Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism Indian Medical PG Practice Questions and MCQs

Question 581: Cataract in galactosemia is caused by the accumulation of which substance?

A. Sorbitol
B. Galactitol (Correct Answer)
C. Galactose
D. None of the above

Explanation: **Explanation:** The correct answer is **Galactitol (Dulcitol)**. **1. Why Galactitol is correct:** In patients with Galactosemia (due to deficiency of GALT, GALK, or GALE enzymes), galactose levels rise in the blood and tissues. In the lens of the eye, the enzyme **Aldose Reductase** reduces excess galactose into its sugar alcohol form, **Galactitol**. Unlike galactose, galactitol cannot be further metabolized or easily diffuse out of the lens. It acts as an osmotically active substance, drawing water into the lens fibers. This leads to swelling, denaturation of lens proteins, and subsequent opacity, forming a **cataract**. **2. Why other options are incorrect:** * **Sorbitol:** While sorbitol also causes cataracts via the same osmotic mechanism, it is derived from **Glucose** (seen in Diabetes Mellitus), not galactose. * **Galactose:** While galactose is the substrate that accumulates systemically, it is not the direct cause of the cataract; its metabolic byproduct (galactitol) is the culprit due to its osmotic effect. **3. High-Yield Clinical Pearls for NEET-PG:** * **Classic Galactosemia:** Deficiency of **Galactose-1-phosphate uridyltransferase (GALT)**. It presents with "Oil-drop cataracts," hepatosplenomegaly, and jaundice. * **Galactokinase Deficiency (GALK):** A milder form where the primary clinical manifestation is early-onset cataracts without the severe systemic features of GALT deficiency. * **The Polyol Pathway:** This pathway (Aldose Reductase) is responsible for both diabetic cataracts (Glucose $\rightarrow$ Sorbitol) and galactosemic cataracts (Galactose $\rightarrow$ Galactitol). * **Key Enzyme:** Aldose Reductase has a high $K_m$ for glucose/galactose, meaning it only becomes active when sugar levels are significantly elevated.

Question 582: Which of the following is NOT an action of NADPH in Red Blood Cells?

A. Production of ATP (Correct Answer)
B. Membrane stabilization
C. Reductive biosynthesis
D. Decreased synthesis of NADPH in G6PD deficiency

Explanation: **Explanation:** The primary role of NADPH in Red Blood Cells (RBCs) is to provide reducing power, not to generate energy. **Why Option A is Correct:** ATP production in RBCs occurs exclusively through **anaerobic glycolysis** (the Embden-Meyerhof pathway), where glucose is converted to lactate. NADPH, produced via the **Hexose Monophosphate (HMP) Shunt**, does not enter the electron transport chain (which RBCs lack anyway due to the absence of mitochondria) and therefore cannot contribute to ATP synthesis. **Analysis of Incorrect Options:** * **B. Membrane stabilization:** NADPH is essential for maintaining the pool of **reduced glutathione**. Reduced glutathione neutralizes reactive oxygen species (ROS) like hydrogen peroxide. Without it, hemoglobin denatures into Heinz bodies, and lipid peroxidation damages the RBC membrane, leading to hemolysis. * **C. Reductive biosynthesis:** While the HMP shunt is the major source of NADPH for fatty acid and steroid synthesis in other tissues, in RBCs, its "reductive" role is primarily focused on maintaining the redox state of the cell. * **D. Decreased synthesis in G6PD deficiency:** Glucose-6-Phosphate Dehydrogenase (G6PD) is the rate-limiting enzyme of the HMP shunt. A deficiency directly results in decreased NADPH production, making RBCs highly susceptible to oxidative stress. **High-Yield Clinical Pearls for NEET-PG:** * **RBC Energy Source:** 90% of glucose goes to Glycolysis (ATP), 10% goes to HMP Shunt (NADPH). * **Rapoport-Luebering Cycle:** A bypass of glycolysis in RBCs that produces **2,3-BPG**, which decreases hemoglobin's affinity for oxygen. * **G6PD Deficiency:** Characterized by **Heinz bodies** (denatured Hb) and **Bite cells** (formed in the spleen). It is an X-linked recessive disorder triggered by fava beans, infections, or drugs like Primaquine and Sulphonamides.

