MCQs on Carbohydrate Metabolism and Diabetes Mellitus

Quick Revision Notes: Carbohydrate Metabolism and Diabetes Mellitus

Why is carbohydrate metabolism important?

Carbohydrate metabolism provides energy to the body and maintains blood glucose within a narrow physiological range. The brain, red blood cells (RBCs), and exercising muscles depend heavily on glucose for energy production.

1. Glycolysis – "Glucose to Pyruvate Pathway"

• Occurs in the cytoplasm of all cells.

• Converts one glucose molecule into two pyruvate molecules.

• Produces 2 ATP and 2 NADH directly.

• It is the only source of ATP in RBCs because RBCs lack mitochondria.

• The rate-limiting enzyme is Phosphofructokinase-1 (PFK-1).

Remember:

"PFK Pushes Fuel Quickly."

PFK-1 is:

• Activated by AMP and Fructose-2,6-bisphosphate

• Inhibited by ATP and Citrate

2. TCA Cycle – "The Energy Factory"

• Occurs in the mitochondrial matrix.

• Oxidizes acetyl-CoA completely to CO₂.

• Produces large amounts of NADH, FADH₂, and GTP, which generate ATP in the electron transport chain.

• The cycle starts when Acetyl-CoA combines with Oxaloacetate to form Citrate.

Remember:

"OAA Opens the TCA Cycle."

3. Gluconeogenesis – "Making New Glucose"

• Occurs mainly in the liver and, during prolonged fasting, in the kidney.

• Produces glucose from:

  • Lactate

  • Glycerol

  • Alanine and other glucogenic amino acids

• Maintains blood glucose during fasting and starvation.

Important Enzymes:

• Pyruvate carboxylase

• PEP carboxykinase

• Fructose-1,6-bisphosphatase

• Glucose-6-phosphatase

Remember:

"The Liver Makes Glucose When the Stomach Sleeps."

4. HMP Shunt (Pentose Phosphate Pathway)

• Occurs in the cytoplasm.

• Produces:

  • NADPH for fatty acid synthesis and antioxidant defence.

  • Ribose-5-phosphate for nucleotide synthesis.

• Does not produce ATP.

Clinical Importance:

G6PD deficiency reduces NADPH production and predisposes RBCs to oxidative haemolysis.

Remember:

"HMP Helps Make Protection (NADPH)."

5. Glycogen Metabolism

Glycogenesis

• Conversion of glucose into glycogen.

• Stimulated by insulin.

• Occurs mainly in the liver and skeletal muscle.

Glycogenolysis

• Breakdown of glycogen to glucose.

• Stimulated by glucagon and adrenaline.

Remember:

"Insulin Stores, Glucagon Restores."

6. Regulation of Blood Glucose

Normal fasting blood glucose is approximately 70–100 mg/dL.

Hormones that Lower Blood Glucose:

• Insulin only

Hormones that Raise Blood Glucose:

• Glucagon

• Adrenaline

• Cortisol

• Growth hormone

Easy Memory Trick:

"Insulin is Alone; All Others Raise Sugar."

7. Metabolic Changes During Fed State

The fed state occurs after a meal when insulin levels are high.

Major pathways activated:

• Glycolysis

• Glycogenesis

• Fatty acid synthesis

• Protein synthesis

Remember:

"Fed State = Build and Store."

8. Metabolic Changes During Fasting

After 8–24 hours of fasting:

• Glycogenolysis becomes the major source of blood glucose.

• Lipolysis increases.

• Gluconeogenesis begins to rise.

Remember:

"Short Fast Uses Stored Sugar."

9. Metabolic Changes During Prolonged Starvation

After several days of starvation:

• Liver glycogen stores become depleted.

• Gluconeogenesis becomes dominant.

• Brain starts using ketone bodies.

• Protein breakdown decreases to preserve muscle mass.

Remember:

"Long Starvation Uses Fat to Save Protein."

10. Diabetes Mellitus and Metabolic Derangements

Diabetes mellitus is characterized by either:

• Lack of insulin secretion, or

• Reduced response to insulin.

Major metabolic abnormalities include:

• Hyperglycemia

• Glycosuria

• Lipolysis

• Ketogenesis

• Protein breakdown

Classical Symptoms:

• Polyuria

• Polydipsia

• Polyphagia

• Weight loss

Remember:

"Three Ps Plus Weight Loss = Diabetes."

11. Why Does Diabetic Ketoacidosis Occur?

In insulin deficiency:

• Fat breakdown increases.

