Carbohydrate Metabolism — MCQs

A 42-year-old man presented with symptoms of weakness, fatigue, shortness of breath, and dizziness. His hemoglobin level was less than 7 g/dl (normal for a male being greater than 13.5 g/dl). Red blood cells of the patient showed abnormally low levels of lactate production. Heinz bodies were not found in peripheral blood film. Deficiency of which one of the following enzymes would be the most likely cause of this patient's anemia?

Q357Easy

All of the following are enzymes of the TCA cycle located in the mitochondrial matrix, EXCEPT?

Q358Easy

Cyclic AMP increases the rate of glycogenolysis by which of the following mechanisms?

Q359Easy

Starch is a:

Q360Easy

Which of the following is an action of insulin?

Carbohydrate Metabolism Indian Medical PG Practice Questions and MCQs

Question 351: Which of the following is NOT a key enzyme in glycolysis?

A. Phosphofructokinase
B. Hexokinase
C. Pyruvate kinase
D. Glucose-1,6-diphosphatase (Correct Answer)

Explanation: **Explanation:** In biochemistry, "key enzymes" of a metabolic pathway refer to those that catalyze **irreversible, rate-limiting steps** and serve as primary sites for regulation. **Why Option D is Correct:** **Glucose-1,6-diphosphatase** is not an enzyme involved in the glycolytic pathway. In fact, Glucose-1,6-bisphosphate acts primarily as a cofactor for the enzyme phosphoglucomutase in glycogen metabolism. The enzyme that opposes glycolysis (in gluconeogenesis) is **Fructose-1,6-bisphosphatase**, which converts Fructose-1,6-BP back to Fructose-6-P. The absence of Glucose-1,6-diphosphatase in the glycolytic sequence makes it the correct answer. **Analysis of Incorrect Options:** * **A. Phosphofructokinase-1 (PFK-1):** This is the **most important rate-limiting enzyme** of glycolysis. It catalyzes the irreversible conversion of Fructose-6-P to Fructose-1,6-BP. * **B. Hexokinase/Glucokinase:** This catalyzes the first irreversible step (phosphorylation of glucose to Glucose-6-P), trapping glucose inside the cell. * **C. Pyruvate Kinase:** This catalyzes the final irreversible step, converting Phosphoenolpyruvate (PEP) to Pyruvate, yielding one molecule of ATP. **High-Yield Clinical Pearls for NEET-PG:** * **Rate-limiting step:** PFK-1 is inhibited by high ATP and Citrate, and activated by AMP and **Fructose-2,6-bisphosphate** (the most potent activator). * **Rapoport-Luebering Cycle:** In RBCs, 1,3-BPG can be converted to 2,3-BPG, which shifts the oxygen dissociation curve to the right. * **Pyruvate Kinase Deficiency:** The second most common cause of enzyme-deficient hemolytic anemia (after G6PD deficiency). * **Fluoride Inhibition:** Sodium fluoride (used in blood collection vials) inhibits **Enolase**, preventing glycolysis to ensure accurate blood glucose measurement.

Question 352: Which of the following is a non-reducing sugar?

A. Glucose
B. Lactose
C. Maltose
D. Sucrose (Correct Answer)

Explanation: ### Explanation **Concept Overview:** A sugar is classified as **reducing** if it has a free or potentially free aldehyde or ketone group. This group allows the sugar to act as a reducing agent in chemical tests (like Benedict’s or Fehling’s). In disaccharides, if the **anomeric carbons** of both monosaccharides are involved in a glycosidic bond, the sugar becomes **non-reducing**. **Why Sucrose is the Correct Answer:** Sucrose is a disaccharide composed of **$\alpha$-D-glucose** and **$\beta$-D-fructose**. The glycosidic linkage occurs between the **C1 of glucose** (aldehyde group) and the **C2 of fructose** (keto group). Since both functional groups are locked in the bond, there is no free reactive group available to reduce copper or silver ions. **Analysis of Incorrect Options:** * **A. Glucose:** A monosaccharide with a free aldehyde group at C1; it is a classic reducing sugar. * **B. Lactose:** A disaccharide (Galactose + Glucose) with a **$\beta$(1$\rightarrow$4) linkage**. The anomeric carbon (C1) of the glucose unit remains free. * **C. Maltose:** A disaccharide (Glucose + Glucose) with an **$\alpha$(1$\rightarrow$4) linkage**. The anomeric carbon of the second glucose unit is free. **High-Yield Clinical Pearls for NEET-PG:** * **Benedict’s Test:** Used to detect reducing sugars in urine (e.g., glucosuria in Diabetes Mellitus). * **Invert Sugar:** Sucrose is dextrorotatory, but upon hydrolysis, it produces a levorotatory mixture of glucose and fructose; hence, hydrolyzed sucrose is called "invert sugar." * **Trehalose:** Another high-yield non-reducing sugar (found in mushrooms) where two glucose units are linked via an **$\alpha$1$\rightarrow$1 bond**. * **Seliwanoff’s Test:** Sucrose gives a positive result (cherry red color) because it contains fructose (a ketose).