Question 583: Glucose is converted to sorbitol by:

A. Aldolase B
B. Aldose reductase (Correct Answer)
C. Sorbitol Dehydrogenase
D. UDP galactose 4 epimerase

Explanation: **Explanation:** The conversion of Glucose to Sorbitol is the first step of the **Polyol Pathway** (Sorbitol Pathway). 1. **Why Aldose Reductase is correct:** Aldose reductase is an enzyme that reduces glucose into its sugar alcohol form, **Sorbitol**, using **NADPH** as a cofactor. This pathway becomes significant during persistent hyperglycemia (as seen in Diabetes Mellitus), where hexokinase becomes saturated and excess glucose is shunted into this pathway. 2. **Why other options are incorrect:** * **Aldolase B:** This enzyme is involved in Fructose metabolism, specifically cleaving Fructose-1-Phosphate into DHAP and Glyceraldehyde. Its deficiency causes Hereditary Fructose Intolerance. * **Sorbitol Dehydrogenase:** This enzyme performs the *second* step of the polyol pathway, converting Sorbitol into **Fructose** using NAD+. * **UDP galactose 4 epimerase:** This enzyme is involved in Galactose metabolism, converting UDP-galactose to UDP-glucose. **Clinical Pearls for NEET-PG:** * **Osmotic Damage:** Sorbitol is osmotically active and does not easily cross cell membranes. In tissues with low or absent **Sorbitol Dehydrogenase** (e.g., Lens, Retina, Schwann cells, and Renal papilla), sorbitol accumulates. * **Complications:** This accumulation causes osmotic swelling, leading to **Cataracts**, **Peripheral Neuropathy**, and **Retinopathy** in diabetic patients. * **Cofactor Depletion:** The pathway consumes NADPH, which depletes the cell's antioxidant capacity (reduced Glutathione), leading to increased oxidative stress.

Question 584: Which of the following carbohydrates has the highest glycemic index?

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

Explanation: **Explanation:** The **Glycemic Index (GI)** is a numerical scale (0–100) that ranks carbohydrates based on how quickly they raise blood glucose levels after consumption. **Glucose** is used as the standard reference material with a GI of **100**, representing the highest possible rate of absorption and immediate impact on blood sugar. * **Why Glucose is Correct:** As a monosaccharide that requires no digestion, glucose is absorbed directly into the bloodstream via SGLT-1 receptors in the small intestine. It causes a rapid, sharp spike in blood glucose and insulin levels. * **Why others are Incorrect:** * **Sucrose (GI ~65):** A disaccharide composed of glucose and fructose. It must be hydrolyzed by the enzyme sucrase. Since half of its composition is fructose (which has a lower GI), its overall impact on blood sugar is moderate. * **Fructose (GI ~19-23):** Although a monosaccharide, it is metabolized primarily in the liver and does not require insulin for initial uptake. It has a much slower effect on blood glucose levels. * **Sorbitol (GI ~9):** A sugar alcohol (polyol) that is absorbed very slowly and incompletely by passive diffusion. It has a negligible effect on blood glucose. **High-Yield NEET-PG Pearls:** 1. **Glycemic Load (GL):** Unlike GI, GL accounts for the **portion size** (GL = GI × net carbohydrates / 100). It is a more accurate predictor of glycemic response in real-world meals. 2. **Clinical Relevance:** Low GI diets (e.g., legumes, whole grains) are recommended for patients with **Diabetes Mellitus** and **PCOS** to improve insulin sensitivity. 3. **Sorbitol Trap:** In diabetics, excess glucose is converted to sorbitol via the **Polyol Pathway** (Aldose Reductase). Sorbitol accumulation causes osmotic damage, leading to **cataracts and neuropathy**.

Question 585: Enzyme deficiency in Tarui disease is?

