Carbohydrate Metabolism Practice Questions

Q: Regarding proteoglycans, which statement is false?

They hold a small amount of water.. **Explanation** Proteoglycans are complex macromolecules consisting of a core protein with one or more covalently attached **glycosaminoglycan (GAG)** chains. **Why Option B is the correct (false) statement:** Proteoglycans are highly hydrophilic. Due to the presence of sulfate and carboxyl groups, they carry a high density of negative charges. these charges repel each other and attract a large cloud of cations (like $Na^+$), which creates high osmotic pressure. Consequently, proteoglycans **hold a large amount of water**, forming a hydrated "gel" that provides structural support and shock absorption in tissues like cartilage and the vitreous humor. **Analysis of other options:** * **Option A:** Chondroitin sulfate is the most abundant GAG in the body and is a primary component of proteoglycans found in cartilage and bone. * **Option C:** They are composed of sugars (specifically repeating disaccharide units of GAGs) which make up about 95% of their weight. * **Option D:** They carry a strong **negative electrical charge** (polyanionic) due to the sulfate and uronic acid groups. **High-Yield NEET-PG Pearls:** * **Hyaluronic Acid:** The only GAG that is **not sulfated** and not covalently attached to a protein core (it exists as a free carbohydrate chain). * **Aggrecan:** The major proteoglycan in cartilage; it associates with hyaluronic acid to form massive aggregates. * **Clinical Correlation:** Deficiencies in enzymes that degrade GAGs lead to **Mucopolysaccharidoses** (e.g., Hurler and Hunter Syndromes), characterized by the accumulation of these molecules in lysosomes.

Q: What is the net generation of ATP up to pyruvate in aerobic glycolysis?

7. **Explanation:** In aerobic glycolysis, the net ATP yield is calculated by accounting for both direct substrate-level phosphorylation and the oxidative phosphorylation of reduced coenzymes. **The Calculation:** 1. **ATP Consumption:** 2 ATP are consumed in the preparatory phase (Hexokinase and Phosphofructokinase-1 reactions). 2. **ATP Production (Substrate-level):** 4 ATP are produced (2 from Phosphoglycerate kinase and 2 from Pyruvate kinase). 3. **NADH Production:** 2 NADH are generated at the Glyceraldehyde-3-phosphate dehydrogenase step. 4. **The Yield:** In aerobic conditions, these 2 NADH enter the electron transport chain via the **Malate-Aspartate shuttle**, yielding **2.5 ATP per NADH** (Total = 5 ATP). 5. **Net Total:** (4 Substrate ATP + 5 Oxidative ATP) – 2 Consumed ATP = **7 ATP**. *Note: If the Glycerol-3-phosphate shuttle is used (common in muscle/brain), the yield is 1.5 ATP per NADH, totaling 5 net ATP. However, 7 is the standard "high-yield" answer for aerobic glycolysis in most medical exams.* **Analysis of Incorrect Options:** * **Option A (2):** This is the net ATP yield for **anaerobic glycolysis**, where NADH is consumed to reduce pyruvate to lactate, leaving only substrate-level ATP. * **Option C (15):** This represents the ATP yield for one molecule of Acetyl-CoA entering the TCA cycle plus its associated oxidative phosphorylation. * **Option D (35):** This is closer to the total ATP yield for the complete oxidation of one glucose molecule to $CO_2$ and $H_2O$ (approx. 30–32 ATP). **Clinical Pearls for NEET-PG:** * **Rate-limiting step:** Phosphofructokinase-1 (PFK-1). * **Rapoport-Luebering Cycle:** In RBCs, glycolysis can bypass the phosphoglycerate kinase step to produce 2,3-BPG, resulting in **zero net ATP** production for that molecule of glucose. * **Arsenic Poisoning:** Inhibits ATP production in glycolysis by competing with inorganic phosphate at the GAPDH step.

Q: A child with increased conjugated bilirubin develops seizures and cataract. What is the probable diagnosis?

Galactosemia. **Explanation:** The clinical triad of **conjugated hyperbilirubinemia (jaundice), cataracts, and seizures** in an infant is a classic presentation of **Classic Galactosemia**, caused by a deficiency of the enzyme **Galactose-1-phosphate uridyltransferase (GALT)**. 1. **Why Galactosemia is correct:** * **Cataracts:** Excess galactose is diverted to the polyol pathway, where **aldose reductase** converts it into **galactitol**. Galactitol is osmotically active, causing water to enter the lens, leading to cataracts (often "oil-drop" appearance). * **Jaundice:** Accumulation of Galactose-1-phosphate is toxic to hepatocytes, leading to liver dysfunction and conjugated hyperbilirubinemia. * **Seizures:** These occur due to secondary **hypoglycemia**, as accumulated galactose-1-phosphate inhibits phosphoglucomutase, impairing glycogenolysis. 2. **Why other options are incorrect:** * **Tyrosinemia:** Presents with liver failure, renal tubular dysfunction (Fanconi syndrome), and a "cabbage-like" odor, but cataracts are not a feature. * **Fructosemia (Hereditary Fructose Intolerance):** Presents with jaundice and hypoglycemia after introducing fruit juice/sucrose, but **does not cause cataracts** because fructose is not converted to a polyol in the lens. * **Glycogen Storage Disorders (GSD):** Primarily present with hepatomegaly and severe hypoglycemia (e.g., Von Gierke’s), but do not typically present with cataracts. **NEET-PG High-Yield Pearls:** * **Screening Test:** Benedict’s test is positive for reducing sugars in urine (but glucose oxidase dipstick is negative). * **Increased Risk:** Patients are highly susceptible to **E. coli neonatal sepsis**. * **Management:** Immediate withdrawal of lactose/galactose from the diet (switch to soy milk). * **Galactokinase deficiency:** Causes cataracts only, without the systemic "sick baby" features (no jaundice or seizures).

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).

Question 1

Regarding proteoglycans, which statement is false?

Accepted Answer

They hold a small amount of water.

Answer

Chondroitin sulfate is a component of proteoglycans.

Answer

They are composed of sugars.

Answer

They carry an electrical charge.

Question 2

What is the net generation of ATP up to pyruvate in aerobic glycolysis?

Accepted Answer

7

Answer

2

Answer

15

Answer

35

Question 3

A child with increased conjugated bilirubin develops seizures and cataract. What is the probable diagnosis?

Accepted Answer

Galactosemia

Answer

Tyrosinemia

Answer

Fructosemia

Answer

Glycogen storage disorder

Question 4

How is fructose transported from the intestine into enterocytes?

Accepted Answer

GLUT 5

Answer

GLUT 1

Answer

GLUT 4

Answer

GLUT 7

Question 5

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 6

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 7

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

Accepted Answer

Mitochondrial matrix

Answer

Intermembrane space

Answer

Cytosol

Answer

Ribosome

Question 8

Which glucose transporter is primarily found in neurons?

Accepted Answer

GLUT-3

Answer

GLUT-1

Answer

GLUT-2

Answer

GLUT-4

Question 9

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 10

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

Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism — MCQs

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