Question 353: Which of the following enzymes found in the liver is involved in gluconeogenesis during the postabsorptive state?

A. Glucose-6-phosphate dehydrogenase
B. 6-phosphogluconate dehydrogenase
C. Glucose-6-phosphatase (Correct Answer)
D. Glucokinase

Explanation: ### Explanation **Correct Answer: C. Glucose-6-phosphatase** **Why it is correct:** Gluconeogenesis is the metabolic pathway that generates glucose from non-carbohydrate precursors (like lactate, glycerol, and amino acids) during fasting or the postabsorptive state. **Glucose-6-phosphatase** is one of the four "key" or "bottleneck" enzymes of gluconeogenesis. It catalyzes the final step: the hydrolysis of Glucose-6-phosphate into free glucose and inorganic phosphate. This enzyme is primarily located in the lumen of the endoplasmic reticulum of the liver and kidneys, allowing these organs to release free glucose into the bloodstream to maintain glycemic levels. **Why the other options are incorrect:** * **A & B (G6PD and 6-phosphogluconate dehydrogenase):** These are the rate-limiting enzymes of the **Pentose Phosphate Pathway (Hexose Monophosphate Shunt)**. They are involved in generating NADPH and ribose-5-phosphate, not in the synthesis of glucose. * **D (Glucokinase):** This enzyme is involved in **glycolysis** and glycogenesis. It catalyzes the conversion of glucose to glucose-6-phosphate. In the postabsorptive state, glucokinase activity is low to prevent a futile cycle, as its action is the exact opposite of Glucose-6-phosphatase. **High-Yield Clinical Pearls for NEET-PG:** * **The Four Key Gluconeogenic Enzymes:** Pyruvate carboxylase, PEP carboxykinase, Fructose-1,6-bisphosphatase, and Glucose-6-phosphatase. * **Von Gierke Disease (GSD Type I):** Caused by a deficiency of Glucose-6-phosphatase. It presents with severe fasting hypoglycemia, hepatomegaly, and lactic acidosis because the liver cannot export glucose. * **Muscle Metabolism:** Muscle lacks Glucose-6-phosphatase; therefore, muscle glycogen cannot contribute directly to blood glucose levels.

Question 354: Gluconeogenesis does not occur significantly from which of the following in humans?

A. Lactate
B. Fatty acids (Correct Answer)
C. Pyruvate
D. Amino acids

Explanation: **Explanation:** The correct answer is **Fatty acids**. In humans, even-chain fatty acids cannot be converted into glucose because the breakdown of fatty acids yields **Acetyl-CoA**. The conversion of Pyruvate to Acetyl-CoA (via the Pyruvate Dehydrogenase complex) is **irreversible**. Humans lack the enzymes (Isocitrate lyase and Malate synthase) of the **Glyoxylate cycle**, which would allow the conversion of Acetyl-CoA into oxaloacetate for gluconeogenesis. Consequently, Acetyl-CoA enters the TCA cycle and is completely oxidized to $CO_2$. **Why the other options are incorrect:** * **Lactate:** Produced during anaerobic glycolysis (Cori Cycle), lactate is transported to the liver where it is converted back to pyruvate by LDH and enters gluconeogenesis. * **Pyruvate:** This is a primary substrate. It is carboxylated to Oxaloacetate by Pyruvate Carboxylase, the first regulatory step of gluconeogenesis. * **Amino Acids:** Glucogenic amino acids (e.g., Alanine) are deaminated to form pyruvate or TCA cycle intermediates (like $\alpha$-ketoglutarate), which are then converted to glucose. **High-Yield Clinical Pearls for NEET-PG:** * **Exception:** While even-chain fatty acids are non-glucogenic, **Odd-chain fatty acids** are glucogenic because their terminal 3-carbon unit, **Propionyl-CoA**, is converted to Succinyl-CoA. * **Glycerol:** The glycerol backbone of triglycerides *is* glucogenic; it enters the pathway as Dihydroxyacetone phosphate (DHAP). * **Key Regulatory Enzyme:** Fructose-1,6-bisphosphatase is the rate-limiting enzyme of gluconeogenesis. * **Location:** Gluconeogenesis occurs primarily in the **Liver** (90%) and **Kidney** (10%).