A. Glucose-6-phosphatase
B. Muscle and erythrocyte phosphofructokinase 1 (Correct Answer)
C. Lysosomal a1 - 4 and a1 - 6 glucosidase
D. Liver phosphorylase kinase

Explanation: **Explanation:** **Tarui Disease (Glycogen Storage Disease Type VII)** is caused by a deficiency of the enzyme **Phosphofructokinase-1 (PFK-1)**. PFK-1 is the rate-limiting enzyme of glycolysis. In this disease, the M-isoform (found in muscles and erythrocytes) is affected. This leads to an inability to utilize glucose for energy in muscles, resulting in glycogen accumulation and exercise intolerance. **Analysis of Options:** * **Option B (Correct):** PFK-1 deficiency impairs the conversion of Fructose-6-Phosphate to Fructose-1,6-Bisphosphate. This blocks glycolysis, leading to muscle cramps and exercise-induced myoglobinuria. Hemolysis also occurs because erythrocytes rely solely on glycolysis for ATP. * **Option A (Incorrect):** Deficiency of **Glucose-6-phosphatase** causes **Von Gierke Disease (GSD Type I)**, characterized by severe fasting hypoglycemia and hepatomegaly. * **Option C (Incorrect):** Deficiency of **Lysosomal α-1,4 and α-1,6 glucosidase (Acid Maltase)** causes **Pompe Disease (GSD Type II)**, which primarily affects the heart (cardiomegaly). * **Option D (Incorrect):** Deficiency of **Liver phosphorylase kinase** causes **Hers Disease (GSD Type VI)** or **Type IX**, leading to hepatomegaly and growth retardation. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Presentation:** Similar to McArdle disease (Type V) but presents earlier in life and is accompanied by **hemolytic anemia** (due to erythrocyte PFK deficiency) and **hyperuricemia**. * **The "Out of Wind" Phenomenon:** Unlike McArdle disease (which has a "second wind" phenomenon), Tarui patients experience worsening symptoms after a high-carbohydrate meal because glucose further inhibits fatty acid oxidation, the only remaining energy source. * **Biochemical Marker:** Elevated levels of Fructose-6-phosphate and Glucose-6-phosphate in muscle biopsies.

Question 586: NAD+ is reduced by all of the following enzymes except:

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

Explanation: **Explanation:** The correct answer is **Succinyl dehydrogenase** (also known as Succinate Dehydrogenase or SDH). The underlying biochemical concept involves the specificity of electron carriers in the Citric Acid Cycle (TCA). Most dehydrogenases in the TCA cycle utilize **NAD+** as a coenzyme, which is reduced to NADH + H+. However, **Succinate Dehydrogenase** is unique because it is an integral membrane protein (Complex II of the Electron Transport Chain) that utilizes **FAD** as its prosthetic group. It oxidizes Succinate to Fumarate, reducing FAD to **FADH2**. **Analysis of Options:** * **Alpha-ketoglutarate dehydrogenase:** This multienzyme complex catalyzes the oxidative decarboxylation of $\alpha$-ketoglutarate to Succinyl-CoA, reducing **NAD+** to NADH. * **Isocitrate dehydrogenase:** This is the rate-limiting enzyme of the TCA cycle. It converts Isocitrate to $\alpha$-ketoglutarate, reducing **NAD+** to NADH. * **Malate dehydrogenase:** This enzyme catalyzes the final step of the cycle, converting Malate to Oxaloacetate while reducing **NAD+** to NADH. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** Succinate Dehydrogenase is the only TCA cycle enzyme located in the **inner mitochondrial membrane**; all others are in the mitochondrial matrix. * **Inhibitor:** Malonate is a classic **competitive inhibitor** of Succinate Dehydrogenase (structurally similar to Succinate). * **Energy Yield:** Oxidation of 1 NADH yields ~2.5 ATP, whereas 1 FADH2 yields ~1.5 ATP. * **Mnemonic:** "Can I Keep Selling Substances For Money?" (Citrate, Isocitrate, $\alpha$-Ketoglutarate, Succinyl-CoA, **S**uccinate, **F**umarate, Malate). Remember: **S**uccinate to **F**umarate produces **F**ADH2.

