Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism Indian Medical PG Practice Questions and MCQs

Question 281: Which of the following statements about GLUT is false?

A. GLUT-2 is needed in the brain (Correct Answer)
B. GLUT-3 is present in the placenta
C. GLUT-4 is present in adipose tissue
D. GLUT-3 is present in both intestine and testis

Explanation: The correct answer is **A. GLUT-2 is needed in the brain**. This statement is false because the brain primarily relies on **GLUT-1** (for crossing the blood-brain barrier) and **GLUT-3** (for neuronal uptake). GLUT-2 is a high-capacity, low-affinity transporter found in the liver, pancreatic beta cells, small intestine, and renal tubules, where it acts as a "glucose sensor." ### Explanation of Options: * **Option A (False/Correct):** GLUT-2 is not the primary transporter for the brain. The brain requires a constant glucose supply regardless of blood sugar levels; therefore, it utilizes GLUT-3, which has a very low Km (high affinity). * **Option B (True):** GLUT-3 is indeed present in the placenta to ensure a steady transfer of glucose to the fetus. * **Option C (True):** GLUT-4 is the only **insulin-dependent** glucose transporter. It is sequestered in intracellular vesicles and translocates to the cell membrane only in the presence of insulin. It is primarily found in skeletal muscle, cardiac muscle, and **adipose tissue**. * **Option D (True):** GLUT-3 has a wide distribution, including the brain (neurons), placenta, liver, kidneys, and specifically the **testis and intestine**. ### High-Yield Clinical Pearls for NEET-PG: * **GLUT-1 Deficiency Syndrome:** Presents with infantile seizures and developmental delay due to impaired glucose transport across the blood-brain barrier. * **SGLT vs. GLUT:** Remember that SGLT (1 & 2) are active transporters (secondary active) used in the intestine and kidneys, whereas all GLUTs (1–5) facilitate **passive diffusion**. * **GLUT-5:** Unique because it is primarily a **fructose** transporter, located in the small intestine and spermatozoa. * **Bidirectional Transport:** GLUT-2 is unique for its ability to transport glucose in both directions (e.g., during gluconeogenesis in the liver).

Question 282: Regarding the HMP shunt, all of the following statements are true EXCEPT:

A. It occurs in the cytosol.
B. No ATP is produced during the cycle.
C. It is active in adipose tissue, the liver, and gonads.
D. The oxidative phase generates NADPH, while the non-oxidative phase generates pyruvate. (Correct Answer)

Explanation: **Explanation:** The **Hexose Monophosphate (HMP) Shunt**, also known as the Pentose Phosphate Pathway (PPP), is an alternative pathway to glycolysis for glucose oxidation. **Why Option D is the Correct Answer (The False Statement):** The HMP shunt is unique because it **does not produce pyruvate** or lactate. The pathway consists of two phases: 1. **Oxidative Phase (Irreversible):** Converts Glucose-6-Phosphate to Ribulose-5-Phosphate, generating **NADPH**. 2. **Non-oxidative Phase (Reversible):** Recycles pentose phosphates back into glycolytic intermediates like **Fructose-6-Phosphate** and **Glyceraldehyde-3-Phosphate**. Pyruvate is the end product of glycolysis, not the HMP shunt. **Analysis of Other Options:** * **Option A:** True. Like glycolysis, all enzymes of the HMP shunt are located in the **cytosol**. * **Option B:** True. The pathway is focused on biosynthesis and redox balance; it **neither consumes nor produces ATP** directly. * **Option C:** True. The shunt is highly active in tissues requiring NADPH for fatty acid synthesis (**liver, adipose tissue, mammary glands**) or steroid synthesis (**gonads, adrenal cortex**), and in RBCs to maintain reduced glutathione. **High-Yield Clinical Pearls for NEET-PG:** * **Rate-limiting enzyme:** Glucose-6-Phosphate Dehydrogenase (G6PD), stimulated by Insulin. * **G6PD Deficiency:** Leads to hemolytic anemia due to the inability to regenerate reduced glutathione, making RBCs susceptible to oxidative stress (Heinz bodies/Bite cells). * **Transketolase:** A key enzyme in the non-oxidative phase that requires **Thiamine (Vitamin B1)** as a cofactor. Measuring erythrocyte transketolase activity is used to diagnose Thiamine deficiency. * **Major Products:** NADPH (for reductive biosynthesis) and Ribose-5-phosphate (for nucleotide synthesis).

