Carbohydrate Metabolism Practice Questions

Q: How is fructose transported from the intestine into enterocytes?

GLUT 5. ### Explanation **Correct Option: C (GLUT 5)** Fructose is unique among dietary monosaccharides because its absorption is independent of sodium. It is transported from the intestinal lumen into the enterocytes via **facilitated diffusion** using the **GLUT 5** transporter. Unlike glucose and galactose, which use the SGLT-1 (Sodium-Glucose Co-transporter 1) for active transport, fructose does not require ATP. Once inside the enterocyte, fructose (along with glucose and galactose) exits into the portal circulation via the **GLUT 2** transporter located on the basolateral membrane. **Why Incorrect Options are Wrong:** * **GLUT 1:** This is a high-affinity glucose transporter found primarily in **erythrocytes (RBCs)** and the **blood-brain barrier**. It provides a basal level of glucose uptake. * **GLUT 4:** This is the only **insulin-dependent** glucose transporter. It is found in **skeletal muscle** and **adipose tissue**. It is sequestered in intracellular vesicles and moves to the cell surface only in the presence of insulin. * **GLUT 7:** This transporter is located on the **endoplasmic reticulum membrane** of hepatocytes. It transports free glucose (produced by glucose-6-phosphatase) into the cytosol before it is released into the blood. **High-Yield Clinical Pearls for NEET-PG:** * **SGLT-1 vs. GLUT 5:** Remember that SGLT-1 is for Glucose/Galactose (Active), while GLUT 5 is specific for **Fructose** (Passive/Facilitated). * **GLUT 2:** Known as the "bidirectional" or "high-capacity, low-affinity" transporter. It is found in the **Liver, Pancreas (beta cells), Kidney, and Small Intestine**. * **Fructose Malabsorption:** A deficiency or downregulation of GLUT 5 can lead to fructose malabsorption, resulting in osmotic diarrhea and bloating.

Q: In an embryo with a complete deficiency of pyruvate kinase, how many net moles of ATP are generated in the conversion of 1 mole of glucose through the glycolytic pathway?

0. ### Explanation **1. Why the Correct Answer (A) is Right:** In the normal glycolytic pathway, there is an initial **investment phase** where 2 ATPs are consumed (by Hexokinase and Phosphofructokinase-1). This is followed by a **payoff phase** where 4 ATPs are generated: * 2 ATPs at the **Phosphoglycerate Kinase** step. * 2 ATPs at the **Pyruvate Kinase** step. **Pyruvate Kinase (PK)** catalyzes the final irreversible step of glycolysis: the conversion of Phosphoenolpyruvate (PEP) to Pyruvate. In a **complete deficiency** of PK, the second payoff step is blocked. Consequently, the cell only generates the 2 ATPs from the Phosphoglycerate Kinase step. * **Net ATP Calculation:** (2 ATP generated) - (2 ATP invested) = **0 Net ATP.** **2. Why the Incorrect Options are Wrong:** * **Option B (1 ATP):** This does not correspond to any standard stage of glycolysis. * **Option C (2 ATP):** This is the net yield of normal anaerobic glycolysis in a healthy cell (4 generated - 2 invested). * **Option D (3 ATP):** This is the net yield of glycolysis starting from **Glycogen** (1 ATP saved as the Hexokinase step is bypassed), but only if PK is functional. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **RBC Vulnerability:** Mature RBCs lack mitochondria and depend entirely on glycolysis for energy. PK deficiency is the **second most common** cause of enzyme-deficient hemolytic anemia (after G6PD deficiency). * **Mechanism of Anemia:** Without ATP, the Na+/K+ ATPase pump fails, leading to loss of ion balance, cell dehydration (echinocytes), and premature destruction in the spleen. * **Biochemical Marker:** PK deficiency leads to an accumulation of upstream metabolites, most notably **2,3-Bisphosphoglycerate (2,3-BPG)**. This causes a **right shift** in the Oxygen Dissociation Curve, helping oxygen delivery to tissues despite the anemia. * **Inheritance:** Autosomal Recessive.

Q: Where are the maximum number of enzymes of the Krebs cycle found?

