Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism Indian Medical PG Practice Questions and MCQs

Question 531: Impaired glucose tolerance on an oral glucose tolerance test (GTT) is indicated by which of the following criteria?

A. Fasting plasma glucose greater than 126 mg/dL
B. Random blood glucose greater than 200 mg/dL
C. Fasting blood glucose less than 90 mg/dL
D. 2 hours after glucose load between 140-200 mg/dL, with fasting blood glucose less than 126 mg/dL (Correct Answer)

Explanation: **Explanation:** The Oral Glucose Tolerance Test (OGTT) is the gold standard for diagnosing **Impaired Glucose Tolerance (IGT)**, a state of "prediabetes" where blood glucose levels are higher than normal but do not yet meet the threshold for a Diabetes Mellitus diagnosis. **1. Why Option D is Correct:** According to WHO and ADA criteria, IGT is defined by a 2-hour post-load (75g glucose) plasma glucose value between **140 mg/dL and 199 mg/dL**, provided the fasting plasma glucose (FPG) is **less than 126 mg/dL**. This indicates that while the body can maintain relatively normal fasting levels, its ability to handle a concentrated glucose load is diminished. **2. Analysis of Incorrect Options:** * **Option A:** A fasting plasma glucose **≥ 126 mg/dL** is the diagnostic threshold for **Diabetes Mellitus**. * **Option B:** A random blood glucose **≥ 200 mg/dL** (in the presence of classic symptoms like polyuria/polydipsia) is also diagnostic of **Diabetes Mellitus**. * **Option C:** A fasting blood glucose less than 90 mg/dL is considered **Normal** (Normal range is typically 70–100 mg/dL). **3. High-Yield Clinical Pearls for NEET-PG:** * **Impaired Fasting Glucose (IFG):** FPG between **100–125 mg/dL** with a normal 2-hour OGTT (<140 mg/dL). * **HbA1c Ranges:** Normal (<5.7%), Prediabetes (5.7–6.4%), Diabetes (≥6.5%). * **Gestational Diabetes (GDM):** Usually screened between 24–28 weeks of gestation using the O'Sullivan test or DIPSI criteria. * **Standard Load:** The standard OGTT uses **75g** of anhydrous glucose dissolved in water.

Question 532: Long term status of blood sugar is explained by?

A. HbA
B. Serial measurement of fasting blood sugar
C. Oral glucose tolerance test
D. HbA1c (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. HbA1c** **Why it is correct:** HbA1c (Glycated Hemoglobin) is formed by the **non-enzymatic, irreversible covalent binding** of glucose to the N-terminal valine residue of the beta chain of hemoglobin. Since the average lifespan of a Red Blood Cell (RBC) is approximately **120 days**, the level of HbA1c reflects the average blood glucose concentration over the preceding **8 to 12 weeks (2–3 months)**. This makes it the gold standard for monitoring long-term glycemic control and treatment efficacy in diabetic patients. **Why other options are incorrect:** * **HbA:** This is normal adult hemoglobin ($\alpha_2\beta_2$). While it is the precursor that gets glycated, the level of HbA itself does not indicate glucose status. * **Serial measurement of fasting blood sugar:** This provides a series of "snapshots" of blood glucose at specific moments. It is highly susceptible to short-term fluctuations caused by diet, exercise, or acute stress. * **Oral Glucose Tolerance Test (OGTT):** This is used primarily for the diagnosis of Diabetes Mellitus and Gestational Diabetes. It measures the body's acute response to a glucose load but does not reflect long-term history. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnostic Threshold:** An HbA1c of **$\geq$ 6.5%** is diagnostic for Diabetes Mellitus. * **Fructosamine Test:** Measures glycated albumin and reflects glycemic control over the past **2–3 weeks**. It is used when HbA1c is unreliable (e.g., in hemolytic anemia or hemoglobinopathies). * **False Low HbA1c:** Seen in conditions that decrease RBC lifespan (e.g., Hemolytic anemia, recent blood transfusion, or pregnancy). * **False High HbA1c:** Seen in conditions that increase RBC lifespan (e.g., Splenectomy) or Iron deficiency anemia.

