Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism Indian Medical PG Practice Questions and MCQs

Question 511: Which is the major site of expression of GLUT5?

A. Renal tubules
B. Brain
C. Placenta
D. Sperm (Correct Answer)

Explanation: **Explanation:** The correct answer is **Sperm**. GLUT5 is a unique member of the glucose transporter family because it functions primarily as a **fructose transporter** rather than a glucose transporter. 1. **Why Sperm is correct:** Mature spermatozoa utilize fructose as their primary energy source for motility. Fructose is secreted in high concentrations by the seminal vesicles. GLUT5 is highly expressed on the plasma membrane of sperm cells to facilitate the uptake of this specific sugar. It is also found in high concentrations in the **jejunum (small intestine)**, where it mediates the absorption of dietary fructose. 2. **Why other options are incorrect:** * **Renal tubules:** While GLUT2 and GLUT1 are the primary transporters for glucose reabsorption in the kidneys, GLUT5 has minimal expression here. * **Brain:** The brain primarily relies on **GLUT1** (blood-brain barrier) and **GLUT3** (neurons) for a steady supply of glucose. * **Placenta:** The placenta predominantly expresses **GLUT1** to ensure the continuous transfer of glucose from maternal to fetal circulation. **High-Yield Clinical Pearls for NEET-PG:** * **GLUT1:** Found in RBCs, Blood-Brain Barrier, and Placenta (Basal glucose uptake). * **GLUT2:** Bidirectional transporter found in **Liver, Pancreas (B-cells), and Kidney**. It has a high $K_m$ (low affinity). * **GLUT3:** Highest affinity for glucose; found in **Neurons**. * **GLUT4:** The only **insulin-dependent** transporter; found in **Skeletal muscle and Adipose tissue**. * **GLUT5:** Specific for **Fructose**; located in the Small Intestine and Sperm.

Question 512: Severe thiamine deficiency is associated with which of the following?

A. Decreased RBC transketolase activity (Correct Answer)
B. Increased clotting time
C. Decreased RBC transaminase activity
D. Increased xanthic acid excretion

Explanation: **Explanation:** **1. Why Option A is Correct:** Thiamine (Vitamin B1) acts as a coenzyme in its active form, **Thiamine Pyrophosphate (TPP)**, for several key enzymes. One of these is **Transketolase**, a crucial enzyme in the Hexose Monophosphate (HMP) Shunt. Since transketolase is present in red blood cells (RBCs) and its activity is strictly dependent on TPP, measuring **RBC Transketolase activity** is the most reliable diagnostic biochemical marker for thiamine deficiency. In severe deficiency, this activity decreases significantly; if the activity increases by >25% upon adding TPP in vitro (TPP effect), it confirms the deficiency. **2. Why the Other Options are Incorrect:** * **Option B (Increased clotting time):** Clotting time is related to coagulation factors and Vitamin K deficiency, not Thiamine. * **Option C (Decreased RBC transaminase activity):** Transaminases (ALT/AST) require **Pyridoxal Phosphate (Vitamin B6)** as a cofactor, not Thiamine. * **Option D (Increased xanthic acid excretion):** Increased excretion of **Xanthurenic acid** in urine following a tryptophan load is a classic marker for **Vitamin B6 (Pyridoxine) deficiency**, as B6 is required for the kynurenine pathway. **3. High-Yield Clinical Pearls for NEET-PG:** * **Key TPP-dependent enzymes:** 1. Pyruvate Dehydrogenase (Link reaction) 2. alpha-Ketoglutarate Dehydrogenase (TCA cycle) 3. Branched-chain alpha-ketoacid dehydrogenase (Maple Syrup Urine Disease) 4. Transketolase (HMP Shunt) * **Clinical Presentation:** Deficiency leads to **Beriberi** (Dry: neurological; Wet: high-output heart failure) and **Wernicke-Korsakoff Syndrome** (triad of ataxia, ophthalmoplegia, and confusion), commonly seen in chronic alcoholics. * **Biochemical Tip:** Always measure transketolase activity *before* administering glucose to a suspected thiamine-deficient patient to avoid precipitating Wernicke’s encephalopathy.

