Carbohydrate Metabolism Practice Questions

Q: Which of the following steps is specific for gluconeogenesis?

Oxaloacetate to PEP. ***Oxaloacetate to PEP*** - This step, catalyzed by **PEP carboxykinase (PEPCK)**, is a bypass reaction necessary to overcome the irreversible pyruvate kinase step in glycolysis. - It is a key regulatory point in **gluconeogenesis**, allowing the synthesis of glucose from non-carbohydrate precursors. *Oxaloacetate to citrate* - This reaction is part of the **Krebs cycle (citric acid cycle)**, where oxaloacetate combines with acetyl-CoA to form citrate. - It does not directly lead to **glucose synthesis** and is not unique to gluconeogenesis. *Oxaloacetate to glucose* - This is an **overly broad statement** and not a direct, single enzymatic step in gluconeogenesis. - While oxaloacetate is an intermediate in the gluconeogenic pathway, it must first be converted to **PEP** and then proceed through several more steps to become glucose. *Pyruvate to acetyl CoA* - This reaction is catalyzed by the **pyruvate dehydrogenase complex** and represents a committed step into oxidative metabolism, primarily the Krebs cycle. - This step is **irreversible** in mammals and prevents the direct conversion of acetyl-CoA back to pyruvate or glucose, making it not relevant for gluconeogenesis.

Q: Insulin resistance down-regulates the translocation of which glucose transporter to the cell membrane?

GLUT-4. ***GLUT-4*** - **Insulin resistance** primarily affects cells that express **GLUT-4**, such as muscle and adipose tissue, by impairing its translocation from intracellular vesicles to the cell membrane. - This reduced translocation leads to decreased glucose uptake in response to insulin, a hallmark of **type 2 diabetes**. *GLUT-1* - **GLUT-1** is responsible for basal glucose uptake in nearly all cells, including **erythrocytes** and endothelial cells of the blood-brain barrier. - Its activity is largely **insulin-independent** and not significantly affected by insulin resistance in the same way as GLUT-4. *GLUT-2* - **GLUT-2** is found primarily in **pancreatic β-cells**, hepatocytes, renal tubular cells, and enterocytes. - It has a low affinity but high capacity for glucose transport, playing a key role in **glucose sensing** and facilitating glucose flux in and out of these cells, independent of insulin translocation. *GLUT-3* - **GLUT-3** is predominantly expressed in **neurons** and the placenta, where it facilitates high-affinity glucose uptake. - It is crucial for maintaining the brain's glucose supply and its activity is also **insulin-independent**.

Q: In the oxidative phase of pentose phosphate pathway, NADPH is produced in?

Cytosol. ***Cytosol*** - The **oxidative phase** of the **pentose phosphate pathway (PPP)**, which produces **NADPH**, occurs exclusively in the **cytosol**. - Two key enzymes generate NADPH: **glucose-6-phosphate dehydrogenase (G6PD)** and **6-phosphogluconate dehydrogenase**. - **NADPH** is crucial for **reductive biosynthesis** (e.g., fatty acid synthesis, cholesterol synthesis) and for maintaining **redox balance** (e.g., reducing glutathione to protect against oxidative stress). *Mitochondria* - While mitochondria are central to **oxidative phosphorylation** and the **Krebs cycle**, they primarily produce **NADH** and **FADH2** for ATP generation. - The pentose phosphate pathway does not occur in mitochondria. *Ribosome* - **Ribosomes** are responsible for **protein synthesis** (translation) and are not involved in metabolic pathways or NADPH production. - They are cellular machinery for translation, not metabolic compartments. *Peroxisomes* - **Peroxisomes** are involved in **fatty acid β-oxidation** and **detoxification** of hydrogen peroxide. - While peroxisomes have some oxidative enzymes, they are not the site of the pentose phosphate pathway or its NADPH production.

Q: Which of the following is not a step in gluconeogenesis?

