Carbohydrate Metabolism Practice Questions

Q: Long term status of blood sugar is explained by?

HbA1c. ### 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.

Q: What is the composition of Hyaluronic acid?

N-acetyl glucosamine + beta-glucuronic acid. **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.

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

NADH to NAD. **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.

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

Hemolytic anemia. **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).

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

GLUT 2. **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.

Q: Xylitol is a

Natural five carbon sugar. **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).

Question 1

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

Accepted Answer

2 hours after glucose load between 140-200 mg/dL, with fasting blood glucose less than 126 mg/dL

Answer

Fasting plasma glucose greater than 126 mg/dL

Answer

Random blood glucose greater than 200 mg/dL

Answer

Fasting blood glucose less than 90 mg/dL

Question 2

Long term status of blood sugar is explained by?

Accepted Answer

HbA1c

Answer

HbA

Answer

Serial measurement of fasting blood sugar

Answer

Oral glucose tolerance test

Question 3

Which enzyme is not typically found in muscles?

Accepted Answer

Glucose-6-phosphatase

Answer

Phosphorylase b

Answer

Hexokinase

Answer

Glycogen synthase

Question 4

What is the composition of Hyaluronic acid?

Accepted Answer

N-acetyl glucosamine + beta-glucuronic acid

Answer

N-acetyl glucosamine + beta-glucosamine acid

Answer

N-acetyl glucosamine + sulfated glucosamine acid

Answer

N-acetyl glucosamine + iduranic acid

Question 5

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

Accepted Answer

NADH to NAD

Answer

FAD

Answer

ATP

Answer

NAD to NADH

Question 6

G-6-PD deficiency causes which of the following?

Accepted Answer

Hemolytic anemia

Answer

Leukemia

Answer

Hemophilia

Answer

None of the above

Question 7

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

Accepted Answer

GLUT 2

Answer

GLUT 1

Answer

GLUT 3

Answer

SGLT 1

Question 8

Which enzyme of glycolysis is also a part of gluconeogenesis?

Accepted Answer

Phosphoglycerate kinase

Answer

Pyruvate kinase

Answer

PFK (Phosphofructokinase)

Answer

Hexokinase

Question 9

Fructose intolerance is due to which of the following?

Accepted Answer

Fructose and Glucose

Answer

Fructose

Answer

Maltose

Answer

Sucrose

Question 10

Xylitol is a

Accepted Answer

Natural five carbon sugar

Answer

Natural sweet amino acid

Answer

Synthetic sweet amino acid

Answer

Synthetic five carbon sugar

Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism — MCQs

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