Carbohydrate Metabolism Practice Questions

Q: What is the source of ATP in red blood cells?

Anaerobic glycolysis. ### Explanation **Correct Answer: C. Anaerobic glycolysis** **1. Why Anaerobic Glycolysis is Correct:** Mature red blood cells (RBCs) lack **mitochondria**, which are the "powerhouses" required for aerobic respiration (TCA cycle and Electron Transport Chain). Consequently, RBCs cannot utilize oxygen for energy production, despite being the primary carriers of oxygen. They rely exclusively on **anaerobic glycolysis** (the Embden-Meyerhof pathway) in the cytosol to convert glucose into lactate, generating a net gain of **2 ATP** molecules per glucose molecule. This ATP is vital for maintaining ion gradients (Na⁺/K⁺ ATPase pump) and erythrocyte membrane integrity. **2. Why Other Options are Incorrect:** * **A. Beta-oxidation of fatty acids:** This process occurs within the mitochondrial matrix. Since RBCs lack mitochondria, they cannot oxidize fatty acids for energy. * **B. TCA cycle:** The enzymes for the Tricarboxylic Acid (TCA) cycle are located in the mitochondria. Without these organelles, RBCs cannot perform aerobic metabolism. * **D. Gluconeogenesis:** This is the synthesis of glucose from non-carbohydrate precursors (primarily occurring in the liver and kidneys). RBCs are consumers of glucose, not producers. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Rapoport-Luebering Shunt:** A side pathway of glycolysis in RBCs that produces **2,3-BPG**. This molecule is crucial as it decreases the affinity of hemoglobin for oxygen, facilitating oxygen delivery to tissues. * **Lactate Production:** The end product of glycolysis in RBCs is always lactate, which is released into the blood and taken up by the liver for gluconeogenesis (**Cori Cycle**). * **G6PD Deficiency:** The HMP shunt (Pentose Phosphate Pathway) is also vital in RBCs to produce **NADPH**, which maintains reduced glutathione to protect the cell against oxidative damage. Deficiency leads to hemolytic anemia.

Q: Which of the following represents the normal glucose tolerance curve?

Curve B. ***Curve B*** - Demonstrates the normal **glucose tolerance pattern** with fasting glucose around **80-90 mg/dL**, peak at **120-140 mg/dL** at 30-60 minutes, and return to near-fasting levels by **2 hours**. - Represents normal **insulin sensitivity** and **pancreatic beta-cell function** with appropriate glucose clearance from blood. *Curve A* - Shows a **diabetic pattern** with elevated fasting glucose and peak values exceeding **200 mg/dL** during oral glucose tolerance test. - Blood glucose remains **persistently elevated** at 2 hours (>200 mg/dL), indicating **impaired glucose tolerance** or diabetes mellitus. *Curve C* - Demonstrates an **abnormal flat curve** pattern, possibly indicating **renal glycosuria** or **alimentary hypoglycemia**. - May show **minimal glucose rise** despite oral glucose load, suggesting **malabsorption** or rapid glucose clearance without normal physiological response. *None of the above* - This option is incorrect as **Curve B** clearly represents the normal glucose tolerance curve pattern. - The **WHO/ADA criteria** for normal OGTT are well-established, making one of the given curves definitively correct.

Q: Which of the following is NOT a cause of fasting hypoglycemia?