Conversion of pyruvate to acetyl-CoA. ***Conversion of pyruvate to acetyl-CoA*** - This step is a key irreversible reaction catalyzed by the **pyruvate dehydrogenase complex** that commits pyruvate to oxidative metabolism via the **Krebs cycle** or to fatty acid synthesis. - It is **not a part of gluconeogenesis**, as acetyl-CoA cannot be converted back to pyruvate or glucose in mammals. - This reaction is irreversible and represents a point of no return for glucose synthesis. *Conversion of glucose-6-phosphate to glucose* - This is the **final step in gluconeogenesis**, catalyzed by **glucose-6-phosphatase** in the liver and kidney. - This enzyme allows free glucose to be released into the bloodstream. - It is an essential gluconeogenic step that bypasses the irreversible hexokinase/glucokinase reaction of glycolysis. *Conversion of oxaloacetate to phosphoenolpyruvate* - This is a **key bypass step in gluconeogenesis** that overcomes the irreversible pyruvate kinase reaction in glycolysis. - It is catalyzed by **phosphoenolpyruvate carboxykinase (PEPCK)** and requires GTP. - This is crucial for synthesizing glucose from non-carbohydrate precursors like amino acids and lactate. *Conversion of fructose-1,6-bisphosphate to fructose-6-phosphate* - This is an important **bypass step in gluconeogenesis**, catalyzed by **fructose-1,6-bisphosphatase**. - This irreversible reaction bypasses the phosphofructokinase-1 step of glycolysis. - It is one of the three key regulatory steps unique to gluconeogenesis.

Q: Which of the following enzymes participates exclusively in glycolysis?

Pyruvate kinase. ***Pyruvate kinase*** - This enzyme catalyzes the **final step of glycolysis**, irreversibly converting **phosphoenolpyruvate (PEP)** to pyruvate, producing ATP. - **Exclusively participates in glycolysis** - it has no role in any other metabolic pathway, making it the most definitive answer. - All tissue-specific isoforms (M1, M2, L, R) perform the same glycolysis-exclusive function. *Phosphofructokinase* - **Phosphofructokinase-1 (PFK-1)** catalyzes the committed step of glycolysis (Fructose-6-P → Fructose-1,6-BP) and is technically exclusive to the glycolytic pathway. - However, when the question refers to "phosphofructokinase" generically, it could include **PFK-2**, which produces fructose-2,6-bisphosphate (a regulatory molecule, not a glycolytic intermediate) and is part of the regulatory mechanism rather than the pathway itself. - **Pyruvate kinase is more unambiguously exclusive** to glycolysis as a metabolic enzyme. *Hexokinase* - While essential for the initial step of glycolysis, **hexokinase** phosphorylates multiple hexoses (glucose, mannose, fructose) and its product (G6P) can enter **multiple pathways**: glycolysis, pentose phosphate pathway, or glycogen synthesis. - **Not exclusive to glycolysis** - it serves as a branch point enzyme. *Glucose-6-phosphate dehydrogenase* - This enzyme is the rate-limiting step of the **pentose phosphate pathway (PPP)**, not glycolysis. - It catalyzes the oxidation of G6P to produce **NADPH** and ribose-5-phosphate for nucleotide synthesis, thereby diverting glucose-6-phosphate **away from glycolysis**.

Q: When the insulin to glucagon ratio decreases, which enzyme is primarily active?