Mitochondrial matrix. ### Explanation The **Krebs cycle** (also known as the Citric Acid Cycle or TCA cycle) is the final common pathway for the oxidation of carbohydrates, lipids, and proteins. **1. Why the Mitochondrial Matrix is Correct:** The Krebs cycle occurs entirely within the **mitochondria** to ensure that the generated reducing equivalents (NADH and FADH₂) are in close proximity to the Electron Transport Chain (ETC). **Seven out of the eight enzymes** of the cycle—including Citrate Synthase, Isocitrate Dehydrogenase, and α-Ketoglutarate Dehydrogenase—are located in the **mitochondrial matrix** in a soluble form. **2. Analysis of Incorrect Options:** * **Intermembrane Space:** This area primarily serves as a reservoir for protons ($H^+$) pumped during the ETC to create the electrochemical gradient; it does not house metabolic cycle enzymes. * **Cytosol:** While glycolysis occurs here, the pyruvate produced must be transported into the mitochondria (via pyruvate dehydrogenase complex) to enter the Krebs cycle. * **Ribosome:** These are sites of protein synthesis (translation) and have no role in oxidative metabolism. **3. High-Yield Clinical Pearls for NEET-PG:** * **The Exception:** **Succinate Dehydrogenase** is the only enzyme of the Krebs cycle **not** found in the matrix; it is embedded in the **Inner Mitochondrial Membrane** (acting as Complex II of the ETC). * **Rate-Limiting Step:** **Isocitrate Dehydrogenase** is the key rate-limiting enzyme of the cycle. * **Energy Yield:** One turn of the Krebs cycle produces **10 ATPs** (3 NADH = 7.5, 1 FADH₂ = 1.5, 1 GTP = 1). * **Amphibolic Nature:** The cycle is both catabolic (breaking down acetyl-CoA) and anabolic (providing intermediates like Succinyl-CoA for heme synthesis).

Q: Which glucose transporter is primarily found in neurons?

GLUT-3. ### Explanation **Correct Option: C (GLUT-3)** Glucose transporters (GLUTs) are transmembrane proteins that facilitate the transport of glucose across cell membranes via facilitated diffusion. **GLUT-3** is known as the "neuronal glucose transporter." It is primarily expressed in the **neurons** of the brain. It possesses a **very low Km** (high affinity) for glucose, ensuring that neurons—which have a high metabolic demand and limited internal energy stores—can prioritize glucose uptake even when blood glucose levels are significantly low. **Analysis of Incorrect Options:** * **GLUT-1:** Found primarily in **Red Blood Cells (RBCs)** and the **Blood-Brain Barrier (BBB)**. While it brings glucose into the brain tissue, GLUT-3 is the specific transporter that moves it into the neurons themselves. * **GLUT-2:** A high-capacity, high-Km (low affinity) transporter found in the **Liver, Pancreatic beta cells, and Kidney**. It acts as a glucose sensor in the pancreas. * **GLUT-4:** The only **insulin-dependent** glucose transporter. It is primarily located in **Skeletal muscle and Adipose tissue**. **High-Yield Clinical Pearls for NEET-PG:** * **Brain Glucose Supply:** Glucose enters the brain via GLUT-1 (BBB) and enters neurons via GLUT-3. * **Insulin Independence:** The brain (GLUT-1/3), RBCs (GLUT-1), and Liver (GLUT-2) do not require insulin for glucose uptake. * **SGLT vs. GLUT:** Remember that SGLT (Sodium-Glucose Linked Transporters) perform **active transport** (secondary), whereas GLUTs perform **passive transport** (facilitated diffusion). * **GLUT-5:** Specifically functions as a **fructose** transporter, primarily in the small intestine and spermatozoa.

Q: Decreased glucose concentration in hepatic cells triggers all of the following EXCEPT?

Increased fructose-2,6-biphosphate levels. **Explanation:** The regulation of glycolysis and gluconeogenesis in the liver is primarily controlled by the bifunctional enzyme **PFK-2/FBPase-2**. This enzyme dictates the levels of **Fructose-2,6-bisphosphate (F-2,6-BP)**, the most potent allosteric activator of glycolysis. **Why Option D is the Correct Answer:** When glucose levels decrease, the **Glucagon/Insulin ratio increases**. Glucagon triggers a cAMP-mediated signaling cascade that activates Protein Kinase A (PKA). PKA phosphorylates the bifunctional enzyme, leading to the **inhibition of PFK-2** and **activation of FBPase-2**. This results in the degradation of F-2,6-BP. Therefore, decreased glucose leads to **decreased** F-2,6-BP levels, making Option D the "Except" statement. **Analysis of Other Options:** * **Option A:** Low blood glucose directly stimulates alpha cells of the pancreas to secrete glucagon. * **Option B & C:** As described above, phosphorylation by PKA during hypoglycemia activates the FBPase-2 domain and inhibits the PFK-2 domain of the bifunctional enzyme to favor gluconeogenesis. **High-Yield Facts for NEET-PG:** * **F-2,6-BP** is the most potent stimulator of **Phosphofructokinase-1 (PFK-1)** and a potent inhibitor of **Fructose-1,6-bisphosphatase**. * **Fed State (High Insulin):** Dephosphorylated state → PFK-2 active → High F-2,6-BP → Glycolysis stimulated. * **Fasting State (High Glucagon):** Phosphorylated state → FBPase-2 active → Low F-2,6-BP → Gluconeogenesis stimulated. * **Mnemonic:** **P**hosphorylation by **P**KA makes the enzyme act as a **P**hosphatase (FBPase-2 active).