Question 283: Which of the following enzymes are NOT involved in glycogen metabolism?

A. Glycogen phosphorylase b
B. Glycogen synthase I
C. Glycogen synthase C
D. Glycogen synthase A (Correct Answer)

Explanation: ### Explanation In glycogen metabolism, enzymes exist in two interconvertible forms: an active form and an inactive form, regulated primarily by covalent modification (phosphorylation/dephosphorylation). **Why Option D is the Correct Answer:** The term **"Glycogen synthase A"** is a misnomer in standard biochemical nomenclature. While "Glycogen Synthase **a**" (lowercase) refers to the active, dephosphorylated form of the enzyme, "Glycogen Synthase **A**" (uppercase) is not a recognized clinical or biochemical designation for the enzyme. In the context of this specific competitive exam question, it serves as the "distractor" that does not exist in the metabolic pathway. **Analysis of Other Options:** * **Glycogen phosphorylase b (Option A):** This is the **inactive**, dephosphorylated form of the enzyme responsible for glycogenolysis. It is converted to the active 'a' form by phosphorylase kinase. * **Glycogen synthase I (Option B):** The "I" stands for **Independent**. This is the active, dephosphorylated form of glycogen synthase that functions independently of the glucose-6-phosphate concentration. * **Glycogen synthase D (Option C):** The "D" stands for **Dependent**. This is the inactive, phosphorylated form of the enzyme which requires high concentrations of the allosteric activator, glucose-6-phosphate, to function. **High-Yield Clinical Pearls for NEET-PG:** * **Reciprocal Regulation:** Glucagon and Epinephrine trigger phosphorylation, which **activates** Glycogen Phosphorylase (promoting breakdown) but **inactivates** Glycogen Synthase (inhibiting synthesis). * **Insulin Effect:** Insulin triggers dephosphorylation via Protein Phosphatase-1, activating Glycogen Synthase (I-form). * **Rate-Limiting Enzymes:** Glycogen Synthase is the rate-limiting enzyme for glycogenesis; Glycogen Phosphorylase is the rate-limiting enzyme for glycogenolysis.

Question 284: Which of the following reactions generates ATP?

A. Glucose-3-phosphate to 1,3 BPG
B. Glucose-3-phosphate to Dihydroxyacetone phosphate
C. Phosphoenolpyruvate to Pyruvate (Correct Answer)
D. Pyruvate to Lactate

Explanation: **Explanation:** The generation of ATP in glycolysis occurs through **Substrate-Level Phosphorylation**, where a high-energy phosphate group is directly transferred from a metabolic intermediate to ADP. **1. Why Option C is Correct:** The conversion of **Phosphoenolpyruvate (PEP) to Pyruvate** is the final step of glycolysis, catalyzed by the enzyme **Pyruvate Kinase**. PEP contains a high-energy enol-phosphate bond. The breakdown of this bond releases enough energy to drive the phosphorylation of ADP to ATP. This is one of the two substrate-level phosphorylation steps in glycolysis (the other being the conversion of 1,3-BPG to 3-phosphoglycerate). **2. Analysis of Incorrect Options:** * **Option A (Glyceraldehyde-3-phosphate to 1,3-BPG):** This reaction, catalyzed by G3P Dehydrogenase, generates **NADH**, not ATP. It incorporates inorganic phosphate but does not produce energy in the form of ATP at this specific step. * **Option B (Glyceraldehyde-3-phosphate to DHAP):** This is a reversible isomerization reaction catalyzed by **Triose Phosphate Isomerase**. It involves the rearrangement of atoms with no net gain or loss of energy/ATP. * **Option C (Pyruvate to Lactate):** This occurs under anaerobic conditions catalyzed by **Lactate Dehydrogenase**. This reaction actually **consumes NADH** (oxidizing it to NAD+) to allow glycolysis to continue; it does not generate ATP. **High-Yield Clinical Pearls for NEET-PG:** * **Rate-Limiting Step:** Pyruvate Kinase is one of the three irreversible enzymes of glycolysis. * **Clinical Correlation:** **Pyruvate Kinase deficiency** is the second most common cause of enzyme-deficient hemolytic anemia (after G6PD deficiency). Since RBCs lack mitochondria, they rely solely on glycolysis for ATP; a deficiency leads to ATP depletion, causing rigid membranes and hemolysis. * **Net Yield:** The net gain of glycolysis is **2 ATP** and **2 NADH** per molecule of glucose.