Glycogen phosphorylase. ***Glycogen phosphorylase*** - A decrease in the **insulin-to-glucagon ratio** indicates a **low blood glucose** state, signaling the need for glucose production. - **Glycogen phosphorylase** is the key enzyme in **glycogenolysis**, which breaks down stored glycogen into glucose-1-phosphate, thereby elevating blood glucose. - This is the **primary and fastest response** to decreased insulin/glucagon ratio. *Fructose-1,6-bisphosphatase* - This enzyme is crucial for **gluconeogenesis**, specifically catalyzing the dephosphorylation of **fructose-1,6-bisphosphate** to **fructose-6-phosphate**. - While active during low insulin/high glucagon states, it is involved in synthesizing glucose, not directly breaking down stored glycogen as quickly as glycogen phosphorylase. *Pyruvate carboxylase* - This enzyme is the first committed step in **gluconeogenesis**, converting **pyruvate to oxaloacetate** in the mitochondria. - Although active in response to a low insulin-to-glucagon ratio, its role is in synthesizing glucose from non-carbohydrate precursors, which is a slower process than immediate glycogen breakdown. *Glucose-6-phosphatase* - This enzyme is found primarily in the **liver and kidneys** and is responsible for dephosphorylating **glucose-6-phosphate** to free glucose, allowing it to exit the cell into the bloodstream. - While essential for the release of glucose from both gluconeogenesis and glycogenolysis, it acts at a later stage to make glucose available rather than initiating the breakdown of glycogen itself.

Q: An adolescent male patient presents to you with exercise intolerance. He gives a history of developing cramps on exertion. Which of the following enzyme deficiencies could be the cause?

Myophosphorylase. ***Myophosphorylase*** - A deficiency in **myophosphorylase** (McArdle's disease, Glycogen Storage Disease Type V) impairs muscle glycogen breakdown, leading to **exercise intolerance** and **muscle cramps** due to insufficient ATP production during exertion. - Patients often experience a "second wind" phenomenon where symptoms improve after resting, as free fatty acids become an alternative fuel source. *Hexokinase* - A deficiency in **hexokinase** would affect the first step of glycolysis, impacting glucose phosphorylation in all tissues, not specifically causing exercise-induced muscle cramps. - This deficiency is rare and typically presents with **hemolytic anemia** due to impaired erythrocyte metabolism. *Glucose-6-phosphatase* - A deficiency in **glucose-6-phosphatase** (Von Gierke's disease, Glycogen Storage Disease Type Ia) primarily affects the liver and kidneys, leading to **fasting hypoglycemia**, lactic acidosis, and hepatomegaly, not exercise intolerance. - Muscle glycogen metabolism is unaffected in this condition. *Hepatic glycogen phosphorylase* - A deficiency in **hepatic glycogen phosphorylase** (Hers' disease, Glycogen Storage Disease Type VI) mainly causes **hepatomegaly** and **mild hypoglycemia** because the liver cannot effectively mobilize its glycogen stores. - **Muscle glycogen metabolism** remains normal, so exercise intolerance and cramps are not characteristic symptoms.

Q: Which one of the following shows allosteric inhibition of glycolysis?

Citrate. ***Citrate*** - **Citrate** is a classic **allosteric inhibitor** of **phosphofructokinase-1 (PFK-1)**, the key regulatory enzyme in glycolysis - It binds to an allosteric site (distinct from the active site), reducing PFK-1's affinity for **fructose-6-phosphate** - This is a **negative feedback mechanism** - when citrate accumulates (indicating sufficient ATP production via the citric acid cycle), glycolysis slows down *Malonic acid* - **Malonic acid** is a **competitive inhibitor** (NOT allosteric) of succinate dehydrogenase in the citric acid cycle - It structurally resembles succinate and competes for the active site directly *2,3-BPG* - **2,3-Bisphosphoglycerate (2,3-BPG)** is an **allosteric effector** of hemoglobin (decreases oxygen affinity), not an enzyme inhibitor in glycolysis - It binds to hemoglobin, not to glycolytic enzymes *Amino acid alanine* - **Alanine** is an allosteric inhibitor of **pyruvate kinase** (not a glycolytic regulator in this context) - While it does show allosteric inhibition, it acts on gluconeogenesis regulation in the liver, not as a direct glycolytic inhibitor

Q: Classical galactosemia (Type I) is due to deficiency of which enzyme?