Question 513: Sodium fluoride is a good in-vitro preservative of glucose in blood samples because it inhibits which of the following?

A. Enolase (Correct Answer)
B. Hexokinase
C. Phosphofructokinase
D. Pyruvate dehydrogenase

Explanation: **Explanation:** **1. Why Enolase is the Correct Answer:** Sodium fluoride (NaF) is the standard preservative used in blood collection tubes (grey-top) for glucose estimation. Its primary role is to inhibit **glycolysis**, preventing the breakdown of glucose by RBCs and WBCs in the sample. * **Mechanism:** Fluoride ions ($F^-$) bind with magnesium ($Mg^{2+}$) and inorganic phosphate to form a **magnesium-fluorophosphate complex**. This complex competitively inhibits the enzyme **Enolase**, which requires $Mg^{2+}$ as a cofactor to convert 2-phosphoglycerate to phosphoenolpyruvate. By blocking this step, the glycolytic pathway is halted, preserving the glucose concentration for up to 48–72 hours. **2. Why Other Options are Incorrect:** * **B. Hexokinase:** This is the first enzyme of glycolysis. While it is inhibited by its product (Glucose-6-Phosphate), it is not the target of fluoride. * **C. Phosphofructokinase (PFK-1):** This is the rate-limiting enzyme of glycolysis, regulated by ATP/AMP levels and Citrate, not by fluoride. * **D. Pyruvate Dehydrogenase (PDH):** This enzyme links glycolysis to the TCA cycle (converting pyruvate to Acetyl-CoA). It is located in the mitochondria and is not the site of action for fluoride-mediated glucose preservation. **3. High-Yield Clinical Pearls for NEET-PG:** * **Grey-top Vacutainer:** Contains Sodium Fluoride (antiglycolytic agent) and Potassium Oxalate (anticoagulant). * **The "10 mg/dL" Rule:** In unpreserved blood, glucose levels drop by approximately **10 mg/dL per hour** at room temperature due to glycolysis. * **Fluoride & Urease:** Fluoride also inhibits the enzyme **Urease**. Therefore, fluoride-containing tubes should **not** be used for urea estimation if the laboratory uses the urease method. * **Enolase Inhibition:** This is a classic example of **competitive inhibition** in the presence of phosphate.

Question 514: Cori's cycle is another name for which of the following metabolic pathways?

A. Oxidative decarboxylation of pyruvate
B. HMP pathway
C. TCA cycle
D. Lactic acid cycle (Correct Answer)

Explanation: **Explanation:** **Cori’s Cycle (Lactic Acid Cycle)** refers to the metabolic pathway in which lactate produced by anaerobic glycolysis in the muscles (or RBCs) moves to the liver and is converted back to glucose, which then returns to the muscles. 1. **Why the correct answer is right:** In actively contracting skeletal muscle, the rate of glycolysis exceeds the rate of the TCA cycle, leading to the reduction of pyruvate into **lactate** by the enzyme *Lactate Dehydrogenase (LDH)*. This lactate is released into the blood and taken up by the **liver**. In the liver, lactate is oxidized back to pyruvate and converted into glucose via **gluconeogenesis**. This glucose is then released back into the bloodstream for muscle use. This inter-organ cooperation prevents lactic acidosis and maintains blood glucose levels during exercise. 2. **Why the incorrect options are wrong:** * **Oxidative decarboxylation of pyruvate:** This is the conversion of pyruvate to Acetyl-CoA by the *Pyruvate Dehydrogenase (PDH) complex*, linking glycolysis to the TCA cycle. * **HMP pathway (Pentose Phosphate Pathway):** An alternative glucose pathway used to generate NADPH (for fatty acid synthesis) and Ribose-5-phosphate (for nucleotide synthesis). * **TCA cycle (Krebs Cycle):** The final common pathway for the oxidation of carbohydrates, lipids, and proteins occurring in the mitochondria. **High-Yield Facts for NEET-PG:** * **Net Energy Cost:** The Cori cycle consumes **6 ATP** in the liver for every **2 ATP** produced in the muscle (a net loss of 4 ATP). * **Key Enzyme:** *Lactate Dehydrogenase* (Muscle: Pyruvate → Lactate; Liver: Lactate → Pyruvate). * **Glucose-Alanine Cycle (Cahill Cycle):** Similar to the Cori cycle, but involves the transport of amino groups from muscle to liver via **Alanine** instead of lactate.