Question 355: What is the end product of glycolysis in RBCs?

A. Pyruvate
B. Lactic acid (Correct Answer)
C. Acetyl CoA
D. Oxaloacetate

Explanation: **Explanation:** The correct answer is **Lactic acid (Lactate)**. **1. Why Lactic Acid is Correct:** Glycolysis is the sole source of energy for Red Blood Cells (RBCs). Unlike most cells, RBCs lack **mitochondria**. Because mitochondria are the site of the Citric Acid Cycle (TCA) and Oxidative Phosphorylation, RBCs cannot perform aerobic respiration. Consequently, they must rely entirely on **anaerobic glycolysis**. In this pathway, pyruvate produced from glucose is reduced to lactic acid by the enzyme **Lactate Dehydrogenase (LDH)**. This step is crucial because it regenerates **NAD+**, which is required for glycolysis to continue. **2. Why Other Options are Incorrect:** * **Pyruvate:** While pyruvate is the end product of *aerobic* glycolysis, in RBCs, it is immediately converted to lactate to maintain the redox balance (NAD+/NADH ratio). * **Acetyl CoA:** Pyruvate is converted to Acetyl CoA by the Pyruvate Dehydrogenase complex inside the mitochondria. Since RBCs lack mitochondria, this conversion cannot occur. * **Oxaloacetate:** This is an intermediate of the TCA cycle or gluconeogenesis. RBCs do not possess the mitochondrial machinery or enzymes (like Pyruvate Carboxylase) to produce oxaloacetate from pyruvate. **3. Clinical Pearls & High-Yield Facts:** * **Rapoport-Luebering Shunt:** A unique feature of RBC glycolysis where 1,3-bisphosphoglycerate is converted to **2,3-BPG**. This molecule decreases hemoglobin's affinity for oxygen, facilitating oxygen delivery to tissues. * **Energy Yield:** Anaerobic glycolysis in RBCs yields a net of **2 ATP** per glucose molecule. * **Hemolytic Anemia:** Deficiencies in glycolytic enzymes, most commonly **Pyruvate Kinase**, lead to ATP depletion, causing RBC membrane instability and premature destruction (hemolysis).

Question 356: A 42-year-old man presented with symptoms of weakness, fatigue, shortness of breath, and dizziness. His hemoglobin level was less than 7 g/dl (normal for a male being greater than 13.5 g/dl). Red blood cells of the patient showed abnormally low levels of lactate production. Heinz bodies were not found in peripheral blood film. Deficiency of which one of the following enzymes would be the most likely cause of this patient's anemia?

A. Phosphoglucose isomerase
B. Glucose-6-phosphate dehydrogenase (G6PD)
C. Pyruvate kinase (Correct Answer)
D. Hexokinase

Explanation: ### Explanation The patient presents with severe anemia and a critical biochemical finding: **abnormally low levels of lactate production** in Red Blood Cells (RBCs). **1. Why Pyruvate Kinase (PK) is the Correct Answer:** Mature RBCs lack mitochondria and depend entirely on **anaerobic glycolysis** (the Embden-Meyerhof pathway) for ATP production. Pyruvate kinase catalyzes the final step of glycolysis: converting Phosphoenolpyruvate (PEP) to Pyruvate, generating ATP in the process. * A deficiency in PK leads to decreased ATP production, causing failure of the Na⁺/K⁺-ATPase pumps, leading to cell dehydration, rigid RBCs (echinocytes), and premature destruction in the spleen (hemolytic anemia). * Since the glycolytic pathway is blocked at the final step, the conversion of pyruvate to **lactate** is significantly diminished, explaining the low lactate levels. **2. Analysis of Incorrect Options:** * **Glucose-6-phosphate dehydrogenase (G6PD):** This is the most common enzyme deficiency in the HMP shunt. It typically presents with **Heinz bodies** (denatured hemoglobin) and bite cells on a peripheral smear, usually triggered by oxidative stress. It does not directly reduce lactate production. * **Hexokinase:** While a deficiency would decrease glycolysis, it is extremely rare. Furthermore, PK deficiency is the most common glycolytic enzyme defect causing congenital non-spherocytic hemolytic anemia. * **Phosphoglucose isomerase:** Deficiency can cause hemolysis, but it is much less common than PK deficiency and doesn't specifically explain the clinical scenario as classically as PK. **3. NEET-PG High-Yield Pearls:** * **PK Deficiency:** Most common cause of **congenital non-spherocytic hemolytic anemia**. * **Biochemical Hallmark:** Increased levels of **2,3-BPG** (due to backup of glycolytic intermediates), which shifts the oxygen dissociation curve to the **right**, helping the patient tolerate anemia better by increasing O₂ delivery to tissues. * **Lactate Connection:** In RBCs, the end product of glycolysis is always lactate. Any block in the main glycolytic pathway (like PK) reduces total lactate output.

