Carbohydrate Metabolism Practice Questions

Q: Which of the following is the major proteoglycan of synovial fluid?

Hyaluronic acid. ### 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).

Q: Which enzyme is responsible for postprandial glucose utilization?

Glucokinase. **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.

Q: Which GLUT receptor is primarily found on the pancreas?

GLUT 2. **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).

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

Sodium fluoride. **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.

Q: Which form of carbohydrate is present in proteoglycans?

Polysaccharide. **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.

Q: Enzyme deficient in Von-Gierke's disease is:

Glucose-6-phosphatase. **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.

Q: What is true regarding galactosemia?

All the above. **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.

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

Fructose is initially phosphorylated by liver fructokinase.. **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.

Question 1

Which of the following is the major proteoglycan of synovial fluid?

Accepted Answer

Hyaluronic acid

Answer

Chondroitin sulfate

Answer

Dermatan sulfate

Answer

Heparan sulfate

Question 2

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

Accepted Answer

Glycogen phosphorylase is activated, while glycogen synthase is inactivated.

Answer

The net synthesis of glycogen is increased.

Answer

Glycogen phosphorylase is inactivated, while glycogen synthase is activated.

Answer

Both glycogen synthase and phosphorylase are activated.

Question 3

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

Accepted Answer

Glyceraldehyde-3-phosphate Dehydrogenase

Answer

Glucokinase

Answer

Phosphoglucomutase

Answer

Lactate dehydrogenase

Question 4

Which enzyme is responsible for postprandial glucose utilization?

Accepted Answer

Glucokinase

Answer

Hexokinase

Answer

Fructokinase

Answer

All of the above

Question 5

Which GLUT receptor is primarily found on the pancreas?

Accepted Answer

GLUT 2

Answer

GLUT 1

Answer

GLUT 4

Answer

GLUT 5

Question 6

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

Accepted Answer

Sodium fluoride

Answer

EDTA

Answer

Citrate

Answer

0.9% saline

Question 7

Which form of carbohydrate is present in proteoglycans?

Accepted Answer

Polysaccharide

Answer

Monosaccharide

Answer

Disaccharide

Answer

Oligosaccharide

Question 8

Enzyme deficient in Von-Gierke's disease is:

Accepted Answer

Glucose-6-phosphatase

Answer

Phosphofructokinase

Answer

Glucocerebrocidase

Answer

Acid maltase

Question 9

What is true regarding galactosemia?

Accepted Answer

All the above

Answer

Mental retardation occurs

Answer

Defect in epimerase

Answer

Defect in galactose 1-phosphate uridyltransferase

Question 10

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

Accepted Answer

Fructose is initially phosphorylated by liver fructokinase.

Answer

After initial modification, fructose is cleaved by a specific enolase.

Answer

Fructose is converted to UDP-fructose.

Answer

Fructose is ultimately converted to galactose.

Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism — MCQs

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