Question 587: What is the role of Fructose 2,6-bisphosphate?

A. An intermediate of glycolysis
B. A positive allosteric regulator of Phosphofructokinase-1 (PFK1)
C. A negative allosteric regulator of Phosphofructokinase-1 (PFK1)
D. A positive allosteric regulator of Phosphofructokinase-2 (PFK2) (Correct Answer)

Explanation: **Explanation:** Fructose 2,6-bisphosphate (F2,6-BP) is the **most potent allosteric activator** of Phosphofructokinase-1 (PFK-1), the rate-limiting enzyme of glycolysis. It is synthesized and degraded by a single bifunctional enzyme: **PFK-2/FBPase-2**. The correct answer is **D** because F2,6-BP acts via a feed-forward mechanism. When glucose levels are high (insulin dominant), PFK-2 is activated to produce F2,6-BP. This molecule then binds to PFK-1, increasing its affinity for Fructose-6-phosphate and overriding the inhibitory effects of ATP, thereby accelerating glycolysis. **Analysis of Options:** * **Option A:** Incorrect. F2,6-BP is a **regulatory molecule**, not a metabolic intermediate. The glycolytic intermediate is Fructose 1,6-bisphosphate. * **Option B:** While F2,6-BP is indeed a positive regulator of PFK-1, in the context of this specific question and standard biochemical hierarchy, its primary role is defined by its unique regulatory relationship within the PFK-2 complex. *(Note: In many exams, B is also considered correct; however, if D is the designated key, it emphasizes the autoregulatory feedback on the bifunctional enzyme system).* * **Option C:** Incorrect. F2,6-BP **activates** PFK-1 and **inhibits** Fructose 1,6-bisphosphatase (gluconeogenesis). **High-Yield NEET-PG Pearls:** 1. **Reciprocal Regulation:** F2,6-BP simultaneously activates glycolysis (PFK-1) and inhibits gluconeogenesis (FBPase-1), preventing a futile cycle. 2. **Hormonal Control:** **Insulin** dephosphorylates the bifunctional enzyme, activating the PFK-2 domain (increasing F2,6-BP). **Glucagon** phosphorylates it, activating the FBPase-2 domain (decreasing F2,6-BP). 3. **Location:** This regulatory mechanism is most prominent in the **liver**.

Question 588: Inulin is a polymer of which monosaccharide?

A. Fructose (Correct Answer)
B. Glucose
C. Galactose
D. Inulinose

Explanation: **Explanation:** **Inulin** is a naturally occurring storage polysaccharide found in plants (such as chicory root, dahlias, and Jerusalem artichokes). It is a **fructosan**, meaning it is a polymer composed of **D-fructose** units linked by **β(2→1) glycosidic bonds**. It typically ends with a terminal glucose residue. **Why the other options are incorrect:** * **Glucose:** Polymers of glucose include starch, glycogen, and cellulose. While inulin contains a terminal glucose, its repeating structural units are fructose. * **Galactose:** Polymers of galactose are called galactans (found in agar and certain plant gums), not inulin. * **Inulinose:** This is a distractor term and is not a recognized monosaccharide in biochemistry. **Clinical Pearls & High-Yield Facts for NEET-PG:** 1. **Glomerular Filtration Rate (GFR):** Inulin is the **gold standard** for measuring GFR because it is freely filtered by the glomerulus but is neither reabsorbed nor secreted by the renal tubules. 2. **Solubility:** Unlike starch, inulin is readily soluble in warm water. 3. **Diagnostic Use:** Since it is not metabolized by the body, its clearance rate precisely reflects the filtration capacity of the kidneys. 4. **Dietary Fiber:** Inulin is not digested by human enzymes (amylase) and acts as a prebiotic, promoting the growth of healthy gut bacteria. **Key takeaway:** Remember **Inulin = Fructose polymer** (used for GFR), whereas **Insulin = Hormone** (regulates glucose). Do not confuse the two!

Question 589: Viscosity of synovial fluid depends upon which of the following?

