Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism Indian Medical PG Practice Questions and MCQs

Question 111: Which of the following is the major proteoglycan of synovial fluid?

A. Chondroitin sulfate
B. Dermatan sulfate
C. Heparan sulfate
D. Hyaluronic acid (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Hyaluronic Acid** **Medical Concept:** Hyaluronic acid (Hyaluronan) is a unique **Glycosaminoglycan (GAG)** that serves as the primary lubricant and shock absorber in synovial fluid. Unlike other GAGs, hyaluronic acid is **not sulfated** and is not covalently attached to a protein core in its basic form (though it forms the backbone for proteoglycan aggregates like aggrecan). Its high molecular weight and ability to bind large amounts of water create the high viscosity necessary for frictionless joint movement. **Analysis of Incorrect Options:** * **A. Chondroitin Sulfate:** This is the most abundant GAG in the body, primarily found in **cartilage** and bone. While present in the joint complex, it is a structural component of the cartilage matrix rather than the primary lubricant of the fluid. * **B. Dermatan Sulfate:** Found predominantly in the **skin**, blood vessels, and heart valves. It plays a role in coagulation and wound repair but is not a major constituent of synovial fluid. * **C. Heparan Sulfate:** Located on **cell surfaces** and in basement membranes (e.g., the glomerular basement membrane). It acts as a receptors and participates in cell-cell interactions. **High-Yield Clinical Pearls for NEET-PG:** * **Unique Feature:** Hyaluronic acid is the only GAG that is **not sulfated** and is synthesized at the plasma membrane rather than the Golgi apparatus. * **Link Protein:** In cartilage, hyaluronic acid non-covalently binds to multiple **Aggrecan** molecules via "link proteins" to form massive proteoglycan aggregates. * **Clinical Application:** Intra-articular injections of hyaluronic acid (Viscosupplementation) are used to manage pain in **Osteoarthritis**. * **Bacterial Virulence:** Some bacteria (e.g., *Staph. aureus*) produce **Hyaluronidase**, an enzyme that degrades hyaluronic acid, allowing the pathogen to spread through connective tissues (spreading factor).

Question 112: The binding of epinephrine or glucagon to the corresponding membrane receptor has which of the following effects on glycogen metabolism?

A. The net synthesis of glycogen is increased.
B. Glycogen phosphorylase is activated, while glycogen synthase is inactivated. (Correct Answer)
C. Glycogen phosphorylase is inactivated, while glycogen synthase is activated.
D. Both glycogen synthase and phosphorylase are activated.

Explanation: **Explanation:** The binding of **epinephrine** (in muscle/liver) or **glucagon** (in liver) to G-protein coupled receptors (GPCR) triggers a phosphorylation cascade that prioritizes glucose mobilization over storage. **Mechanism:** 1. **Signal Transduction:** Binding activates Adenylyl Cyclase, increasing intracellular **cAMP**. 2. **Kinase Activation:** cAMP activates **Protein Kinase A (PKA)**. 3. **Reciprocal Regulation:** PKA phosphorylates two key enzymes: * **Glycogen Phosphorylase Kinase:** Once phosphorylated, it activates **Glycogen Phosphorylase**, leading to increased glycogenolysis (breakdown). * **Glycogen Synthase:** Once phosphorylated, it becomes **inactive**, halting glycogenesis (synthesis). Thus, the hormonal signal ensures that catabolism is "switched on" while anabolism is "switched off" simultaneously. **Analysis of Incorrect Options:** * **Option A:** Synthesis decreases because Glycogen Synthase is inhibited by phosphorylation. * **Option C:** This describes the effect of **Insulin**, which promotes dephosphorylation via Protein Phosphatase-1 (PP1), activating synthesis and inhibiting breakdown. * **Option D:** These enzymes are regulated reciprocally; activating both simultaneously would create a "futile cycle," wasting ATP. **High-Yield NEET-PG Pearls:** * **Second Messenger:** cAMP is the primary second messenger for glucagon and $\beta$-adrenergic receptors. * **State of Enzymes:** In glycogen metabolism, **phosphorylated = active** for the breakdown enzyme (Phosphorylase), but **phosphorylated = inactive** for the synthesis enzyme (Synthase). * **Calcium Link:** In muscles, $Ca^{2+}$ can activate Phosphorylase Kinase even without cAMP, linking muscle contraction directly to energy mobilization.