Question 515: Which glycolytic enzyme(s) are inhibited by fluoride?

A. Hexokinase
B. Aldolase
C. Enolase (Correct Answer)
D. Pyruvate Kinase

Explanation: **Explanation:** **Enolase** is the correct answer because it is specifically inhibited by fluoride ions. In the glycolytic pathway, Enolase catalyzes the dehydration of 2-phosphoglycerate to phosphoenolpyruvate (PEP). This enzyme requires magnesium ions ($Mg^{2+}$) as a cofactor. Fluoride binds with phosphate and magnesium to form a **magnesium-fluorophosphate complex**, which competitively displaces $Mg^{2+}$ from the enzyme’s active site, thereby halting glycolysis. **Analysis of Incorrect Options:** * **Hexokinase (A):** This is the first regulatory step of glycolysis (Glucose to Glucose-6-P). It is inhibited by its product, Glucose-6-phosphate, but not by fluoride. * **Aldolase (B):** This enzyme cleaves Fructose-1,6-bisphosphate into DHAP and Glyceraldehyde-3-phosphate. It is not a target for fluoride inhibition. * **Pyruvate Kinase (D):** This is the final irreversible step of glycolysis. It is regulated by allosteric effectors (like Fructose-1,6-bisphosphate) and covalent modification, but it is not inhibited by fluoride. **Clinical Pearls & High-Yield Facts for NEET-PG:** * **Blood Glucose Estimation:** In clinical practice, blood samples for glucose estimation are collected in **grey-topped vials** containing **Sodium Fluoride (NaF)**. * **Preservation:** NaF acts as a glycolytic inhibitor, preventing RBCs from consuming the glucose in the sample, ensuring an accurate measurement of the patient's blood sugar levels. * **Anticoagulant Pair:** NaF is usually paired with **Potassium Oxalate**, which acts as the anticoagulant by chelating calcium. * **Note:** Fluoride inhibition is reversible if more magnesium is added, but in laboratory settings, it effectively "fixes" the glucose concentration for up to 48–72 hours.

Question 516: In hereditary fructose intolerance, which enzyme is defective?

A. Phosphofructokinase
B. Fructose 2, 6-biphosphatase
C. Fructokinase
D. Aldolase B (Correct Answer)

Explanation: **Explanation:** **Hereditary Fructose Intolerance (HFI)** is an autosomal recessive disorder caused by a deficiency of **Aldolase B**. In the liver, fructose is first converted to Fructose-1-Phosphate (F1P) by fructokinase. Aldolase B is responsible for cleaving F1P into dihydroxyacetone phosphate (DHAP) and glyceraldehyde. When Aldolase B is defective, **Fructose-1-Phosphate accumulates** intracellularly. This "traps" inorganic phosphate, leading to ATP depletion, inhibition of glycogenolysis, and gluconeogenesis, which clinically manifests as severe postprandial hypoglycemia, vomiting, and jaundice following the introduction of fruit or formula. **Analysis of Incorrect Options:** * **A. Phosphofructokinase:** This is the rate-limiting enzyme of glycolysis. Deficiency (Tarui disease) leads to glycogen storage disease type VII, characterized by exercise intolerance and muscle cramps. * **B. Fructose 2,6-bisphosphatase:** This is a regulatory bifunctional enzyme that controls the levels of Fructose 2,6-bisphosphate, thereby regulating glycolysis and gluconeogenesis; it is not primary to HFI. * **C. Fructokinase:** Deficiency causes **Essential Fructosuria**. This is a benign condition because fructose is not "trapped" in cells; it simply spills into the urine (fructosemia and fructosuria) without causing metabolic crisis. **High-Yield Clinical Pearls for NEET-PG:** * **The "Trapping" Mechanism:** ATP depletion in HFI leads to liver failure and proximal renal tubular acidosis (Fanconi syndrome). * **Dietary Management:** Treatment requires strict avoidance of **fructose, sucrose (glucose + fructose), and sorbitol**. * **Clinical Presentation:** Symptoms typically appear when an infant is weaned from breast milk and introduced to fruits or juices. * **Reducing Sugars:** In HFI, urine dipstick for glucose is negative, but a test for reducing sugars (Benedict’s test) is positive.