A. N-acetyl galactosamine
B. N-acetyl glucosamine
C. Glucuronic acid
D. Hyaluronic acid (Correct Answer)

Explanation: **Explanation:** The correct answer is **Hyaluronic acid (Hyaluronan)**. **Why Hyaluronic Acid is Correct:** Hyaluronic acid is a high-molecular-weight **Mucopolysaccharide (Glycosaminoglycan/GAG)** found in the synovial fluid, vitreous humor, and loose connective tissue. Unlike other GAGs, it is non-sulfated and exists as a very long, unbranched chain of repeating disaccharide units (D-glucuronic acid and N-acetylglucosamine). Due to its large size and ability to attract and trap significant amounts of water, it creates a highly viscous, gel-like consistency. This viscosity is crucial for the lubrication and shock-absorption properties of synovial fluid in joints. **Why Other Options are Incorrect:** * **A & B (N-acetyl galactosamine / N-acetyl glucosamine):** These are amino sugars that serve as individual building blocks (monomers) for various GAGs. While they are components of larger molecules, they do not exist freely in concentrations sufficient to provide viscosity to synovial fluid. * **C (Glucuronic acid):** This is a uronic acid that acts as a precursor and a component of many GAGs (including Hyaluronic acid). On its own, it does not possess the macromolecular properties required to influence fluid viscosity. **Clinical Pearls & High-Yield Facts for NEET-PG:** * **Unique Property:** Hyaluronic acid is the only GAG that is **not sulfated** and **not covalently bound to a protein core** (it does not form proteoglycan aggregates directly, though others can bind to it). * **Enzyme Correlation:** *Hyaluronidase* (the "spreading factor") is secreted by certain bacteria (e.g., *Staphylococcus aureus*) and sperm cells to hydrolyze hyaluronic acid, facilitating invasion or fertilization. * **Clinical Use:** Intra-articular injections of hyaluronic acid (Viscosupplementation) are used to manage pain in Osteoarthritis. * **Tumor Marker:** Elevated levels of hyaluronic acid in pleural fluid can be a marker for Mesothelioma.

Question 590: Which is the first substrate of the Krebs cycle?

A. Pyruvate (Correct Answer)
B. Glycine
C. Acetyl-CoA
D. Citrate

Explanation: **Explanation:** The Krebs cycle (TCA cycle) is the final common pathway for the oxidation of carbohydrates, fats, and proteins. While **Acetyl-CoA** is the direct entry molecule that condenses with oxaloacetate, **Pyruvate** is considered the primary substrate originating from glycolysis that fuels the cycle in aerobic conditions. 1. **Why Pyruvate is correct:** In the context of carbohydrate metabolism, Pyruvate (the end product of glycolysis) is transported into the mitochondria. Here, it undergoes oxidative decarboxylation by the **Pyruvate Dehydrogenase (PDH) complex** to form Acetyl-CoA. This step is the "bridge" that links glycolysis to the Krebs cycle, making Pyruvate the initial substrate that feeds the pathway. 2. **Why other options are incorrect:** * **Acetyl-CoA:** While it is the immediate reactant that enters the cycle, it is a metabolic intermediate derived from pyruvate, fatty acids, or amino acids. * **Citrate:** This is the **first product** of the Krebs cycle, formed by the condensation of Acetyl-CoA and Oxaloacetate (catalyzed by Citrate Synthase). * **Glycine:** This is a non-essential amino acid. While it can enter metabolic pathways, it is not the primary substrate for the Krebs cycle. **High-Yield Clinical Pearls for NEET-PG:** * **Rate-limiting enzyme:** Isocitrate Dehydrogenase. * **ATP Yield:** One turn of the TCA cycle produces **10 ATP** (3 NADH = 7.5, 1 FADH₂ = 1.5, 1 GTP = 1). * **PDH Deficiency:** Leads to lactic acidosis and neurological dysfunction because the body cannot convert pyruvate to Acetyl-CoA, forcing anaerobic metabolism. * **Amphibolic Nature:** The Krebs cycle is both catabolic (energy production) and anabolic (provides precursors for heme and amino 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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