Question 113: Which of the following enzymes is involved in the catabolism of fructose to pyruvate in the liver?

A. Glucokinase
B. Phosphoglucomutase
C. Lactate dehydrogenase
D. Glyceraldehyde-3-phosphate Dehydrogenase (Correct Answer)

Explanation: ### Explanation The catabolism of fructose in the liver follows a specialized pathway known as **fructolysis**, which bypasses the major rate-limiting step of glycolysis (Phosphofructokinase-1). **Why Option D is Correct:** In the liver, fructose is first phosphorylated to Fructose-1-phosphate by **fructokinase**. It is then cleaved by **Aldolase B** into Dihydroxyacetone phosphate (DHAP) and **Glyceraldehyde**. Glyceraldehyde is subsequently phosphorylated to **Glyceraldehyde-3-phosphate (G3P)** by triokinase. From this point, the pathway merges with the standard glycolytic pathway. **Glyceraldehyde-3-phosphate Dehydrogenase (GAPDH)** is the enzyme that catalyzes the conversion of G3P to 1,3-bisphosphoglycerate, eventually leading to the formation of pyruvate. **Why Other Options are Incorrect:** * **A. Glucokinase:** This enzyme phosphorylates glucose to glucose-6-phosphate. While it can act on fructose, its affinity for fructose is extremely low; fructokinase is the primary enzyme for fructose metabolism in the liver. * **B. Phosphoglucomutase:** This enzyme is involved in glycogen metabolism (interconverting glucose-1-phosphate and glucose-6-phosphate), not fructose catabolism. * **C. Lactate dehydrogenase:** This enzyme catalyzes the reversible conversion of pyruvate to lactate under anaerobic conditions; it is not a step in the direct pathway from fructose to pyruvate. **High-Yield Clinical Pearls for NEET-PG:** * **Essential Fructosuria:** Due to **Fructokinase** deficiency. It is a benign, asymptomatic condition where fructose is excreted in the urine. * **Hereditary Fructose Intolerance (HFI):** Due to **Aldolase B** deficiency. It is severe, leading to the accumulation of Fructose-1-phosphate, which depletes intracellular ATP and inorganic phosphate, causing hypoglycemia and jaundice. * **Metabolic Speed:** Fructose is metabolized **faster** than glucose because it bypasses the PFK-1 rate-limiting step.

Question 114: Which enzyme is responsible for postprandial glucose utilization?

A. Hexokinase
B. Glucokinase (Correct Answer)
C. Fructokinase
D. All of the above

Explanation: **Explanation:** The correct answer is **Glucokinase (Hexokinase IV)**. The primary role of glucokinase is to facilitate the uptake and utilization of glucose by the liver and pancreas specifically during the **postprandial (fed) state** when blood glucose levels are high. **Why Glucokinase is the correct answer:** Glucokinase possesses unique kinetic properties that make it ideal for post-meal glucose sensing: 1. **High $K_m$ (Low affinity):** It only becomes active when blood glucose levels are elevated (e.g., after a meal), preventing the liver from consuming glucose during fasting. 2. **High $V_{max}$ (High capacity):** It can rapidly phosphorylate large amounts of glucose, allowing the liver to "clear" postprandial hyperglycemia and store it as glycogen. 3. **Lack of Product Inhibition:** Unlike hexokinase, it is not inhibited by glucose-6-phosphate, allowing continuous glucose uptake even when energy levels are high. **Analysis of Incorrect Options:** * **Hexokinase (Types I, II, III):** These are found in extrahepatic tissues. They have a **low $K_m$** (high affinity), meaning they work at maximum capacity even during fasting to ensure the brain and muscles get glucose first. They are inhibited by glucose-6-phosphate. * **Fructokinase:** This enzyme is specific to fructose metabolism (converting fructose to fructose-1-phosphate) and does not play a direct role in systemic glucose utilization. **NEET-PG High-Yield Pearls:** * **Localization:** Glucokinase is found in the **Liver** and **Pancreatic $\beta$-cells**. * **Glucose Sensor:** In the pancreas, glucokinase acts as the "glucose sensor" that triggers insulin release. * **Clinical Correlation:** Mutations in the glucokinase gene lead to **MODY type 2** (Maturity-Onset Diabetes of the Young), characterized by mild, chronic hyperglycemia. * **Inducibility:** Glucokinase synthesis is **induced by Insulin**, further enhancing its role in the fed state.