Excess glucagon. **Explanation:** The core physiological mechanism of fasting hypoglycemia involves an inability to maintain blood glucose levels during periods of starvation, usually due to defects in glycogenolysis, gluconeogenesis, or hormonal regulation [3]. **Why Option A is correct:** **Glucagon** is a counter-regulatory hormone produced by the alpha cells of the pancreas. Its primary function is to **increase** blood glucose levels by stimulating glycogenolysis and gluconeogenesis in the liver [1]. Therefore, an **excess of glucagon** (as seen in a Glucagonoma) would lead to **hyperglycemia**, not hypoglycemia. **Why the other options are incorrect:** * **B. Glucose-6-phosphatase deficiency (Von Gierke Disease):** This is Type I Glycogen Storage Disease (GSD). This enzyme is essential for the final step of both glycogenolysis and gluconeogenesis [2]. Its absence leads to severe fasting hypoglycemia because the liver cannot release free glucose into the blood. * **C. Uremia:** Chronic kidney disease/uremia causes hypoglycemia through multiple mechanisms, including reduced renal gluconeogenesis (the kidney contributes ~20% of glucose production), impaired insulin clearance, and malnutrition. * **D. Glycogen synthase deficiency:** Known as Type 0 GSD, this condition prevents the liver from storing glycogen [3]. Without glycogen stores to draw upon during a fast, patients develop ketotic hypoglycemia. **High-Yield NEET-PG Pearls:** * **Whipple’s Triad for Hypoglycemia:** 1. Symptoms of hypoglycemia, 2. Low plasma glucose (<55 mg/dL), 3. Relief of symptoms after glucose administration. * **Common causes of fasting hypoglycemia:** Insulinoma, exogenous insulin (factitious), adrenal insufficiency (Addison’s), and severe liver disease. * **Glucagonoma Clinical Triad:** Hyperglycemia (Diabetes), Necrolytic Migratory Erythema (NME), and weight loss.

Q: Which of the following glycosaminoglycans does not contain a sulfur-containing bond?

Hyaluronic acid. **Explanation:** **Hyaluronic acid** (Hyaluronan) is the correct answer because it is the only Glycosaminoglycan (GAG) that is **non-sulfated**. Unlike other GAGs, it is not synthesized in the Golgi apparatus by sulfotransferases; instead, it is synthesized by integral membrane proteins called hyaluronan synthases directly into the extracellular space. Additionally, it is the only GAG that is not covalently attached to a protein core (i.e., it does not form proteoglycans). **Analysis of Incorrect Options:** * **Chondroitin (Chondroitin Sulfate):** The most abundant GAG in the body, found in cartilage and bone. It is heavily sulfated at the carbon-4 or carbon-6 positions. * **Keratan (Keratan Sulfate):** Found in the cornea and loose connective tissue. It contains sulfate groups and is unique because its repeating disaccharide unit contains galactose instead of uronic acid. * **Dermatan (Dermatan Sulfate):** Found in skin, blood vessels, and heart valves. It is a sulfated GAG formed by the epimerization of glucuronic acid to iduronic acid. **High-Yield Clinical Pearls for NEET-PG:** * **Hyaluronic Acid:** Acts as a lubricant and shock absorber in synovial fluid and the vitreous humor. It plays a vital role in cell migration during embryogenesis and wound healing. * **Heparin:** The GAG with the **highest negative charge** and highest degree of sulfation; it acts as an intracellular anticoagulant. * **Mucopolysaccharidoses (MPS):** Genetic deficiencies in lysosomal enzymes that degrade sulfated GAGs (e.g., Hurler and Hunter syndromes). Note that Hyaluronic acid is typically not involved in these storage disorders. * **Unique Feature:** Hyaluronic acid is the largest GAG by molecular weight, often consisting of thousands of sugar residues.

Q: The hydrolysis of Glucose-6-phosphate is catalyzed by a specific phosphatase which is found only in which locations?