• Large amounts of acetyl-CoA are produced.

• Oxaloacetate is diverted for gluconeogenesis.

• Excess acetyl-CoA is converted to ketone bodies.

Remember:

"No Insulin → Fat Burns → Ketones Rise."

12. High-Yield Competitive Exam Facts

✓ PFK-1 is the rate-limiting enzyme of glycolysis.
✓ Fructose-1,6-bisphosphatase is the rate-limiting enzyme of gluconeogenesis.
✓ G6PD is the rate-limiting enzyme of the HMP shunt.
✓ Glycogen phosphorylase is the rate-limiting enzyme of glycogenolysis.
✓ Glycogen synthase is the rate-limiting enzyme of glycogenesis.
✓ GLUT-4 is insulin-dependent.
✓ The brain cannot utilise fatty acids.
✓ RBCs lack mitochondria and depend entirely on glycolysis and the HMP shunt.
✓ HMP shunt produces NADPH but not ATP.
✓ Diabetic ketoacidosis is more common in Type 1 diabetes mellitus.

Exam Booster Mnemonic

"Glycolysis Gives ATP, TCA Gives More, HMP Gives NADPH, and Gluconeogenesis Gives Glucose Again."

MCQs

1. Which enzyme catalyses the committed and rate-limiting step of glycolysis?

A. Hexokinase
B. Pyruvate kinase
C. Phosphofructokinase-1 (PFK-1)
D. Aldolase

Answer: C. Phosphofructokinase-1 (PFK-1)
Explanation: PFK-1 controls the flow of glucose through glycolysis and is the major regulatory enzyme of the pathway.

2. Which of the following activates phosphofructokinase-1?

A. ATP
B. Citrate
C. AMP
D. Glucagon

Answer: C. AMP
Explanation: AMP signals low cellular energy and stimulates glycolysis by activating PFK-1.

3. NADPH required for maintaining reduced glutathione in erythrocytes is mainly generated by:

A. Glycolysis
B. TCA cycle
C. HMP shunt
D. Glycogenolysis

Answer: C. HMP shunt
Explanation: The HMP shunt produces NADPH, which protects RBCs from oxidative injury.

4. Deficiency of glucose-6-phosphate dehydrogenase primarily affects:

A. Hepatocytes
B. Skeletal muscle
C. Erythrocytes
D. Adipose tissue

Answer: C. Erythrocytes
Explanation: RBCs depend exclusively on the HMP shunt for NADPH production because they lack mitochondria.

5. Which TCA cycle enzyme directly produces GTP?

A. Citrate synthase
B. Isocitrate dehydrogenase
C. Succinyl-CoA synthetase
D. Fumarase

Answer: C. Succinyl-CoA synthetase
Explanation: This reaction generates one GTP by substrate-level phosphorylation.

6. The net ATP yield from aerobic glycolysis of one glucose molecule is approximately:

A. 2 ATP
B. 4 ATP
C. 6 ATP
D. 8 ATP

Answer: D. 8 ATP
Explanation: Classical calculations consider 2 ATP plus 2 NADH equivalents, giving about 8 ATP.

7. Which enzymes bypass pyruvate kinase in gluconeogenesis?

A. Hexokinase
B. Fructose-1,6-bisphosphatase
C. Pyruvate carboxylase and PEP carboxykinase
D. Glucose-6-phosphatase

Answer: C. Pyruvate carboxylase and PEP carboxykinase
Explanation: These enzymes convert pyruvate to phosphoenolpyruvate during glucose synthesis.

8. Which tissue cannot contribute directly to blood glucose during fasting?

A. Kidney
B. Liver
C. Skeletal muscle
D. Intestinal mucosa

Answer: C. Skeletal muscle
Explanation: Muscle lacks glucose-6-phosphatase and cannot release free glucose into blood.

9. The Cori cycle involves transport of:

A. Lactate from muscle to liver
B. Glucose from liver to kidney
C. Fatty acids from adipose tissue to liver
D. Ketone bodies from liver to brain

Answer: A. Lactate from muscle to liver
Explanation: Lactate formed during anaerobic glycolysis is converted back to glucose in the liver.

10. Which metabolite activates pyruvate carboxylase?

A. Citrate
B. ATP
C. Acetyl-CoA
D. NADH

Answer: C. Acetyl-CoA
Explanation: High acetyl-CoA concentrations stimulate gluconeogenesis.