Question 115: Which GLUT receptor is primarily found on the pancreas?

A. GLUT 1
B. GLUT 2 (Correct Answer)
C. GLUT 4
D. GLUT 5

Explanation: **Explanation:** **GLUT 2** is the correct answer because it serves as the primary glucose sensor for the body. It is a high-capacity, low-affinity (high $K_m$) bidirectional transporter. In the **pancreatic beta cells**, GLUT 2 allows glucose entry proportional to blood glucose levels. Once inside, glucose is metabolized to ATP, leading to the closure of ATP-sensitive $K^+$ channels, depolarization, and subsequent **insulin secretion**. This high $K_m$ ensures that insulin is released only when blood glucose levels are elevated. **Analysis of Incorrect Options:** * **GLUT 1:** Found in the **Blood-Brain Barrier (BBB)** and **RBCs**. It provides basal glucose uptake required for cellular respiration. * **GLUT 4:** The only **insulin-dependent** transporter. It is primarily located in **skeletal muscle and adipose tissue**. In the presence of insulin, GLUT 4 translocates from intracellular vesicles to the cell membrane. * **GLUT 5:** A specialized transporter primarily responsible for **fructose** absorption in the small intestine and spermatozoa. **High-Yield Clinical Pearls for NEET-PG:** * **Locations of GLUT 2:** Remember the mnemonic **"KLiP"** — **K**idney (PCT), **L**iver, **i**ntestine (basolateral side), and **P**ancreas. * **Fanconi-Bickel Syndrome:** A rare glycogen storage disease caused by a congenital defect in the **GLUT 2** transporter. * **SGLT vs. GLUT:** SGLT (1 & 2) are active transporters (secondary active) used for glucose absorption against a gradient, whereas GLUTs are passive transporters (facilitated diffusion).

Question 116: For glucose estimation in blood, what is the appropriate mode of transport from a primary health center to a laboratory?

A. Sodium fluoride (Correct Answer)
B. EDTA
C. Citrate
D. 0.9% saline

Explanation: **Explanation:** The estimation of blood glucose requires the prevention of **in vitro glycolysis**. Even after blood is drawn, RBCs and WBCs continue to consume glucose at a rate of approximately 5–7% per hour. **Why Sodium Fluoride (NaF) is the correct choice:** Sodium fluoride acts as a **glycolytic inhibitor**. It works by inhibiting the enzyme **Enolase** in the glycolytic pathway (specifically by forming a complex with magnesium and phosphate, depriving the enzyme of its cofactor). This "locks" the glucose level at the time of collection, making it the ideal preservative for transport. It is typically used in a **Grey-top vacutainer**, often combined with Potassium Oxalate (an anticoagulant). **Why the other options are incorrect:** * **EDTA (Ethylenediaminetetraacetic acid):** Primarily used for Hematology (CBC) as it chelates calcium. It does not inhibit glycolysis; thus, glucose levels will falsely decrease during transport. * **Citrate:** Used for coagulation studies (PT/APTT) and ESR. Like EDTA, it has no effect on the glycolytic enzymes. * **0.9% Saline:** This is an isotonic crystalloid used for fluid resuscitation or as a diluent. It has no preservative properties for glucose. **High-Yield NEET-PG Pearls:** 1. **Enzyme Inhibition:** NaF inhibits **Enolase**. 2. **The "1-hour" Rule:** If blood is not collected in NaF, plasma must be separated from cells within 1 hour to prevent significant glucose drop. 3. **Grey Top Tube:** Contains NaF (antiglycolytic) and Potassium Oxalate (anticoagulant). 4. **Clinical Caveat:** NaF inhibition of enolase is delayed for the first 1–2 hours; therefore, some initial glycolysis still occurs.