Liver, intestines, and kidneys. **Explanation:** The enzyme **Glucose-6-Phosphatase (G6Pase)** is the key regulatory enzyme of the final step in both **Gluconeogenesis** and **Glycogenolysis**. It catalyzes the conversion of Glucose-6-phosphate into free glucose. **1. Why Option A is Correct:** The primary physiological role of G6Pase is to maintain blood glucose levels during fasting. This requires the release of free glucose into the systemic circulation. Therefore, the enzyme is localized specifically in the **Liver, Kidneys, and Intestinal mucosa**. These are the only tissues capable of contributing to the blood glucose pool. The enzyme is located on the luminal surface of the **Endoplasmic Reticulum (ER)**. **2. Why Other Options are Incorrect:** * **Option C (Striated Muscle):** This is a high-yield distinction. Muscle lacks G6Pase; therefore, muscle glycogen cannot be used to maintain blood glucose. Instead, G6P enters glycolysis to provide ATP for contraction. * **Option B & D:** Brain, spleen, and plasma do not perform gluconeogenesis or significant glycogen storage for systemic use. They lack the gene expression for this specific phosphatase. **Clinical Pearls for NEET-PG:** * **Von Gierke’s Disease (GSD Type Ia):** Caused by a deficiency of Glucose-6-Phosphatase. It presents with severe fasting hypoglycemia, hepatomegaly, lactic acidosis, and hyperuricemia. * **Type Ib GSD:** Caused by a deficiency of the **G6P translocase** (the transporter that moves G6P into the ER). * **Metabolic Significance:** Because muscles lack G6Pase, they export lactate (via the Cori Cycle) or alanine (via the Glucose-Alanine Cycle) to the liver to be converted into glucose.

Q: Hypoglycemia is more severe in type 1 Glycogen storage disease as compared to type 6 Glycogen storage disease because:

No gluconeogenesis in type 1 disease. **Explanation:** The severity of hypoglycemia in Glycogen Storage Diseases (GSD) depends on whether the body can utilize alternative pathways to maintain blood glucose levels during fasting. **1. Why Option A is correct:** * **Type 1 GSD (von Gierke Disease)** is caused by a deficiency of **Glucose-6-Phosphatase**. This enzyme is the "final common gateway" for both **Glycogenolysis** (breakdown of glycogen) and **Gluconeogenesis** (synthesis of glucose from non-carbohydrate sources like lactate and amino acids). * Because this enzyme is missing, the liver cannot release free glucose into the blood from *either* pathway. This leads to profound, life-threatening fasting hypoglycemia. **2. Why other options are incorrect:** * **Option B:** **Type 6 GSD (Hers Disease)** is a deficiency of **Liver Glycogen Phosphorylase**. This enzyme is only involved in glycogenolysis. In Type 6, the gluconeogenesis pathway remains **intact** because Glucose-6-Phosphatase is functional. The liver can still produce glucose from lactate and alanine, making the hypoglycemia much milder. * **Option D:** Type 1a affects the liver, kidney, and intestinal mucosa. It does **not** affect muscles because muscles lack Glucose-6-Phosphatase even in healthy individuals (muscles do not contribute to blood glucose). **High-Yield Clinical Pearls for NEET-PG:** * **Biochemical Hallmarks of Type 1:** Hyperuricemia (Gout), Hyperlactatemia, Hyperlipidemia (doll-like facies), and Hepatomegaly. * **Lactate Paradox:** In Type 1, administration of glucagon increases lactate but not glucose. In Type 6, lactate levels remain relatively normal because gluconeogenesis consumes it. * **Type 1b:** Includes the same features as 1a plus **neutropenia** and recurrent infections due to a glucose-6-phosphate translocase deficiency.

Q: Which of the following events does not occur when the concentration of glucose in the liver decreases?