11. During prolonged fasting, the brain increasingly utilizes:

A. Glycogen
B. Fatty acids
C. Ketone bodies
D. Amino acids

Answer: C. Ketone bodies
Explanation: Ketone body utilisation reduces the need for muscle protein breakdown.

12. Which hormone promotes glycogen synthesis?

A. Cortisol
B. Glucagon
C. Epinephrine
D. Insulin

Answer: D. Insulin
Explanation: Insulin promotes glucose uptake and storage as glycogen.

13. Glucagon stimulates all except

A. Glycogenolysis
B. Gluconeogenesis
C. Lipolysis
D. Glycolysis in the liver

Answer: D. Glycolysis in the liver
Explanation: Glucagon inhibits hepatic glycolysis and promotes glucose production.

14. Acetyl-CoA combines with which molecule to enter the TCA cycle?

A. Malate
B. Oxaloacetate
C. Succinate
D. α-Ketoglutarate

Answer: B. Oxaloacetate
Explanation: Citrate synthase catalyses the condensation of acetyl-CoA with oxaloacetate.

15. Which enzyme is deficient in Von Gierke disease?

A. Glycogen phosphorylase
B. Debranching enzyme
C. Glucose-6-phosphatase
D. Branching enzyme

Answer: C. Glucose-6-phosphatase
Explanation: Deficiency causes severe fasting hypoglycemia and hepatomegaly.

16. Severe fasting hypoglycaemia with hepatomegaly is characteristic of:

A. McArdle disease
B. Pompe disease
C. Von Gierke disease
D. Hers disease

Answer: C. Von Gierke disease
Explanation: Inability to release glucose from liver glycogen causes hypoglycemia.

17. Deficiency of muscle glycogen phosphorylase causes:

A. McArdle disease
B. Pompe disease
C. Cori disease
D. Andersen disease

Answer: A. McArdle disease
Explanation: Patients experience exercise intolerance and muscle cramps.

18. The major source of blood glucose after 24 hours of fasting is:

A. Dietary glucose
B. Glycogenolysis only
C. Gluconeogenesis
D. TCA cycle

Answer: C. Gluconeogenesis
Explanation: Liver glycogen stores become depleted after about one day.

19. Besides the liver, which organ contributes significantly to gluconeogenesis during prolonged starvation?

A. Spleen
B. Pancreas
C. Kidney
D. Heart

Answer: C. Kidney
Explanation: The kidney becomes an important glucose-producing organ during starvation.

20. In uncontrolled diabetes mellitus, increased ketone body production occurs because:

A. Glycogen synthesis increases
B. Oxaloacetate is diverted to gluconeogenesis
C. Glycolysis becomes excessive
D. Protein synthesis increases

Answer: B. Oxaloacetate is diverted to gluconeogenesis
Explanation: Acetyl-CoA accumulates and is converted into ketone bodies.

21. Diabetic ketoacidosis occurs mainly because:

A. Insulin stimulates ketogenesis
B. Acetyl-CoA cannot efficiently enter the TCA cycle
C. Glycolysis is accelerated
D. Glycogen synthesis is increased

Answer: B. Acetyl-CoA cannot efficiently enter the TCA cycle
Explanation: Lack of oxaloacetate forces acetyl-CoA toward ketone body formation.

22. Which glucose transporter is insulin-dependent?

A. GLUT-1
B. GLUT-2
C. GLUT-3
D. GLUT-4

Answer: D. GLUT-4
Explanation: GLUT-4 is found in skeletal muscle and adipose tissue and responds to insulin.

23. Which tissue takes up glucose independently of insulin?

A. Adipose tissue
B. Skeletal muscle
C. Brain
D. Cardiac muscle

Answer: C. Brain
Explanation: The brain mainly uses GLUT-1 and GLUT-3 transporters that do not require insulin.

24. During the fed state, excess glucose is mainly converted into:

A. Ketone bodies
B. Glycogen and fatty acids
C. Amino acids only
D. Lactate only

Answer: B. Glycogen and fatty acids
Explanation: Insulin promotes storage of excess energy.

25. Which glycolytic enzyme is inhibited by alanine?

A. Hexokinase
B. Pyruvate kinase
C. PFK-1
D. Aldolase

Answer: B. Pyruvate kinase
Explanation: Alanine signals adequate energy and slows glycolysis.

26. Which of the following is not produced in the HMP shunt?

A. NADPH
B. Ribose-5-phosphate
C. ATP
D. CO₂

Answer: C. ATP
Explanation: The pentose phosphate pathway produces NADPH but no ATP.