Question 117: Which form of carbohydrate is present in proteoglycans?

A. Monosaccharide
B. Disaccharide
C. Oligosaccharide
D. Polysaccharide (Correct Answer)

Explanation: **Explanation:** **1. Why Polysaccharide is Correct:** Proteoglycans are complex macromolecules consisting of a core protein covalently attached to one or more **glycosaminoglycan (GAG)** chains. GAGs are long, unbranched **polysaccharides** composed of repeating disaccharide units (usually an amino sugar and a uronic acid). Because these GAG chains consist of hundreds of sugar units, they are classified as polysaccharides. Their high negative charge (due to sulfate and carboxyl groups) allows them to attract water, providing the "cushioning" effect essential for the extracellular matrix and cartilage. **2. Why Other Options are Incorrect:** * **Monosaccharide (A):** These are single sugar units (e.g., glucose). While they are the building blocks of GAGs, the functional carbohydrate unit in a proteoglycan is the long chain, not the individual monomer. * **Disaccharide (B):** GAGs are made of *repeating* disaccharide units, but the final structure is a long-chain polymer. A single disaccharide does not constitute a proteoglycan. * **Oligosaccharide (C):** These are short chains (typically 3–10 units). Oligosaccharides are the carbohydrate component of **Glycoproteins**, not Proteoglycans. This is a common point of confusion in exams. **3. NEET-PG High-Yield Clinical Pearls:** * **Proteoglycan vs. Glycoprotein:** In Proteoglycans, the carbohydrate content is dominant (up to 95%), whereas, in Glycoproteins, the protein content is dominant. * **Hyaluronic Acid:** The only GAG that is **not sulfated** and not covalently attached to a protein core. * **Mucopolysaccharidoses (MPS):** These are lysosomal storage disorders (e.g., Hurler and Hunter syndromes) caused by the deficiency of enzymes required to degrade these GAG polysaccharides. * **Heparin:** A naturally occurring anticoagulant GAG found in mast cells.

Question 118: Enzyme deficient in Von-Gierke's disease is:

A. Phosphofructokinase
B. Glucocerebrocidase
C. Acid maltase
D. Glucose-6-phosphatase (Correct Answer)

Explanation: **Explanation:** **Von Gierke’s Disease (GSD Type I)** is the most common glycogen storage disease. It is caused by a deficiency of the enzyme **Glucose-6-phosphatase**, which is responsible for the final step in both glycogenolysis and gluconeogenesis: converting Glucose-6-phosphate into free glucose. This enzyme is primarily located in the liver and kidneys. Without it, the body cannot release glucose into the bloodstream, leading to severe fasting hypoglycemia and an accumulation of glycogen in the liver and kidneys (hepatorenal megaly). **Analysis of Incorrect Options:** * **A. Phosphofructokinase:** Deficiency of the muscle isoform leads to **Tarui’s disease (GSD Type VII)**, characterized by exercise intolerance and muscle cramps. * **B. Glucocerebrosidase:** This enzyme is deficient in **Gaucher’s disease**, which is a lysosomal storage disorder (sphingolipidosis), not a glycogen storage disease. * **C. Acid maltase (α-1,4-glucosidase):** Deficiency leads to **Pompe’s disease (GSD Type II)**, which primarily affects the heart and muscles, causing cardiomegaly. **High-Yield Clinical Pearls for NEET-PG:** * **Biochemical Triad:** Severe fasting hypoglycemia, Lactic acidosis (due to shunting of G6P to glycolysis), Hyperuricemia (leading to gout), and Hyperlipidemia (doll-like facies). * **Diagnosis:** Characterized by a lack of increase in blood glucose following administration of glucagon or epinephrine. * **Management:** Frequent feedings with uncooked cornstarch to maintain glucose levels and prevent nocturnal hypoglycemia.

Question 119: What is true regarding galactosemia?