Question 285: What is the effect of oral glucose administration on the body?

A. Decrease ketone body production (Correct Answer)
B. Increased lactate production upon exercise
C. Decreased gluconeogenesis
D. Increased gluconeogenesis

Explanation: **Explanation:** The administration of oral glucose triggers a rapid rise in blood glucose levels, which stimulates the pancreas to secrete **insulin** and inhibits the release of **glucagon**. **Why Option A is Correct:** Insulin is a potent anti-ketogenic hormone. It inhibits **Hormone-Sensitive Lipase (HSL)** in adipose tissue, reducing the breakdown of triglycerides into free fatty acids (FFAs). Since FFAs are the primary substrates for ketogenesis in the liver, their reduction leads to a significant **decrease in ketone body production**. Furthermore, insulin promotes the synthesis of Malonyl-CoA, which inhibits *Carnitine Palmitoyltransferase-1 (CPT-1)*, preventing fatty acids from entering the mitochondria for β-oxidation. **Analysis of Incorrect Options:** * **Option B:** Lactate production during exercise is primarily determined by muscle oxygen availability and intensity (anaerobic glycolysis), not by the immediate administration of oral glucose. * **Option C & D:** While glucose administration *does* eventually suppress gluconeogenesis via insulin, the most immediate and physiologically profound metabolic shift in the context of "sparing" effects is the suppression of ketogenesis and lipolysis. In many NEET-PG contexts, the "glucose-sparing effect" specifically refers to the reduction of fat utilization and ketone formation. **High-Yield Clinical Pearls for NEET-PG:** * **Antiketogenic effect of Carbohydrates:** Carbohydrates are described as "fat-sparing." In the absence of glucose (starvation/Diabetes), Oxaloacetate is diverted toward gluconeogenesis, depleting the TCA cycle and forcing Acetyl-CoA into the ketogenic pathway. * **Key Enzyme:** Insulin dephosphorylates (activates) **Acetyl-CoA Carboxylase**, increasing Malonyl-CoA, which is the "gatekeeper" that stops fatty acid oxidation. * **Ketone Bodies:** Acetone, Acetoacetate, and β-hydroxybutyrate. Note that Acetone is a non-metabolizable waste product excreted via the lungs.

Question 286: In what form does the product of glycolysis enter the TCA cycle?

A. Acetyl-CoA (Correct Answer)
B. Pyruvate
C. NADH
D. Glucose

Explanation: **Explanation:** The end product of aerobic glycolysis is **Pyruvate**. However, the TCA cycle (Krebs cycle) occurs in the mitochondrial matrix and cannot directly utilize pyruvate. **1. Why Acetyl-CoA is correct:** Before entering the TCA cycle, pyruvate must undergo **oxidative decarboxylation** to form **Acetyl-CoA**. This reaction is catalyzed by the **Pyruvate Dehydrogenase (PDH) Complex**, a multi-enzyme cluster located in the inner mitochondrial membrane. Acetyl-CoA then condenses with Oxaloacetate (OAA) to form Citrate, marking the official start of the TCA cycle. Therefore, Acetyl-CoA is the "connecting link" or the actual substrate that enters the cycle. **2. Why other options are incorrect:** * **Pyruvate:** While it is the product of glycolysis, it is a 3-carbon molecule that must be converted to the 2-carbon Acetyl-CoA before it can participate in the TCA cycle. * **NADH:** This is a coenzyme produced during glycolysis and the TCA cycle. It enters the Electron Transport Chain (ETC) to generate ATP but does not "enter" the TCA cycle as a substrate. * **Glucose:** This is the starting substrate for glycolysis, not the product. **3. High-Yield Clinical Pearls for NEET-PG:** * **PDH Complex Requirements:** It requires five cofactors: **T**hiamine (B1), **R**iboflavin (B2), **N**iacin (B3), **P**antothenic acid (B5), and **L**ipoic acid (**T**ender **R**eeds **N**ever **P**lay **L**oose). * **Arsenic Poisoning:** Arsenite inhibits the PDH complex by binding to lipoic acid, leading to lactic acidosis and neurological symptoms. * **Regulation:** PDH is inhibited by its products (Acetyl-CoA and NADH) and activated by ADP and $Ca^{2+}$.

Question 287: Phosphofructokinase is the key enzyme of which metabolic pathway?

