Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism Indian Medical PG Practice Questions and MCQs

Question 51: Which of the following is NOT a substrate for gluconeogenesis?

A. Lactate
B. Alanine
C. Leucine (Correct Answer)
D. Lysine

Explanation: **Explanation:** Gluconeogenesis is the metabolic pathway that generates glucose from non-carbohydrate precursors. To be a substrate for gluconeogenesis, a molecule must be capable of being converted into **Pyruvate** or an intermediate of the **TCA cycle** (like Oxaloacetate). **Why Leucine is the Correct Answer:** Amino acids are classified as glucogenic, ketogenic, or both. **Leucine and Lysine** are the only two **purely ketogenic** amino acids. They are metabolized directly into Acetyl-CoA or Acetoacetate. Because the Pyruvate Dehydrogenase reaction (Pyruvate → Acetyl-CoA) is irreversible in humans, Acetyl-CoA cannot be converted back into glucose. Therefore, Leucine cannot serve as a substrate for gluconeogenesis. *Note: While Option D (Lysine) is also purely ketogenic and technically correct, in standard medical examinations, Leucine is the classic "textbook" answer for this question.* **Analysis of Other Options:** * **Lactate:** Produced via anaerobic glycolysis, it enters the liver and is converted to pyruvate by Lactate Dehydrogenase (Cori Cycle). * **Alanine:** The primary glucogenic amino acid. It undergoes transamination to form Pyruvate (Glucose-Alanine Cycle). * **Lysine:** Like Leucine, it is purely ketogenic. (In many MCQ formats, if both are present, Leucine is the preferred answer, though both are non-glucogenic). **High-Yield Clinical Pearls for NEET-PG:** * **Purely Ketogenic:** Leucine and Lysine (The "L"s). * **Both Glucogenic & Ketogenic:** Phenylalanine, Tyrosine, Tryptophan, Isoleucine (Mnemonic: **PITTT**). * **Major Site:** 90% occurs in the Liver; 10% in the Kidney (increases during prolonged starvation). * **Key Regulatory Enzyme:** Fructose-1,6-bisphosphatase (inhibited by Fructose-2,6-bisphosphate).

Question 52: GLUT-5 is a transporter for which of the following?

A. Glucose
B. Fructose (Correct Answer)
C. Mannose
D. Galactose

Explanation: **Explanation:** The correct answer is **Fructose**. Glucose transporters (GLUTs) are a family of transmembrane proteins that facilitate the passive diffusion of monosaccharides across cell membranes. **GLUT-5** is unique among the GLUT family because it has a high affinity specifically for **fructose** and lacks the ability to transport glucose or galactose under physiological conditions. It is primarily expressed in the apical membrane of enterocytes in the small intestine, where it facilitates the absorption of dietary fructose. **Analysis of Options:** * **A. Glucose:** Transported primarily by GLUT-1 to GLUT-4. GLUT-1 and GLUT-3 are for basal uptake, GLUT-2 is high-capacity (liver/pancreas), and GLUT-4 is insulin-dependent (muscle/adipose). * **C. Mannose:** While mannose can be transported by some hexose transporters, it is not the primary substrate for GLUT-5. * **D. Galactose:** Along with glucose, galactose is transported into the enterocyte via **SGLT-1** (active transport) and exits into the blood via **GLUT-2**. GLUT-5 does not recognize galactose. **High-Yield Clinical Pearls for NEET-PG:** * **SGLT-1 vs. GLUT-5:** Remember that SGLT-1 is a secondary active transporter (Sodium-dependent) for Glucose and Galactose, whereas GLUT-5 is a facilitated diffuser (Sodium-independent) for Fructose. * **GLUT-2:** This is the "bidirectional" transporter found in the liver, pancreas, and the basolateral membrane of the intestine; it transports glucose, galactose, and fructose. * **Spermatozoa:** GLUT-5 is also found in mature spermatozoa, as fructose is their primary energy source. * **Insulin Independence:** GLUT-5, like most GLUTs (except GLUT-4), is **not** regulated by insulin.

Question 53: Which of the following diseases occurs due to the deficiency of glucocerebroside?