Question 533: Which enzyme is not typically found in muscles?

A. Phosphorylase b
B. Hexokinase
C. Glucose-6-phosphatase (Correct Answer)
D. Glycogen synthase

Explanation: ### Explanation The correct answer is **Glucose-6-phosphatase**. #### Why Glucose-6-phosphatase is the Correct Answer Glucose-6-phosphatase is the enzyme responsible for converting Glucose-6-Phosphate into free Glucose. This enzyme is primarily located in the **liver** and **kidneys** (within the endoplasmic reticulum). * **The Concept:** Muscle tissue lacks this enzyme. Consequently, muscles cannot release free glucose into the bloodstream to maintain systemic blood glucose levels. Instead, the glucose-6-phosphate derived from muscle glycogenolysis enters the glycolytic pathway to provide ATP locally for muscle contraction. This makes the muscle a "selfish" consumer of its own glycogen stores. #### Why Other Options are Incorrect * **Phosphorylase b:** This is the inactive form of glycogen phosphorylase, the rate-limiting enzyme of glycogenolysis. It is abundant in muscles to break down glycogen into glucose-1-phosphate during exercise. * **Hexokinase:** This enzyme is universal in extrahepatic tissues, including muscle. It phosphorylates glucose entering the cell to "trap" it as glucose-6-phosphate. * **Glycogen synthase:** This is the rate-limiting enzyme for glycogenesis (glycogen synthesis). Since muscles store significant amounts of glycogen (the largest reservoir by mass in the body), this enzyme is essential. #### NEET-PG High-Yield Pearls * **Von Gierke’s Disease (GSD Type I):** Caused by a deficiency of Glucose-6-phosphatase. It presents with severe fasting hypoglycemia, hepatomegaly, and hyperlactatemia. * **Glucose-6-phosphate Dehydrogenase (G6PD):** Do not confuse this with the phosphatase; G6PD is the rate-limiting enzyme of the HMP Shunt. * **Muscle vs. Liver:** Liver glycogen maintains **blood glucose**; muscle glycogen provides **energy for contraction**. * **Cori Cycle:** Since muscles lack glucose-6-phosphatase, they export lactate to the liver, where it is converted back to glucose via gluconeogenesis.

Question 534: What is the composition of Hyaluronic acid?

A. N-acetyl glucosamine + beta-glucosamine acid
B. N-acetyl glucosamine + beta-glucuronic acid (Correct Answer)
C. N-acetyl glucosamine + sulfated glucosamine acid
D. N-acetyl glucosamine + iduranic acid

Explanation: **Explanation:** Hyaluronic acid (Hyaluronan) is a unique **Glycosaminoglycan (GAG)**. It consists of repeating disaccharide units of **D-glucuronic acid** and **N-acetylglucosamine** linked by $\beta(1 \to 3)$ and $\beta(1 \to 4)$ glycosidic bonds. **Why Option B is correct:** The fundamental structure of Hyaluronic acid is a non-sulfated polymer of [Glucuronic acid + N-acetylglucosamine]. Unlike other GAGs, it is not covalently attached to a protein core (it does not form proteoglycans directly) and is the only GAG synthesized at the plasma membrane rather than the Golgi apparatus. **Why other options are incorrect:** * **Option A:** "Beta-glucosamine acid" is not a standard physiological component of GAGs; the acidic sugar required is glucuronic acid. * **Option C:** Hyaluronic acid is the only GAG that is **non-sulfated**. Sulfated sugars are found in Chondroitin sulfate, Keratan sulfate, and Heparin. * **Option D:** Iduronic acid is the epimer of glucuronic acid and is a characteristic component of **Dermatan sulfate** and **Heparin**, but not Hyaluronic acid. **High-Yield Clinical Pearls for NEET-PG:** 1. **Location:** Found in the vitreous humor of the eye, synovial fluid (acts as a lubricant/shock absorber), and umbilical cord (Wharton’s jelly). 2. **Tumor Marker:** Hyaluronidase is secreted by certain bacteria (e.g., *Staphylococcus aureus*) and sperm (to penetrate the ovum), acting as a "spreading factor." 3. **Unique Features:** It is the largest GAG, the only one that is non-sulfated, and the only one not found as a proteoglycan.