A. Glycogenolysis
B. Glycogenesis
C. Glycolysis (Correct Answer)
D. TCA cycle

Explanation: **Explanation:** **Phosphofructokinase-1 (PFK-1)** is the most important regulatory and rate-limiting enzyme of **Glycolysis** (the Embden-Meyerhof pathway). It catalyzes the irreversible conversion of Fructose-6-phosphate to Fructose-1,6-bisphosphate using one molecule of ATP. This step is known as the "committed step" because once phosphorylated by PFK-1, the glucose metabolite is destined to complete the glycolytic pathway. **Analysis of Incorrect Options:** * **Glycogenolysis:** The rate-limiting enzyme is **Glycogen Phosphorylase**, which breaks down glycogen into glucose-1-phosphate. * **Glycogenesis:** The rate-limiting enzyme is **Glycogen Synthase**, responsible for forming $\alpha$-1,4-glycosidic bonds to synthesize glycogen. * **TCA Cycle:** The key regulatory enzyme is **Isocitrate Dehydrogenase**, which catalyzes the oxidative decarboxylation of isocitrate to $\alpha$-ketoglutarate. **High-Yield Clinical Pearls for NEET-PG:** * **Allosteric Regulation:** PFK-1 is allosterically **inhibited by ATP and Citrate** (signaling high energy status) and **activated by AMP and Fructose-2,6-bisphosphate**. * **Potent Activator:** Fructose-2,6-bisphosphate is the most potent physiological activator of PFK-1, produced by the bifunctional enzyme PFK-2. * **Clinical Correlation:** Deficiency of the M-isoform of PFK-1 in muscles leads to **Tarui Disease (Glycogen Storage Disease Type VII)**, characterized by exercise intolerance and muscle cramping. * **Insulin vs. Glucagon:** Insulin increases PFK-1 activity (promoting glycolysis), while glucagon decreases it.

Question 288: Which test is used to differentiate monosaccharides from disaccharides?

A. Benedict's test
B. Seliwanoff's test
C. Barfoed's test (Correct Answer)
D. Rapid furfural test

Explanation: **Explanation:** The correct answer is **Barfoed’s test**. This test is specifically designed to distinguish between reducing monosaccharides and reducing disaccharides based on the speed of the reaction. **1. Why Barfoed’s test is correct:** Barfoed’s reagent consists of cupric acetate in dilute acetic acid (an acidic medium). Both monosaccharides and disaccharides can reduce cupric ions to cuprous oxide, forming a red precipitate. However, because the medium is acidic, monosaccharides (being stronger reducing agents) react much faster, typically within **2–3 minutes** of boiling. Reducing disaccharides (like lactose or maltose) require prolonged boiling (7–10 minutes) to show a reaction. **2. Analysis of Incorrect Options:** * **Benedict’s test:** Used to detect **reducing sugars** in general (e.g., glucose, fructose, lactose). It cannot differentiate between a monosaccharide and a disaccharide. * **Seliwanoff’s test:** Used to differentiate **keto-hexoses** (like fructose) from aldo-hexoses. It produces a cherry-red complex with ketoses. * **Rapid Furfural test:** Used to distinguish between **fructose (a keto-hexose)** and sucrose. It is a faster version of the Molisch test specifically for ketoses. **High-Yield Clinical Pearls for NEET-PG:** * **Barfoed’s Reagent:** Cupric acetate + Glacial acetic acid. * **Key distinction:** Monosaccharides = Scanty red precipitate in <3 mins; Disaccharides = Precipitate only after >7 mins. * **Osazone Test:** Another high-yield test where glucose and fructose form needle-shaped crystals, while lactose forms "powder-puff" or "hedgehog" shaped crystals. * **Bial’s Test:** Used specifically to detect **Pentoses** (e.g., ribose).

Question 289: Glyconeogenic capability of a cell is determined by the presence of which enzyme?