Increased levels of Fructose 2, 6 - Bisphosphate. ### Explanation **Core Concept: The Glucagon-Mediated Response to Low Glucose** When blood glucose levels decrease, the pancreas releases **glucagon**. In the liver, glucagon triggers a cAMP-mediated phosphorylation cascade via Protein Kinase A (PKA). This cascade targets the bifunctional enzyme complex **PFK-2/FBPase-2**. Phosphorylation of this complex leads to the **inactivation of PFK-2** and the **activation of FBPase-2**. The active FBPase-2 then degrades **Fructose 2,6-bisphosphate (F2,6-BP)** into Fructose-6-phosphate. Since F2,6-BP is the most potent allosteric activator of glycolysis (PFK-1) and inhibitor of gluconeogenesis (FBPase-1), its **decrease** effectively halts glycolysis and promotes gluconeogenesis to restore blood glucose. Therefore, **increased levels of F2,6-BP (Option C) do not occur**; rather, levels significantly drop. **Analysis of Other Options:** * **Option A (Inactivation of PFK-2):** This occurs because phosphorylation by PKA inhibits the kinase domain of the bifunctional enzyme. * **Option B (Activation of FBPase-2):** This occurs because phosphorylation by PKA activates the phosphatase domain of the bifunctional enzyme. * **Option D (Increased Glucagon):** This is the primary hormonal trigger released by alpha cells of the pancreas in response to hypoglycemia. **High-Yield Clinical Pearls for NEET-PG:** * **Fructose 2,6-bisphosphate** is a "signaling molecule," not a metabolic intermediate of the TCA cycle or glycolysis. * **Insulin vs. Glucagon:** Insulin dephosphorylates the bifunctional enzyme (activating PFK-2), increasing F2,6-BP and stimulating glycolysis. Glucagon phosphorylates it, decreasing F2,6-BP and stimulating gluconeogenesis. * **Mnemonic:** **P**hosphorylation by Glucagon makes the **P**hosphatase (FBPase-2) active.

Question 1

What is the source of ATP in red blood cells?

Accepted Answer

Anaerobic glycolysis

Answer

Beta oxidation of fatty acids

Answer

TCA cycle

Answer

Gluconeogenesis

Question 2

Which of the following represents the normal glucose tolerance curve?

Accepted Answer

Curve B

Answer

Curve A

Answer

Curve C

Answer

None of the above

Question 3

In the TCA cycle, which two carbon atoms leave in the form of CO2 are derived from:

Accepted Answer

Oxaloacetate

Answer

Acetyl CoA

Answer

CO2

Answer

Citrate

Question 4

Which of the following is NOT a cause of fasting hypoglycemia?

Accepted Answer

Excess glucagon

Answer

Glucose-6-phosphatase deficiency

Answer

Uremia

Answer

Glycogen synthase deficiency

Question 5

Which of the following glycosaminoglycans does not contain a sulfur-containing bond?

Accepted Answer

Hyaluronic acid

Answer

Chondroitin

Answer

Keratan

Answer

Dermatan

Question 6

Glycogenolysis is best described by which of the following statements?

Accepted Answer

It requires a bifunctional enzyme (debranching and transferase).

Answer

It involves enzymes cleaving beta(1-4) glycosidic linkages.

Answer

It requires activation of glycogen synthase.

Answer

It requires inactivation of phosphorylase kinase.

Question 7

Familial fructokinase deficiency causes no symptoms because:

Accepted Answer

Hexokinase can phosphorylate fructose

Answer

Liver aldolase can metabolize it

Answer

Excess fructose does not escape into the urine

Answer

Excess fructose is excreted through feces

Question 8

The hydrolysis of Glucose-6-phosphate is catalyzed by a specific phosphatase which is found only in which locations?

Accepted Answer

Liver, intestines, and kidneys

Answer

Brain, spleen, and adrenals

Answer

Striated muscle

Answer

Plasma

Question 9

Hypoglycemia is more severe in type 1 Glycogen storage disease as compared to type 6 Glycogen storage disease because:

Accepted Answer

No gluconeogenesis in type 1 disease

Answer

No gluconeogenesis in type 6 disease

Answer

Both

Answer

Type 1 disease affects muscles and liver both

Question 10

Which of the following events does not occur when the concentration of glucose in the liver decreases?

Accepted Answer

Increased levels of Fructose 2, 6 - Bisphosphate

Answer

Inactivation of phosphofructokinase-2 (PFK-2)

Answer

Activation of Fructose Bisphosphatase-2 (Fructose 2, 6 Bisphosphatase)

Answer

Increased levels of Glucagon

Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism — MCQs

On this page

Practice by Chapter

Want unlimited practice?