Question 357: All of the following are enzymes of the TCA cycle located in the mitochondrial matrix, EXCEPT?

A. Alpha-ketoglutarate dehydrogenase
B. Isocitrate dehydrogenase
C. Succinate dehydrogenase (Correct Answer)
D. Malate dehydrogenase

Explanation: ### Explanation **Core Concept:** The Citric Acid Cycle (TCA cycle) occurs primarily in the **mitochondrial matrix**. However, **Succinate Dehydrogenase (Option C)** is the unique exception. It is the only enzyme of the TCA cycle that is **integral to the inner mitochondrial membrane**. This enzyme serves a dual role: 1. **In the TCA Cycle:** It catalyzes the oxidation of succinate to fumarate. 2. **In the Electron Transport Chain (ETC):** It is also known as **Complex II**. It transfers electrons from succinate via FADH₂ directly into the Coenzyme Q pool. **Analysis of Incorrect Options:** * **A. Alpha-ketoglutarate dehydrogenase:** A multi-enzyme complex located in the mitochondrial matrix. It requires five cofactors (Thiamine, Lipoic acid, CoA, FAD, NAD). * **B. Isocitrate dehydrogenase:** The rate-limiting enzyme of the TCA cycle, located within the mitochondrial matrix. * **D. Malate dehydrogenase:** Catalyzes the final step of the cycle (Malate to Oxaloacetate) and is located in the mitochondrial matrix. (Note: A cytosolic isoenzyme also exists for the malate-aspartate shuttle). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for TCA Enzymes:** "**C**an **I** **K**eep **S**elling **S**ubstances **F**or **M**oney?" (**C**itrate synthase, **I**socitrate DH, alpha-**K**etoglutarate DH, **S**uccinyl-CoA synthetase, **S**uccinate DH, **F**umarase, **M**alate DH). * **Inhibitor:** Succinate dehydrogenase is competitively inhibited by **Malonate** (a classic example of competitive inhibition). * **FADH₂ Linkage:** Succinate dehydrogenase is the only TCA enzyme that produces FADH₂ instead of NADH. * **Riboflavin Connection:** Since it uses FAD as a prosthetic group, its activity is impaired in Vitamin B2 deficiency.

Question 358: Cyclic AMP increases the rate of glycogenolysis by which of the following mechanisms?

A. Promoting the activation of phosphorylase kinase, which then activates glycogen phosphorylase. (Correct Answer)
B. Acting as a cofactor for glycogen phosphorylase.
C. Furnishing phosphate for the phosphorylysis of glycogen.
D. Acting as a precursor of 5' AMP, which is a cofactor for glycogen phosphorylase.

Explanation: ### Explanation **Mechanism of Action (The Correct Answer):** Glycogenolysis is regulated by a reversible phosphorylation cascade. When hormones like **glucagon** (in the liver) or **epinephrine** (in the muscle) bind to their receptors, they activate adenylate cyclase, increasing intracellular **cyclic AMP (cAMP)**. 1. cAMP activates **Protein Kinase A (PKA)**. 2. PKA phosphorylates and activates **Phosphorylase Kinase**. 3. Active Phosphorylase Kinase then phosphorylates **Glycogen Phosphorylase *b*** (inactive) into **Glycogen Phosphorylase *a*** (active). 4. Active Glycogen Phosphorylase catalyzes the rate-limiting step of glycogen breakdown. **Analysis of Incorrect Options:** * **Option B:** cAMP is a second messenger, not a cofactor. The essential cofactor for glycogen phosphorylase is **Pyridoxal Phosphate (PLP/Vitamin B6)**. * **Option C:** The phosphate used in phosphorylysis is inorganic phosphate ($P_i$), not derived from cAMP. * **Option D:** While 5' AMP can allosterically activate glycogen phosphorylase in muscle during states of low energy, it is a breakdown product of ATP/ADP, not the primary mechanism by which cAMP exerts its hormonal effect. **NEET-PG High-Yield Pearls:** * **Rate-limiting enzyme:** Glycogen Phosphorylase. * **Cofactor:** Pyridoxal Phosphate (PLP) is mandatory for its activity. * **Covalent Regulation:** Phosphorylation **activates** glycogen phosphorylase but **inactivates** glycogen synthase (reciprocal regulation). * **Allosteric Activator in Muscle:** 5' AMP (signals low energy) and $Ca^{2+}$ (signals muscle contraction) can activate glycogenolysis even without cAMP-mediated phosphorylation.