A. Pyruvate dehydrogenase
B. Glucose 6 phosphatase
C. Pyruvate carboxylase
D. Fructose 1,6-bisphosphatase (Correct Answer)

Explanation: ### Explanation **Why Fructose 1,6-bisphosphatase is the correct answer:** Gluconeogenesis is the synthesis of glucose from non-carbohydrate precursors. While several enzymes are involved, **Fructose 1,6-bisphosphatase (F1,6-BPase)** is considered the **key regulatory and rate-limiting enzyme** of this pathway. Its presence is the definitive marker of a cell's gluconeogenic capability because it bypasses the irreversible step of glycolysis catalyzed by Phosphofructokinase-1 (PFK-1). While Glucose 6-phosphatase is also essential, F1,6-BPase is the primary site of metabolic control (inhibited by Fructose 2,6-bisphosphate and AMP). **Analysis of Incorrect Options:** * **A. Pyruvate dehydrogenase (PDH):** This is a mitochondrial enzyme that converts pyruvate to Acetyl-CoA. It is a link reaction between glycolysis and the TCA cycle. It is **not** part of gluconeogenesis; in fact, Acetyl-CoA cannot be converted back into glucose in humans. * **B. Glucose 6-phosphatase:** While this enzyme is necessary for the final step of gluconeogenesis (releasing free glucose into the blood), it is absent in muscle. However, in many competitive exams, F1,6-BPase is prioritized as the "determinant" of the pathway's flux. * **C. Pyruvate carboxylase:** This enzyme converts pyruvate to oxaloacetate. While it is the first step of gluconeogenesis, it also serves an **anaplerotic** role (replenishing TCA cycle intermediates), meaning its presence alone does not strictly define a cell as gluconeogenic. **High-Yield Clinical Pearls for NEET-PG:** * **Major sites of Gluconeogenesis:** Liver (90%) and Kidney cortex (10%). During prolonged starvation, the kidney's contribution increases significantly. * **Deficiency:** Fructose 1,6-bisphosphatase deficiency leads to fasting hypoglycemia and lactic acidosis (due to inability to utilize lactate for glucose synthesis). * **Obligatory Activator:** Pyruvate carboxylase requires **Acetyl-CoA** for activation. * **Inhibitor:** Alcohol inhibits gluconeogenesis by increasing the NADH/NAD+ ratio, shifting the equilibrium from pyruvate to lactate, leading to hypoglycemia.

Question 290: What is the primary location of GLUT 5?

A. RBC
B. Liver
C. Small intestine (Correct Answer)
D. Placenta

Explanation: **Explanation:** Glucose transporters (GLUT) are a family of transmembrane proteins that facilitate the transport of glucose and other hexoses across cell membranes. **Why the Small Intestine is Correct:** **GLUT 5** is unique among the GLUT family because it is primarily a **fructose transporter** rather than a glucose transporter. Its primary location is the apical membrane of the enterocytes in the **small intestine**, where it facilitates the absorption of dietary fructose from the intestinal lumen. It is also found in high concentrations in **spermatozoa** (testis), as fructose is their main energy source. **Analysis of Incorrect Options:** * **A. RBC:** The primary transporter in Red Blood Cells is **GLUT 1**, which provides a basal glucose uptake independent of insulin. * **B. Liver:** The liver primarily utilizes **GLUT 2**. This is a high-capacity, high-Km (low affinity) transporter that allows the liver to "sense" and respond to high postprandial blood glucose levels. * **D. Placenta:** The placenta predominantly expresses **GLUT 1** and **GLUT 3** to ensure a continuous supply of glucose to the fetus, even during maternal hypoglycemia. **High-Yield Clinical Pearls for NEET-PG:** * **GLUT 4** is the only **insulin-dependent** transporter, located in skeletal muscle and adipose tissue. * **GLUT 2** is bidirectional and found in the "Liver, Kidney, and Pancreatic Beta cells." * **SGLT-1 vs. GLUT 5:** Remember that glucose and galactose are absorbed via SGLT-1 (active transport), while fructose is absorbed via GLUT 5 (facilitated diffusion). * **Mnemonic:** "GLUT **5** is for **F**ructose" (Both start with the 'F' sound).

Practice by Chapter

Carbohydrate Chemistry and Classification

Practice Questions

Glycolysis: Reactions and Regulation

Practice Questions

Gluconeogenesis: Reactions and Regulation

Practice Questions

Glycogen Metabolism: Synthesis and Breakdown

Practice Questions

Glycogen Storage Diseases

Practice Questions

Pentose Phosphate Pathway

Practice Questions

Metabolism of Fructose and Galactose

Practice Questions

Disorders of Fructose and Galactose Metabolism

Practice Questions

Blood Glucose Regulation

Practice Questions

Diabetes Mellitus: Biochemical Aspects

Practice Questions

Glycosylation and Glycoproteins

Practice Questions

Lactose Intolerance and Galactosemia

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free