Question 535: What is the importance of pyruvate to lactate formation in anaerobic glycolysis?

A. FAD
B. NADH to NAD (Correct Answer)
C. ATP
D. NAD to NADH

Explanation: **Explanation:** In anaerobic glycolysis, the conversion of pyruvate to lactate is catalyzed by the enzyme **Lactate Dehydrogenase (LDH)**. This step is crucial not for the production of energy, but for the **regeneration of NAD+**. **Why Option B is Correct:** During the payoff phase of glycolysis, the enzyme *Glyceraldehyde-3-phosphate dehydrogenase* requires **NAD+** as a co-factor to function. Under anaerobic conditions (like in exercising muscle or erythrocytes lacking mitochondria), the NADH produced cannot be oxidized by the electron transport chain. To prevent glycolysis from coming to a halt due to a lack of NAD+, LDH reduces pyruvate to lactate, simultaneously **oxidizing NADH back to NAD+**. This ensures a continuous supply of NAD+ for glycolysis to proceed and generate ATP. **Why Other Options are Incorrect:** * **Option A (FAD):** FAD is primarily involved in the Citric Acid Cycle (Succinate Dehydrogenase) and the Electron Transport Chain, not in the glycolytic pathway. * **Option C (ATP):** While glycolysis produces a net of 2 ATP, the specific step of pyruvate to lactate conversion does not generate ATP; it consumes reducing equivalents. * **Option D (NAD to NADH):** This is the reverse of what occurs. NAD is reduced to NADH earlier in glycolysis (at the GAPDH step). The lactate step must reverse this to maintain redox balance. **High-Yield Clinical Pearls for NEET-PG:** * **Erythrocytes:** Since RBCs lack mitochondria, they depend entirely on anaerobic glycolysis and the LDH reaction for energy. * **Lactic Acidosis:** Occurs when there is excessive production or decreased clearance of lactate (e.g., in shock or hypoxia). * **LDH Isoenzymes:** LDH has 5 isoenzymes; LDH-1 is predominant in the heart, while LDH-5 is predominant in the liver and skeletal muscle.

Question 536: G-6-PD deficiency causes which of the following?

A. Leukemia
B. Hemolytic anemia (Correct Answer)
C. Hemophilia
D. None of the above

Explanation: **Explanation:** **Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency** is an X-linked recessive disorder and the most common enzyme deficiency worldwide. **Why Hemolytic Anemia is Correct:** G6PD is the rate-limiting enzyme of the **Hexose Monophosphate (HMP) Shunt**. Its primary role is to produce **NADPH**. In red blood cells (RBCs), NADPH is essential to maintain a pool of **reduced glutathione**, which neutralizes reactive oxygen species (ROS) like hydrogen peroxide. In G6PD deficiency, the lack of NADPH leads to oxidative stress. This causes hemoglobin to denature and precipitate as **Heinz bodies**. These damaged RBCs are then "bitten" by splenic macrophages (forming **Bite cells**) and prematurely destroyed, resulting in **acute hemolytic anemia**, typically triggered by infections, fava beans, or oxidant drugs (e.g., Primaquine, Sulphonamides). **Why Other Options are Incorrect:** * **Leukemia:** This is a malignant neoplasm of hematopoietic stem cells, primarily caused by genetic mutations (e.g., Philadelphia chromosome) or environmental factors, not enzyme deficiencies in the HMP shunt. * **Hemophilia:** This is a bleeding disorder caused by deficiencies in clotting factors (Factor VIII in Hemophilia A; Factor IX in Hemophilia B), not metabolic pathways of the RBC. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** X-linked Recessive (mostly affects males). * **Peripheral Smear:** Look for **Heinz bodies** (supravital stain) and **Bite cells** (degluticytes). * **Protective Effect:** G6PD deficiency provides a survival advantage against *Plasmodium falciparum* malaria. * **Diagnosis:** Quantitative spectrophotometric assay (Note: Do not test during an acute hemolytic episode as young reticulocytes have normal enzyme levels, leading to a false negative).

Question 537: Glucose increases plasma insulin by a process that involves which glucose transporter?