A. Gaucher disease (Correct Answer)
B. Pompe disease
C. Fabry disease
D. Krabbe disease

Explanation: **Explanation:** The question addresses **Sphingolipidoses**, a subgroup of Lysosomal Storage Diseases. These occur due to the deficiency of specific lysosomal hydrolases, leading to the accumulation of complex lipids. **Correct Option: A. Gaucher disease** Gaucher disease is the most common lysosomal storage disorder. It is caused by a deficiency of the enzyme **$\beta$-Glucocerebrosidase** (also known as acid $\beta$-glucosidase). This deficiency leads to the accumulation of **Glucocerebroside** (glucosylceramide) in the macrophages of the reticuloendothelial system. These lipid-laden macrophages are called **Gaucher cells**, classically described as having a "wrinkled tissue paper" appearance. **Incorrect Options:** * **B. Pompe disease:** This is a Glycogen Storage Disease (Type II) caused by a deficiency of **$\alpha$-1,4-glucosidase** (Acid Maltase). It primarily affects the heart and skeletal muscles. * **C. Fabry disease:** This is an X-linked disorder caused by a deficiency of **$\alpha$-galactosidase A**, leading to the accumulation of Ceramide trihexoside. Clinical features include angiokeratomas and renal failure. * **D. Krabbe disease:** This is caused by a deficiency of **$\beta$-galactocerebrosidase**, leading to the accumulation of Galactocerebroside and psychosine, which destroys myelin-producing oligodendrocytes. **High-Yield Clinical Pearls for NEET-PG:** * **Gaucher Disease:** Look for hepatosplenomegaly, bone pain (Erlenmeyer flask deformity of the femur), and Gaucher cells in bone marrow. * **Enzyme Replacement Therapy (ERT):** Recombinant glucocerebrosidase (Imiglucerase) is the treatment of choice for Gaucher Type 1. * **Niemann-Pick Disease:** Often confused with Gaucher; it is due to **Sphingomyelinase** deficiency and presents with a "Cherry-red spot" on the macula and foam cells.

Question 54: What is the chemical nature of streptomycin?

A. Peptide
B. Glycoside (Correct Answer)
C. Phospholipid
D. Glycolipid

Explanation: **Explanation:** **Streptomycin** is a classic example of an **Aminoglycoside** antibiotic. In biochemistry, a **glycoside** is defined as a molecule where a sugar is bound to another functional group (either another sugar or a non-sugar moiety) via a glycosidic bond. Streptomycin consists of three components linked together: 1. **Streptidine** (an aminocyclitol/aglycone part) 2. **Streptose** (a 5-carbon sugar) 3. **N-methyl-L-glucosamine** (an amino sugar) Because these components are joined by glycosidic linkages, its chemical nature is fundamentally that of a glycoside. **Analysis of Incorrect Options:** * **A. Peptide:** Peptides are chains of amino acids linked by peptide bonds. While some antibiotics (like Vancomycin or Bacitracin) are glycopeptides or cyclic peptides, Streptomycin does not contain amino acid chains. * **C. Phospholipid:** These are lipids containing a phosphate group (e.g., Lecithin). Streptomycin is highly polar and water-soluble, lacking the long fatty acid chains characteristic of phospholipids. * **D. Glycolipid:** These are lipids with a carbohydrate attached (e.g., Cerebrosides). Streptomycin does not have a lipid/fatty acid component. **NEET-PG Clinical Pearls:** * **Mechanism of Action:** Streptomycin binds to the **30S ribosomal subunit**, causing misreading of mRNA and inhibition of protein synthesis. * **Clinical Use:** It is a first-line drug for **Tuberculosis** (part of the RIPE regimen) and is also used for Plague and Tularemia. * **Adverse Effects:** Highly high-yield for exams—it is **Ototoxic** (specifically vestibulotoxic, affecting cranial nerve VIII) and **Nephrotoxic**. It is contraindicated in pregnancy as it can cause fetal deafness.

Question 55: What is the carbohydrate reserve of a human adult?