Galactose-1-phosphate uridyltransferase. ***Galactose-1-phosphate uridyltransferase*** - **Galactosemia Type I** (**classical galactosemia**) is caused by a deficiency in **galactose-1-phosphate uridyltransferase (GALT)**. - This enzyme is crucial for converting **galactose-1-phosphate** to **glucose-1-phosphate** in the Leloir pathway of galactose metabolism. *Adenine phosphoribosyltransferase (APRT)* - Deficiency in **adenine phosphoribosyltransferase (APRT)** leads to **APRT deficiency**, characterized by **kidney stones** composed of 2,8-dihydroxyadenine. - This enzyme is involved in **purine salvage pathways**, not carbohydrate metabolism. *Fructose-1,6-bisphosphatase* - A deficiency in **fructose-1,6-bisphosphatase** causes **fructose-1,6-bisphosphatase deficiency**, a disorder of **gluconeogenesis**. - It results in **hypoglycemia** and **lactic acidosis**, especially during fasting. *Hexokinase* - **Hexokinase** phosphorylates glucose to **glucose-6-phosphate**, the first step in glycolysis. - Deficiency is rare but can lead to **nonspherocytic hemolytic anemia**.

Question 1

Which of the following steps is specific for gluconeogenesis?

Accepted Answer

Oxaloacetate to PEP

Answer

Oxaloacetate to citrate

Answer

Oxaloacetate to glucose

Answer

Pyruvate to acetyl CoA

Question 2

Insulin resistance down-regulates the translocation of which glucose transporter to the cell membrane?

Accepted Answer

GLUT-4

Answer

GLUT-1

Answer

GLUT-2

Answer

GLUT-3

Question 3

In the oxidative phase of pentose phosphate pathway, NADPH is produced in?

Accepted Answer

Cytosol

Answer

Mitochondria

Answer

Ribosome

Answer

Peroxisomes

Question 4

Which of the following is not a step in gluconeogenesis?

Accepted Answer

Conversion of pyruvate to acetyl-CoA

Answer

Conversion of glucose-6-phosphate to glucose

Answer

Conversion of oxaloacetate to phosphoenolpyruvate

Answer

Conversion of fructose-1,6-bisphosphate to fructose-6-phosphate

Question 5

Which of the following enzymes participates exclusively in glycolysis?

Accepted Answer

Pyruvate kinase

Answer

Phosphofructokinase

Answer

Glucose-6-phosphate dehydrogenase

Answer

Hexokinase

Question 6

When the insulin to glucagon ratio decreases, which enzyme is primarily active?

Accepted Answer

Glycogen phosphorylase

Answer

Glucose-6-phosphatase

Answer

Pyruvate carboxylase

Answer

Fructose 1,6-bisphosphatase

Question 7

An adolescent male patient presents to you with exercise intolerance. He gives a history of developing cramps on exertion. Which of the following enzyme deficiencies could be the cause?

Accepted Answer

Myophosphorylase

Answer

Hexokinase

Answer

Glucose-6-phosphatase

Answer

Hepatic glycogen phosphorylase

Question 8

Which one of the following shows allosteric inhibition of glycolysis?

Accepted Answer

Citrate

Answer

Amino acid alanine

Answer

2,3 BPG

Answer

Malonic acid

Question 9

Classical galactosemia (Type I) is due to deficiency of which enzyme?

Accepted Answer

Galactose-1-phosphate uridyltransferase

Answer

Fructose-1,6-bisphosphatase

Answer

Adenine phosphoribosyltransferase (APRT)

Answer

Hexokinase

Question 10

Glycemic index is defined as:

Accepted Answer

Measure of the change in the blood glucose following ingestion of carbohydrate.

Answer

Measure of the change in blood glucose following ingestion of protein.

Answer

Measure of the change in blood glucose following ingestion of fat.

Answer

Measure of glucose control over a period of time.

Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism — MCQs

On this page

Practice by Chapter

Want unlimited practice?