A. GLUT 1
B. GLUT 2 (Correct Answer)
C. GLUT 3
D. SGLT 1

Explanation: **Explanation:** The correct answer is **GLUT 2**. The process of glucose-stimulated insulin secretion (GSIS) occurs in the **Beta cells of the pancreas**. **Why GLUT 2 is correct:** GLUT 2 is a high-capacity, low-affinity (high $K_m$) glucose transporter. In the pancreatic beta cells, it acts as a **"glucose sensor."** Because of its high $K_m$, the rate of glucose entry into the cell is proportional to the blood glucose concentration. Once inside, glucose is phosphorylated by **Glucokinase**, leading to ATP production. Increased ATP closes ATP-sensitive $K^+$ channels, causing depolarization, $Ca^{2+}$ influx, and subsequent insulin exocytosis. **Why other options are incorrect:** * **GLUT 1:** Found primarily in RBCs and the blood-brain barrier. It provides basal glucose uptake but is not the primary sensor for insulin release. * **GLUT 3:** Found in neurons. It has a very low $K_m$ (high affinity), ensuring the brain receives glucose even during hypoglycemia. * **SGLT 1:** This is a Sodium-Glucose Linked Transporter (active transport) found in the small intestine and renal tubules, responsible for glucose absorption/reabsorption, not insulin signaling. **High-Yield Clinical Pearls for NEET-PG:** * **GLUT 2 Locations:** Liver, Pancreas, Small Intestine, and Kidney (Mnemonic: **Li**ttle **Pa**ns **I**n **Ki**tchen). * **Glucokinase vs. Hexokinase:** Glucokinase (Hexokinase IV) also acts as a glucose sensor in the pancreas. Mutations in Glucokinase lead to **MODY type 2** (Maturity-Onset Diabetes of the Young). * **GLUT 4:** The only **insulin-dependent** glucose transporter, found in skeletal muscle and adipose tissue.

Question 538: Which enzyme of glycolysis is also a part of gluconeogenesis?

A. Pyruvate kinase
B. PFK (Phosphofructokinase)
C. Hexokinase
D. Phosphoglycerate kinase (Correct Answer)

Explanation: ### Explanation In carbohydrate metabolism, glycolysis and gluconeogenesis share several enzymes. The key to answering this question lies in distinguishing between **reversible** and **irreversible** steps. **1. Why Phosphoglycerate Kinase is Correct:** Glycolysis consists of ten steps, seven of which are reversible and three of which are irreversible. **Phosphoglycerate kinase** catalyzes the reversible conversion of 1,3-bisphosphoglycerate to 3-phosphoglycerate. Because this reaction operates near equilibrium, the same enzyme is utilized in both glycolysis (producing ATP) and gluconeogenesis (consuming ATP). **2. Why the Other Options are Incorrect:** The other three options represent the "bottleneck" or regulatory steps of glycolysis. These are **irreversible** and must be bypassed in gluconeogenesis by specific gluconeogenic enzymes: * **Hexokinase (Option C):** Bypassed by *Glucose-6-phosphatase*. * **Phosphofructokinase-1 (Option B):** The rate-limiting step of glycolysis; bypassed by *Fructose-1,6-bisphosphatase*. * **Pyruvate Kinase (Option A):** Bypassed by a two-step process involving *Pyruvate carboxylase* and *PEP carboxykinase (PEPCK)*. **3. NEET-PG Clinical Pearls & High-Yield Facts:** * **Reversible Enzymes:** Apart from Phosphoglycerate kinase, other shared enzymes include Phosphohexose isomerase, Aldolase B, Glyceraldehyde-3-phosphate dehydrogenase, Phosphoglycerate mutase, and Enolase. * **ATP Paradox:** Although named a "kinase," Phosphoglycerate kinase is unique because it performs substrate-level phosphorylation in glycolysis but consumes ATP during gluconeogenesis. * **Localization:** Glycolysis occurs entirely in the cytosol, whereas gluconeogenesis begins in the mitochondria (Pyruvate carboxylase) before moving to the cytosol. * **Arsenic Poisoning:** Arsenate competes with inorganic phosphate in the GAPDH reaction, bypassing the Phosphoglycerate kinase step, resulting in zero net ATP gain during glycolysis.