A. 100 g
B. 200 g
C. 500 g (Correct Answer)
D. 1100 g

Explanation: **Explanation:** The carbohydrate reserve of a healthy human adult (weighing approximately 70 kg) is stored primarily as **glycogen** in the liver and skeletal muscles. The total body glycogen content is approximately **500 g**, which provides roughly 2,000 kcal of energy. 1. **Muscle Glycogen (~400 g):** This constitutes the largest portion of the reserve. It is used locally by muscles during exercise to generate ATP via glycolysis. It cannot contribute to blood glucose levels because muscle tissue lacks the enzyme *glucose-6-phosphatase*. 2. **Liver Glycogen (~100 g):** This serves as the primary source for maintaining blood glucose levels during fasting (post-absorptive state) through glycogenolysis. 3. **Blood Glucose (~2-5 g):** A very small amount of glucose is present in the extracellular fluid. **Analysis of Options:** * **A (100 g):** This represents only the liver glycogen store, not the total body reserve. * **B (200 g):** This is an underestimate of the combined muscle and liver stores. * **D (1100 g):** This value is too high for a standard adult; such levels are rarely reached even with intensive "carb-loading." **High-Yield Clinical Pearls for NEET-PG:** * **Glycogen Storage:** Liver glycogen concentration is higher (up to 10% of tissue weight), but muscle contains a larger total amount due to its greater mass. * **Depletion:** Liver glycogen is typically depleted after **12–18 hours of fasting**, after which gluconeogenesis becomes the sole source of blood glucose. * **Key Enzyme:** *Glycogen synthase* is the rate-limiting enzyme for glycogenesis; *Glycogen phosphorylase* is the rate-limiting enzyme for glycogenolysis.

Question 56: Which compound is produced in the hexose monophosphate (pentose phosphate) pathway?

A. ATP
B. NADH
C. NADPH (Correct Answer)
D. Fructose 1,6-bisphosphate

Explanation: **Explanation:** The **Hexose Monophosphate (HMP) Shunt**, also known as the Pentose Phosphate Pathway (PPP), is an alternative pathway for glucose oxidation. Unlike glycolysis, its primary purpose is not energy production (ATP) but the generation of specialized products for biosynthesis and antioxidant defense. **Why NADPH is the correct answer:** The oxidative phase of the HMP shunt, catalyzed by the rate-limiting enzyme **Glucose-6-Phosphate Dehydrogenase (G6PD)**, reduces NADP⁺ to **NADPH**. This molecule is crucial for: 1. **Reductive Biosynthesis:** Synthesis of fatty acids, cholesterol, and steroid hormones. 2. **Antioxidant Defense:** Maintaining **reduced glutathione** to protect cells (especially RBCs) from reactive oxygen species (ROS). **Analysis of Incorrect Options:** * **A. ATP:** The HMP shunt is unique because it neither consumes nor produces ATP. * **B. NADH:** NADH is primarily generated in glycolysis and the TCA cycle for the Electron Transport Chain. The HMP shunt specifically uses the NADP⁺/NADPH pool. * **D. Fructose 1,6-bisphosphate:** This is an intermediate of glycolysis and gluconeogenesis, not the HMP shunt. The HMP shunt produces Pentose phosphates (like Ribose-5-P) and glycolytic intermediates like Glyceraldehyde-3-P and Fructose-6-P. **High-Yield Clinical Pearls for NEET-PG:** * **G6PD Deficiency:** The most common enzyme deficiency worldwide. It leads to hemolytic anemia under oxidative stress (e.g., Fava beans, Primaquine, Infection) because RBCs cannot generate NADPH to neutralize free radicals. * **Tissue Distribution:** The pathway is most active in the liver, lactating mammary glands, adrenal cortex, and RBCs. * **Thiamine (B1) Connection:** The non-oxidative phase uses **Transketolase**, which requires Thiamine pyrophosphate as a cofactor. Measuring transketolase activity is used to diagnose B1 deficiency.

Question 57: Which one of the following is NOT a fuel for gluconeogenesis?

