *Pentose phosphate pathway* - The **pentose phosphate pathway** is a metabolic pathway parallel to glycolysis that generates **NADPH** and the precursor for nucleotide biosynthesis. - It is not depicted in this diagram, which focuses on glucose-lactate interconversion between muscle and liver. *Pyruvate decarboxylation* - **Pyruvate decarboxylation** is the conversion of pyruvate to acetyl-CoA, primarily occurring when oxygen is available for aerobic respiration. - The cycle shown specifically highlights the **anaerobic metabolism** in muscle producing lactate and its subsequent processing.

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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