Question 539: Fructose intolerance is due to which of the following?

A. Fructose
B. Fructose and Glucose (Correct Answer)
C. Maltose
D. Sucrose

Explanation: **Explanation:** **Hereditary Fructose Intolerance (HFI)** is an autosomal recessive disorder caused by a deficiency of the enzyme **Aldolase B**. This enzyme is responsible for cleaving Fructose-1-phosphate into dihydroxyacetone phosphate (DHAP) and glyceraldehyde. When deficient, Fructose-1-phosphate accumulates in the liver, trapping inorganic phosphate and inhibiting both glycogenolysis and gluconeogenesis, leading to severe hypoglycemia. The correct answer is **Fructose and Glucose** because the clinical management of HFI requires the strict elimination of any dietary source that yields fructose. 1. **Fructose:** Directly restricted as it is the primary substrate. 2. **Sucrose:** This is a disaccharide composed of **Fructose and Glucose**. Upon ingestion, it is broken down in the gut, releasing fructose into the system and triggering symptoms. Therefore, patients must avoid both fructose and sucrose-containing foods. **Analysis of Incorrect Options:** * **A. Fructose:** While correct, it is incomplete. Excluding only pure fructose without excluding sucrose (which contains glucose) would still lead to toxic accumulation. * **C. Maltose:** This is a disaccharide of **Glucose + Glucose**. It does not contain fructose and is generally safe for these patients. * **D. Sucrose:** Like option A, this is incomplete. Both free fructose and the fructose derived from sucrose must be avoided. **High-Yield Clinical Pearls for NEET-PG:** * **The "Weaning" Clue:** Symptoms (vomiting, jaundice, hypoglycemia, seizures) typically appear when an infant is **weaned** from breast milk and introduced to fruits or formula containing sucrose. * **Enzyme Deficiency:** Aldolase B (Liver). (Note: Aldolase A is in muscle; Aldolase C is in the brain). * **Urine Test:** Positive for reducing sugars (Benedict's test) but **negative** on the glucose oxidase dipstick. * **Protective Effect:** Interestingly, children with HFI often develop a natural aversion to sweets and have remarkably healthy teeth (no dental caries).

Question 540: Xylitol is a

A. Natural sweet amino acid
B. Synthetic sweet amino acid
C. Natural five carbon sugar (Correct Answer)
D. Synthetic five carbon sugar

Explanation: **Explanation:** **Xylitol** is a five-carbon sugar alcohol (polyol) derived from **xylose**. It occurs naturally in various fruits (berries), vegetables (corn husks), and mushrooms. In the human body, it is an intermediate in the **Uronic Acid Pathway**, where it is produced by the reduction of L-xylulose. **Why Option C is correct:** Xylitol is classified as a **natural five-carbon sugar** (specifically a sugar alcohol or pentitol). It is not "synthetic" because it is found in nature and produced endogenously in humans (about 5–15 grams daily) during carbohydrate metabolism. **Why other options are incorrect:** * **Options A & B:** Xylitol is a carbohydrate (polyol), not an **amino acid**. It lacks the amino (–NH2) and carboxyl (–COOH) groups characteristic of amino acids. * **Option D:** While xylitol is used as a commercial sweetener, it is extracted from natural sources like birch trees or corn cobs rather than being a purely "synthetic" laboratory creation. **Clinical Pearls for NEET-PG:** 1. **Uronic Acid Pathway:** Xylitol is formed from **L-xylulose** by the enzyme *xylulose reductase* (using NADPH). 2. **Essential Pentosuria:** A deficiency of *L-xylulose reductase* leads to the accumulation of L-xylulose in urine. This is a benign condition but can give a false-positive Benedict's test. 3. **Cariostatic Property:** Xylitol is "tooth-friendly" because oral bacteria (like *S. mutans*) cannot ferment it into acid, thus preventing dental caries. 4. **Glycemic Index:** It has a very low glycemic index, making it a preferred sweetener for diabetic patients. 5. **Caloric Value:** It provides roughly 2.4 kcal/g, which is less than sucrose (4 kcal/g).

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

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