Question 517: Which glycolytic enzyme is inhibited by fluoride?

A. Hexokinase
B. Aldolase
C. Enolase (Correct Answer)
D. All of the above

Explanation: **Explanation:** **1. Why Enolase is the Correct Answer:** Enolase is the glycolytic enzyme responsible for the dehydration of **2-phosphoglycerate (2-PG) to phosphoenolpyruvate (PEP)**. Fluoride acts as a potent competitive inhibitor of this enzyme. The mechanism involves fluoride ions forming a complex with magnesium ($Mg^{2+}$) and inorganic phosphate. Since Enolase requires $Mg^{2+}$ as a cofactor for its catalytic activity, the formation of this **magnesium-fluorophosphate complex** traps the metal ion, rendering the enzyme inactive and halting glycolysis. **2. Why Other Options are Incorrect:** * **Hexokinase:** This is the first regulatory step of glycolysis (Glucose to Glucose-6-Phosphate). It is inhibited by its product, Glucose-6-Phosphate, but not by fluoride. * **Aldolase:** This enzyme cleaves Fructose-1,6-bisphosphate into DHAP and Glyceraldehyde-3-phosphate. It is not sensitive to fluoride inhibition. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Blood Glucose Estimation:** In clinical practice, blood samples for glucose estimation are collected in **vacutainers containing Sodium Fluoride (grey-top tubes)**. This prevents "in vitro" glycolysis by RBCs and WBCs, ensuring the measured glucose level reflects the patient's actual blood sugar at the time of collection. * **Potassium Oxalate:** Often added alongside Sodium Fluoride as an anticoagulant; while fluoride inhibits glycolysis, oxalate prevents clotting by chelating calcium. * **Dental Health:** Fluoride's ability to inhibit bacterial enolase (specifically in *Streptococcus mutans*) is one of the mechanisms by which it prevents dental caries. * **Reversibility:** The inhibition of Enolase by fluoride is reversible if the fluoride concentration decreases.

Question 518: Which of the following pathways yields the maximum number of energy-rich phosphate molecules?

A. Glycolysis
B. Gluconeogenesis
C. HMP shunt
D. Citric acid cycle (Correct Answer)

Explanation: ### Explanation The **Citric Acid Cycle (TCA cycle)**, also known as the Krebs cycle, is the final common pathway for the oxidation of carbohydrates, lipids, and proteins. It is the most efficient energy-yielding pathway in the cell. **1. Why Citric Acid Cycle is Correct:** For every turn of the TCA cycle (per acetyl CoA), the following energy-rich molecules are produced: * **3 NADH** (yielding ~7.5 ATP via oxidative phosphorylation) * **1 FADH₂** (yielding ~1.5 ATP via oxidative phosphorylation) * **1 GTP** (equivalent to 1 ATP via substrate-level phosphorylation) Total yield: **10 ATP per acetyl CoA**. Since one glucose molecule produces two acetyl CoA, the TCA cycle contributes **20 ATP** out of the total ~30-32 ATP generated during aerobic respiration. **2. Why Other Options are Incorrect:** * **Glycolysis:** This pathway occurs in the cytosol and has a much lower net yield. Aerobic glycolysis yields only **7 or 5 ATP** (depending on the shuttle used), while anaerobic glycolysis yields only **2 ATP**. * **Gluconeogenesis:** This is an **anabolic (energy-consuming)** pathway. It requires the input of 6 high-energy phosphate bonds (4 ATP and 2 GTP) to synthesize one molecule of glucose from pyruvate. * **HMP Shunt:** This pathway does **not produce ATP**. Its primary functions are the generation of **NADPH** (for reductive biosynthesis) and **Ribose-5-phosphate** (for nucleotide synthesis). **High-Yield Clinical Pearls for NEET-PG:** * **Rate-limiting enzyme of TCA:** Isocitrate Dehydrogenase. * **Substrate-level phosphorylation in TCA:** Catalyzed by **Succinate Thiokinase** (Succinyl CoA synthetase). * **Only membrane-bound enzyme of TCA:** Succinate Dehydrogenase (also part of Complex II of the Electron Transport Chain). * **Inhibitor of TCA:** Fluoroacetate (inhibits Aconitase) and Arsenite (inhibits α-ketoglutarate dehydrogenase).