Question 359: Starch is a:

A. Polysaccharide (Correct Answer)
B. Disaccharide
C. Protein
D. None of these

Explanation: **Explanation:** **Starch** is a **homopolysaccharide** composed of D-glucose units. It serves as the primary storage form of carbohydrates in plants. It consists of two main components: **Amylose** (linear chains with $\alpha$-1,4-glycosidic bonds) and **Amylopectin** (branched chains with $\alpha$-1,4 and $\alpha$-1,6-glycosidic bonds). Since it is a complex polymer made of more than ten monosaccharide units, it is classified as a polysaccharide. **Analysis of Incorrect Options:** * **B. Disaccharide:** These consist of only two monosaccharide units (e.g., Sucrose, Lactose, Maltose). Starch contains thousands of glucose units. * **C. Protein:** Proteins are polymers of amino acids linked by peptide bonds, whereas starch is a carbohydrate made of sugar units linked by glycosidic bonds. **High-Yield Clinical Pearls for NEET-PG:** * **Digestion:** Starch digestion begins in the mouth via **salivary $\alpha$-amylase** (Ptyalin) and continues in the small intestine via **pancreatic $\alpha$-amylase**. * **End Products:** Amylase acts on $\alpha$-1,4 bonds but cannot cleave $\alpha$-1,6 (branch) points, resulting in products like maltose, maltotriose, and **$\alpha$-limit dextrins**. * **Iodine Test:** Starch gives a characteristic **blue-black color** with iodine due to the helical structure of amylose trapping iodine molecules. * **Glycogen vs. Starch:** Glycogen is the animal equivalent of starch but is more highly branched (every 8–12 residues) compared to amylopectin (every 24–30 residues).

Question 360: Which of the following is an action of insulin?

A. Gluconeogenesis
B. Increased glucose uptake in muscle (Correct Answer)
C. Glycogenolysis
D. Increased glucose uptake in endothelium

Explanation: **Explanation:** Insulin is the body’s primary **anabolic hormone**, secreted by the beta cells of the pancreas in response to high blood glucose levels. Its primary goal is to lower blood glucose by promoting storage and utilization. **1. Why Option B is Correct:** Insulin facilitates glucose uptake in **skeletal muscle** and **adipose tissue** by stimulating the translocation of **GLUT-4** (an insulin-dependent glucose transporter) from intracellular vesicles to the plasma membrane. Without insulin, GLUT-4 remains sequestered inside the cell, making these tissues the primary sites for insulin-mediated glucose disposal. **2. Why Other Options are Incorrect:** * **A & C (Gluconeogenesis and Glycogenolysis):** These are **catabolic** processes that increase blood glucose levels. They are stimulated by counter-regulatory hormones like **glucagon** and epinephrine during fasting. Insulin actively inhibits these pathways to prevent hyperglycemia. * **D (Glucose uptake in endothelium):** Glucose uptake in the endothelium (as well as the brain, liver, and RBCs) is **insulin-independent**. These tissues utilize transporters like **GLUT-1, GLUT-2, or GLUT-3**, which are always present on the cell membrane regardless of insulin levels. **High-Yield Clinical Pearls for NEET-PG:** * **GLUT-4** is the only insulin-dependent glucose transporter. * **Exercise** can also trigger GLUT-4 translocation in muscles via an insulin-independent pathway (AMPK-mediated), which is why exercise helps manage Type 2 Diabetes. * **Brain and RBCs** rely on GLUT-1/3; they do not require insulin for glucose entry, ensuring a constant energy supply even during starvation. * **Liver (GLUT-2)**: Insulin does not increase glucose *uptake* via transporters here (GLUT-2 is bidirectional), but it promotes glucose *utilization* by inducing Glucokinase.

Practice by Chapter

Carbohydrate Chemistry and Classification

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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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