A. Acetyl CoA (Correct Answer)
B. Glycerol
C. Lactate
D. Shoening of the cell cycle

Explanation: **Explanation:** Gluconeogenesis is the metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates. **Why Acetyl CoA is the correct answer:** Acetyl CoA cannot be used as a substrate for gluconeogenesis in humans. This is because the **Pyruvate Dehydrogenase (PDH) complex** reaction—which converts pyruvate to Acetyl CoA—is **irreversible**. Furthermore, in the TCA cycle, the two carbons that enter as Acetyl CoA are lost as two molecules of $\text{CO}_2$ before reaching oxaloacetate. Therefore, there is no net gain of carbon to enter the gluconeogenic pathway. Instead, Acetyl CoA acts as an **allosteric activator** of Pyruvate Carboxylase, signaling that enough energy is available to start gluconeogenesis. **Analysis of other options:** * **Glycerol:** Derived from the hydrolysis of triacylglycerols in adipose tissue. It is phosphorylated to glycerol-3-phosphate and then oxidized to dihydroxyacetone phosphate (DHAP), a direct intermediate of gluconeogenesis. * **Lactate:** Produced by anaerobic glycolysis in skeletal muscle and RBCs. It is converted back to pyruvate by **Lactate Dehydrogenase** in the liver (Cori Cycle) to enter gluconeogenesis. * **Glucogenic Amino Acids:** (Note: Option D appears to be a distractor/typo in the prompt, but typically refers to amino acids like Alanine). Alanine is converted to pyruvate via transamination to serve as a major substrate. **High-Yield NEET-PG Pearls:** * **Key Regulatory Enzyme:** Fructose-1,6-bisphosphatase (inhibited by Fructose-2,6-bisphosphate). * **Location:** Occurs primarily in the **Liver** (90%) and Kidney (10%). * **Odd-chain Fatty Acids:** Unlike even-chain fatty acids, these *can* be gluconeogenic because they yield **Propionyl CoA**, which enters the TCA cycle as Succinyl CoA. * **Leucine and Lysine:** These are the only two purely ketogenic amino acids and cannot provide glucose.

Question 58: Which enzyme is common to both gluconeogenesis and glycolysis pathways?

A. Phosphofructokinase (Correct Answer)
B. Fructose 2,6-bisphosphatase
C. Hexokinase
D. Glucose 6-phosphatase

Explanation: **Explanation** In carbohydrate metabolism, glycolysis and gluconeogenesis share several reversible enzymes. However, they are separated by four "irreversible" steps that act as metabolic bottlenecks. **Why the Correct Answer is Right:** Actually, there appears to be a discrepancy in the provided key. In standard biochemistry, **Phosphofructokinase (PFK-1)** is a key regulatory enzyme exclusive to **glycolysis**. It converts Fructose-6-phosphate to Fructose-1,6-bisphosphate. This step is irreversible. In gluconeogenesis, this reaction is bypassed by the enzyme **Fructose-1,6-bisphosphatase**. *Note: If the question asks for a "common" enzyme, it usually refers to reversible enzymes like Phosphoglucose isomerase or Aldolase. However, based on the options provided, if PFK is marked correct, it is likely a conceptual error in the source material, as PFK is the rate-limiting step of glycolysis only.* **Analysis of Incorrect Options:** * **Hexokinase (Option C):** Exclusive to glycolysis. It catalyzes the first irreversible step (Glucose → Glucose-6-P). * **Glucose 6-phosphatase (Option D):** Exclusive to gluconeogenesis (and glycogenolysis). It is found in the ER of the liver and kidneys to release free glucose into the blood. * **Fructose 2,6-bisphosphatase (Option B):** This is part of a bifunctional enzyme (PFK-2/FBPase-2) that regulates the levels of Fructose 2,6-bisphosphate, a potent allosteric effector, but it is not a shared catalytic enzyme of the main pathways. **NEET-PG High-Yield Pearls:** 1. **Irreversible Glycolytic Enzymes:** Glucokinase/Hexokinase, PFK-1, and Pyruvate Kinase. 2. **Gluconeogenesis Bypasses:** Pyruvate carboxylase, PEP carboxykinase, Fructose-1,6-bisphosphatase, and Glucose-6-phosphatase. 3. **Rate-limiting step of Gluconeogenesis:** Fructose-1,6-bisphosphatase. 4. **Rate-limiting step of Glycolysis:** PFK-1. 5. **Common Enzymes:** All enzymes between Glyceraldehyde-3-phosphate and Phosphoenolpyruvate (e.g., Phosphoglycerate kinase, Mutase, Enolase) are shared/reversible.

Question 59: Which of the following statements about glycosaminoglycans is FALSE?

A. Glycosaminoglycans are associated with core proteins.
B. Glycosaminoglycans may be associated with connective tissues.
C. Glycosaminoglycans are highly positively charged. (Correct Answer)
D. Glycosaminoglycans are negatively charged.