Q: Which of the following is a reversible enzyme?

Lactate dehydrogenase. **Explanation:** In metabolic pathways, enzymes are classified as either **reversible** (catalyzing reactions in both directions depending on substrate concentration) or **irreversible** (acting as metabolic "checkpoints" or rate-limiting steps). **Correct Option: C. Lactate Dehydrogenase (LDH)** Lactate dehydrogenase catalyzes the interconversion of **Pyruvate to Lactate** (and vice versa) with the coupled interconversion of NADH and NAD+. This reaction is a classic example of a reversible reaction in anaerobic glycolysis and the Cori cycle. The direction depends on the NAD+/NADH ratio and the tissue type (e.g., LDH-1 in the heart favors pyruvate formation, while LDH-5 in the muscle favors lactate). **Incorrect Options:** * **A. Pyruvate Kinase:** This is the final irreversible step of glycolysis, converting Phosphoenolpyruvate (PEP) to Pyruvate. It is a key regulatory point. * **B. Pyruvate Dehydrogenase (PDH):** This multienzyme complex converts Pyruvate to Acetyl-CoA. This reaction is strictly irreversible in humans, preventing the net synthesis of glucose from acetyl-CoA (fatty acids). * **D. Hexokinase:** This is the first irreversible "priming" step of glycolysis, trapping glucose inside the cell by phosphorylating it to Glucose-6-Phosphate. **NEET-PG High-Yield Pearls:** 1. **Irreversible Steps of Glycolysis:** Remember the "Big Three"—**Hexokinase/Glucokinase, Phosphofructokinase-1 (PFK-1), and Pyruvate Kinase.** These must be bypassed by different enzymes during Gluconeogenesis. 2. **Clinical Correlation:** LDH is a tetramer with five isoenzymes. An elevation in **LDH-1 > LDH-2** (flipped pattern) is a classic (though older) marker for Myocardial Infarction. 3. **Metabolic Logic:** Most "Dehydrogenases" in the TCA cycle are irreversible, but LDH and Malate Dehydrogenase are notable reversible exceptions.

Q: G6PD helps in maintaining the integrity of RBC by:

Controlling oxidative stress on RBC. **Explanation:** **Glucose-6-Phosphate Dehydrogenase (G6PD)** is the rate-limiting enzyme of the **Hexose Monophosphate (HMP) Shunt**. Its primary function in Red Blood Cells (RBCs) is the production of **NADPH**. 1. **Why Option A is Correct:** RBCs are constantly exposed to Reactive Oxygen Species (ROS) like hydrogen peroxide ($H_2O_2$). To neutralize these, the cell uses **Reduced Glutathione**. During this process, glutathione becomes oxidized. To regenerate reduced glutathione, the enzyme **Glutathione Reductase** requires **NADPH** (produced by G6PD) as a cofactor. Without G6PD, NADPH levels drop, oxidized glutathione accumulates, and oxidative stress causes hemoglobin to denature, forming **Heinz bodies** and leading to hemolysis. 2. **Why Other Options are Incorrect:** * **Option B:** "Reduction stress" is not a physiological challenge for RBCs; the threat is always oxidative damage from free radicals. * **Option C:** While G6PD deficiency eventually leads to membrane damage (via Heinz body removal by splenic macrophages), membrane flexibility is primarily maintained by cytoskeletal proteins like **Spectrin and Ankyrin** (defective in Hereditary Spherocytosis). * **Option D:** The Electron Transport Chain (ETC) is located in the mitochondria. Mature RBCs lack mitochondria and rely solely on glycolysis for energy. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** G6PD deficiency is an **X-linked Recessive** disorder. * **Triggers:** Hemolysis is triggered by **Fava beans**, infections, or drugs (e.g., **Primaquine**, Sulfa drugs, Nitrofurantoin). * **Morphology:** Look for **Heinz Bodies** (denatured Hb) and **Bite Cells** (deformed RBCs after splenic macrophages "bite" out the Heinz bodies). * **Protection:** G6PD deficiency offers a selective advantage against **Falciparum malaria**.

Q: A hypotonic baby shows an increased ratio of Pyruvate to Acetyl CoA. The baby also exhibits features of lactic acidosis. The underlying defect prevents pyruvate from forming Acetyl CoA in fibroblasts. Which of the following can revert this situation?