A. Mental retardation occurs
B. Defect in epimerase
C. Defect in galactose 1-phosphate uridyltransferase
D. All the above (Correct Answer)

Explanation: **Explanation:** Galactosemia is an autosomal recessive disorder of galactose metabolism. The "Classic Galactosemia" (Type 1) is the most common and severe form, caused by a deficiency of the enzyme **Galactose 1-phosphate uridyltransferase (GALT)**. **Why "All the above" is correct:** 1. **Defect in GALT (Option C):** This is the hallmark of Classic Galactosemia. The deficiency leads to the accumulation of Galactose 1-phosphate and galactitol in tissues like the liver, brain, and kidneys. 2. **Mental Retardation (Option A):** The accumulation of toxic metabolites (specifically Galactose 1-phosphate) in the central nervous system leads to intellectual disability and developmental delays if not managed early with a lactose-free diet. 3. **Defect in Epimerase (Option B):** While GALT deficiency is most common, **UDP-galactose-4-epimerase deficiency** (Type 3) is a recognized form of galactosemia. Since the question asks what is true regarding "galactosemia" (the broad clinical entity), defects in any of the three enzymes in the Leloir pathway (Galactokinase, GALT, or Epimerase) are technically correct. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad:** Hepatomegaly (Cirrhosis), Cataracts (due to accumulation of **Dulcitol/Galactitol** in the lens), and Intellectual Disability. * **Early Sign:** Infantile jaundice and vomiting shortly after starting milk feeds. * **Infection Risk:** Increased susceptibility to **E. coli sepsis** is a classic association. * **Diagnosis:** Presence of non-glucose reducing sugars in urine (Benedict's test positive, Dipstick negative). * **Treatment:** Immediate lifelong exclusion of lactose and galactose from the diet.

Question 120: Why should individuals with hyperlipidemia and/or gout minimize their intake of sucrose and high fructose syrups?

A. Fructose is initially phosphorylated by liver fructokinase. (Correct Answer)
B. After initial modification, fructose is cleaved by a specific enolase.
C. Fructose is converted to UDP-fructose.
D. Fructose is ultimately converted to galactose.

Explanation: **Explanation:** The metabolic handling of fructose in the liver is the key to understanding its link to hyperlipidemia and gout. Unlike glucose, fructose metabolism bypasses the major rate-limiting step of glycolysis (phosphofructokinase-1). **1. Why Option A is Correct:** Fructose is rapidly phosphorylated by **fructokinase** (ketohexokinase) to Fructose-1-Phosphate (F1P). This reaction is extremely fast and unregulated. * **Hyperlipidemia:** The rapid influx of fructose leads to an overproduction of pyruvate and acetyl-CoA, which serves as a substrate for *de novo* lipogenesis, increasing VLDL and triglyceride levels. * **Gout:** The rapid phosphorylation by fructokinase causes **ATP depletion** and an accumulation of inorganic phosphate. This triggers the purine degradation pathway, leading to increased production of **uric acid**, which exacerbates gout. **2. Why Other Options are Incorrect:** * **Option B:** Fructose-1-Phosphate is cleaved by **Aldolase B** (not enolase) into dihydroxyacetone phosphate (DHAP) and glyceraldehyde. * **Option C:** Fructose is not converted to UDP-fructose; UDP-sugars (like UDP-glucose/galactose) are primarily involved in glycogen synthesis and galactose metabolism. * **Option D:** Fructose is converted into glycolytic intermediates (DHAP/Glyceraldehyde-3-P), not galactose. **Clinical Pearls for NEET-PG:** * **Essential Fructosuria:** Deficiency of Fructokinase (asymptomatic, fructose in urine). * **Hereditary Fructose Intolerance (HFI):** Deficiency of **Aldolase B**. It causes severe hypoglycemia and liver damage because F1P traps intracellular phosphate. * **High-Yield Fact:** Fructose is the only sugar that can bypass the PFK-1 "bottleneck," making it highly lipogenic.

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

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Diabetes Mellitus: Biochemical Aspects

Practice Questions

Glycosylation and Glycoproteins

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Lactose Intolerance and Galactosemia

Practice Questions

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