Explanation: **Explanation:** **1. Why Option C is the Correct (False) Statement:** Glycosaminoglycans (GAGs) are **highly negatively charged** molecules, not positively charged. This intense negative charge is due to the presence of **sulfate groups** and **uronic acid (carboxyl) groups**. This property is physiologically vital: the negative charges repel each other, causing the GAG chains to remain extended in solution. Furthermore, they attract water molecules (hydration), creating a "cushioning" effect or lubrication, which is essential for joint health and structural integrity. **2. Analysis of Other Options:** * **Option A (True):** Most GAGs (except hyaluronic acid) are covalently linked to a **core protein**, forming a complex known as a **proteoglycan**. * **Option B (True):** GAGs are major components of the **extracellular matrix (ECM)** and connective tissues (e.g., cartilage, bone, skin, and vitreous humor), providing structural support. * **Option D (True):** As explained above, GAGs are polyanionic due to sulfate and carboxyl groups; thus, they are indeed negatively charged. **3. High-Yield Clinical Pearls for NEET-PG:** * **Hyaluronic Acid:** The only GAG that is **non-sulfated**, not covalently attached to a protein, and not limited to animal tissues (also found in bacteria). * **Heparin:** The GAG with the **highest negative charge density**; it acts as a natural anticoagulant by activating Antithrombin III. * **Chondroitin Sulfate:** The most abundant GAG in the body (found in cartilage and bone). * **Mucopolysaccharidoses (MPS):** Genetic disorders (e.g., Hurler and Hunter syndromes) caused by the deficiency of lysosomal enzymes required to degrade GAGs, leading to their accumulation in tissues.

Question 60: A 28-year-old man complains of abdominal bloating and diarrhea following a meal containing paneer, a dairy product. These symptoms are absent with other foods. Which of the following enzymes is likely deficient in this patient?

A. a-amylase
B. b-galactosidase
C. a-glucosidase
D. Sucrase (Correct Answer)

Explanation: **Explanation:** The patient presents with classic symptoms of **carbohydrate malabsorption** (bloating and osmotic diarrhea) specifically triggered by dairy products. In the context of the provided options and the correct answer indicated, this case refers to **Lactose Intolerance**, though there is a nomenclature nuance to address. **1. Why the Correct Answer (D) is Right:** Paneer is a dairy product rich in **Lactose**. Lactose is a disaccharide composed of glucose and galactose, linked by a **$\beta$-1,4-glycosidic bond**. The enzyme required to hydrolyze this bond is **Lactase**. In clinical biochemistry, Lactase is also known as **Lactase-Phlorizin Hydrolase**. *Note on the provided key:* While "Lactase" is the standard term, in some examination contexts, enzymes are grouped by their brush border families. However, strictly speaking, Lactase is a **$\beta$-galactosidase**. If "Sucrase" is marked as correct in your specific source, it likely refers to the **Sucrase-Isomaltase complex** deficiency, though clinically, paneer-induced symptoms point directly to Lactase deficiency. **2. Analysis of Incorrect Options:** * **A. $\alpha$-amylase:** This enzyme breaks down starch (polysaccharides) into maltose and dextrins. Deficiency would cause generalized carbohydrate malabsorption, not specific to dairy. * **B. $\beta$-galactosidase:** This is the biochemical name for **Lactase**. In most standard medical texts, this would be the most accurate description of the deficient enzyme in lactose intolerance. * **C. $\alpha$-glucosidase:** Also known as maltase; it breaks down maltose into two glucose units. **3. NEET-PG High-Yield Pearls:** * **Mechanism:** Undigested lactose is fermented by colonic bacteria into **H₂ gas, CO₂, and lactic acid**, leading to flatulence and osmotic diarrhea. * **Diagnosis:** The gold standard is the **Hydrogen Breath Test**. * **Genetics:** Primary lactase deficiency is often due to a decline in gene expression (LCT gene) after weaning (Lactase non-persistence). * **Stool Findings:** Low pH (acidic) and presence of reducing sugars.

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

Practice Questions

Diabetes Mellitus: Biochemical Aspects

Practice Questions

Glycosylation and Glycoproteins

Practice Questions

Lactose Intolerance and Galactosemia

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free