Thiamin. ### Explanation **Correct Option: D (Thiamin)** The clinical presentation of hypotonia, lactic acidosis, and a high Pyruvate/Acetyl CoA ratio indicates a defect in the **Pyruvate Dehydrogenase (PDH) Complex**. This multienzyme complex is responsible for the oxidative decarboxylation of pyruvate into Acetyl CoA, bridging glycolysis and the TCA cycle. The PDH complex requires five essential cofactors: **T**hiamine pyrophosphate (TPP/B1), **R**iboflavin (FAD/B2), **N**iacin (NAD/B3), **P**antothenic acid (CoA/B5), and **L**ipoic acid (Mnemonic: **T**ender **R**oving **N**ights **P**lease **L**uck). In many cases of PDH deficiency, the E1 subunit (pyruvate decarboxylase) has a reduced affinity for its cofactor, **Thiamin (TPP)**. Administering high doses of Thiamin can stabilize the enzyme, increase its catalytic activity, and effectively lower lactate levels by diverting pyruvate toward Acetyl CoA formation. **Analysis of Incorrect Options:** * **A. Biotin:** A cofactor for carboxylases (e.g., Pyruvate Carboxylase). Deficiency would impair gluconeogenesis, not the conversion of pyruvate to Acetyl CoA. * **B. Pyridoxine (B6):** Primarily involved in transamination (ALT/AST) and heme synthesis. It does not play a role in the PDH complex. * **C. Free fatty acids:** These are metabolized into Acetyl CoA via beta-oxidation. While they provide an alternative fuel source, they do not fix the enzymatic defect or reduce the accumulation of pyruvate/lactate. **Clinical Pearls for NEET-PG:** * **PDH Deficiency:** The most common cause of congenital lactic acidosis. It is often an **X-linked dominant** inheritance (E1-alpha subunit mutation). * **Dietary Management:** Patients are often placed on a **Ketogenic Diet** (high fat, low carb) to provide energy via ketones/Acetyl CoA, bypassing the PDH block. * **Leucine and Lysine:** These are purely ketogenic amino acids and are preferred in PDH deficiency as they do not contribute to pyruvate formation.

Question 1

How is fructose transported from the intestine into enterocytes?

Accepted Answer

GLUT 5

Answer

GLUT 1

Answer

GLUT 4

Answer

GLUT 7

Question 2

In an embryo with a complete deficiency of pyruvate kinase, how many net moles of ATP are generated in the conversion of 1 mole of glucose through the glycolytic pathway?

Accepted Answer

0

Answer

1

Answer

2

Answer

3

Question 3

A 12-year-old boy rapidly develops hypoglycemia after moderate activity. On physical examination, his kidneys and liver are found to be enlarged. Histopathology of the liver shows deposits of glycogen in excess. Blood examination reveals raised ketone bodies, lactic acid, and triglycerides. What is the diagnosis?

Accepted Answer

Von Gierke's disease

Answer

Pompe's disease

Answer

McArdle's disease

Answer

Cori's disease

Question 4

Where are the maximum number of enzymes of the Krebs cycle found?

Accepted Answer

Mitochondrial matrix

Answer

Intermembrane space

Answer

Cytosol

Answer

Ribosome

Question 5

Which glucose transporter is primarily found in neurons?

Accepted Answer

GLUT-3

Answer

GLUT-1

Answer

GLUT-2

Answer

GLUT-4

Question 6

Decreased glucose concentration in hepatic cells triggers all of the following EXCEPT?

Accepted Answer

Increased fructose-2,6-biphosphate levels

Answer

Increased glucagon levels in blood

Answer

Activation of fructose-2,6-biphosphatase

Answer

Inhibition of phosphofructokinase-2

Question 7

All of the following are true about fructose-1,6-bisphosphatase, EXCEPT?

Accepted Answer

Fructose-2,6-bisphosphate is an allosteric activator of this enzyme

Answer

Key gluconeogenic enzyme

Answer

Catalyses a hydrolysis reaction

Answer

Requires magnesium for catalysis

Question 8

Which of the following is a reversible enzyme?

Accepted Answer

Lactate dehydrogenase

Answer

Pyruvate kinase

Answer

Pyruvate dehydrogenase

Answer

Hexokinase

Question 9

G6PD helps in maintaining the integrity of RBC by:

Accepted Answer

Controlling oxidative stress on RBC

Answer

Controlling reduction stress on RBC

Answer

Maintaining flexibility of cell membrane

Answer

Component of electron transport chain

Question 10

A hypotonic baby shows an increased ratio of Pyruvate to Acetyl CoA. The baby also exhibits features of lactic acidosis. The underlying defect prevents pyruvate from forming Acetyl CoA in fibroblasts. Which of the following can revert this situation?

Accepted Answer

Thiamin

Answer

Biotin

Answer

Pyridoxine

Answer

Free fatty acid

Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism — MCQs

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