Question 519: The D-xylose test is diagnostic of which condition?

A. Coeliac disease (Correct Answer)
B. Lactose intolerance
C. Bacterial overgrowth
D. Whipple disease

Explanation: **Explanation:** The **D-xylose test** is a classic biochemical investigation used to differentiate between **malabsorption caused by intestinal mucosal disease** and malabsorption due to **pancreatic insufficiency**. **Why Coeliac Disease is correct:** D-xylose is a pentose sugar that is absorbed via passive diffusion in the proximal small intestine without requiring pancreatic enzymes. In **Coeliac disease**, the destruction of intestinal villi (villous atrophy) reduces the surface area available for absorption. Consequently, D-xylose is not absorbed into the blood, leading to **low levels in both blood and urine**. This confirms a primary mucosal defect. **Why other options are incorrect:** * **Lactose Intolerance:** This is a deficiency of the enzyme lactase. It does not affect the passive absorption of pentose sugars like D-xylose. Diagnosis is typically made via the Hydrogen Breath Test. * **Bacterial Overgrowth (SIBO):** While bacteria can sometimes metabolize D-xylose (leading to a false positive), the test is not "diagnostic" for SIBO. SIBO is better diagnosed with the Glucose or Lactulose breath test. * **Whipple Disease:** While it can cause malabsorption, the D-xylose test is classically associated with Coeliac disease in medical examinations. Whipple disease is definitively diagnosed via PAS-positive macrophages on biopsy. **High-Yield NEET-PG Pearls:** * **Normal Results:** If D-xylose levels are normal in the urine/blood despite fat malabsorption, the cause is likely **Pancreatic Insufficiency** (e.g., Chronic Pancreatitis). * **Prerequisite:** The test requires normal renal function; impaired kidneys will result in falsely low urinary D-xylose levels. * **Site of Absorption:** D-xylose is primarily absorbed in the **duodenum and jejunum**.

Question 520: Which of the following does not depend on GLUT4 for glucose uptake?

A. Brain (Correct Answer)
B. Skeletal muscles
C. Cardiac muscle
D. Adipose tissue

Explanation: **Explanation:** The core concept tested here is the distinction between **insulin-dependent** and **insulin-independent** glucose transport. **Why the Brain is the Correct Answer:** The brain is a vital organ that requires a continuous supply of glucose regardless of insulin levels. Glucose uptake in the brain (specifically across the blood-brain barrier and into neurons) is mediated primarily by **GLUT1** and **GLUT3**. These transporters are insulin-independent and have a low $K_m$ (high affinity), ensuring that the brain can sequester glucose even during fasting or hypoglycemic states. Therefore, the brain does not depend on GLUT4. **Why the Other Options are Incorrect:** * **Skeletal Muscle, Cardiac Muscle, and Adipose Tissue:** These tissues are the primary sites for **GLUT4** expression. GLUT4 is the only insulin-responsive glucose transporter. In the resting state, GLUT4 is sequestered in intracellular vesicles. Upon insulin signaling, these vesicles translocate to the plasma membrane to allow glucose entry. Consequently, these tissues are highly dependent on GLUT4 for post-prandial glucose disposal. **High-Yield NEET-PG Pearls:** * **GLUT4 Location:** Remember the mnemonic **"Muscle and Fat need 4"** (Skeletal, Cardiac, and Adipose). * **Exercise Exception:** In skeletal muscle, exercise/muscle contraction can trigger GLUT4 translocation to the membrane via an **AMPK-mediated pathway**, independent of insulin. This is why exercise helps manage blood sugar in Type 2 Diabetes. * **GLUT2:** Found in the Liver, Pancreas ($\beta$-cells), and Kidney. It has a high $K_m$ (low affinity) and acts as a glucose sensor. * **SGLT1/2:** These are active transporters (sodium-glucose co-transporters) found in the small intestine and renal tubules, unlike the GLUT family which facilitates passive diffusion.

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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