27. Fasting hypoglycaemia with elevated ketone bodies suggests increased:

A. Glycolysis
B. Glycogenesis
C. Gluconeogenesis and lipolysis
D. HMP shunt

Answer: C. Gluconeogenesis and lipolysis
Explanation: Fasting activates glucose production and fat breakdown.

28. Which metabolite inhibits PFK-1 and links TCA cycle activity with glycolysis?

A. Oxaloacetate
B. Succinate
C. Citrate
D. Malate

Answer: C. Citrate
Explanation: High citrate levels indicate sufficient energy and slow glycolysis.

29. Which hormone is primarily responsible for preventing postprandial hyperglycaemia?

A. Cortisol
B. Growth hormone
C. Insulin
D. Epinephrine

Answer: C. Insulin
Explanation: Insulin lowers blood glucose by promoting uptake and storage.

30. In prolonged starvation, protein breakdown decreases because:

A. Glucose requirement disappears completely
B. The brain adapts to ketone body utilisation.
C. Fatty acids cross the blood-brain barrier
D. Glycolysis stops completely

Answer: B. The brain adapts to ketone body utilisation.
Explanation: Ketone bodies spare body proteins from excessive degradation

Assertion–Reason and Match-the-Following MCQs on Carbohydrate Metabolism and Diabetes Mellitus

Assertion–Reason Questions

Directions:
Choose the correct option:

A. Both assertion and reason are true and Reason is the correct explanation of Assertion.
B. Both Assertion and Reason are true but Reason is not the correct explanation of Assertion.
C. Assertion is true but Reason is false.
D. Assertion is false but Reason is true.

1.

Assertion: Glycolysis increases during hypoxia.
Reason: Under hypoxic conditions ATP production from oxidative phosphorylation decreases.

✅ Answer: A

Explanation: Cells compensate for reduced oxidative phosphorylation by increasing glycolysis.

2.

Assertion: RBCs cannot utilize fatty acids as an energy source.
Reason: RBCs lack mitochondria.

✅ Answer: A

Explanation: β-Oxidation occurs in mitochondria, which are absent in mature erythrocytes.

3.

Assertion: The HMP shunt is highly active in adipose tissue and liver.
Reason: These tissues require large amounts of NADPH for fatty acid synthesis.

✅ Answer: A

4.

Assertion: Muscle glycogen cannot maintain blood glucose during fasting.
Reason: Skeletal muscle lacks glucose-6-phosphatase.

✅ Answer: A

5.

Assertion: Glucagon stimulates gluconeogenesis.
Reason: Glucagon increases fructose-2,6-bisphosphate concentration in liver.

✅ Answer: C

Explanation: Glucagon actually decreases fructose-2,6-bisphosphate concentration.

6.

Assertion: Brain glucose utilization decreases during prolonged starvation.
Reason: Brain adapts to utilize ketone bodies.

✅ Answer: A

7.

Assertion: Diabetic ketoacidosis is more common in type 1 diabetes mellitus.
Reason: Absolute insulin deficiency promotes lipolysis and ketogenesis.

✅ Answer: A

8.

Assertion: ATP inhibits phosphofructokinase-1.
Reason: ATP acts as an allosteric inhibitor indicating high energy status.

✅ Answer: A

9.

Assertion: Citrate inhibits glycolysis.
Reason: Citrate activates phosphofructokinase-1.

✅ Answer: C

Explanation: Citrate inhibits PFK-1 and slows glycolysis.

10.

Assertion: Pyruvate carboxylase is activated by acetyl-CoA.
Reason: High acetyl-CoA signals the need for gluconeogenesis.

✅ Answer: A

11.

Assertion: G6PD deficiency causes hemolytic anemia.
Reason: NADPH generated by G6PD protects RBCs against oxidative injury.

✅ Answer: A

12.

Assertion: Glycogen phosphorylase is active in the fasting state.
Reason: Insulin activates glycogen phosphorylase by dephosphorylation.

✅ Answer: C

Explanation: Glucagon and epinephrine activate glycogen phosphorylase.

13.

Assertion: Oxaloacetate depletion promotes ketogenesis in diabetes mellitus.
Reason: Oxaloacetate is diverted toward gluconeogenesis.

✅ Answer: A

14.

Assertion: Kidney contributes significantly to glucose production during prolonged starvation.
Reason: Renal gluconeogenesis increases during starvation.

✅ Answer: A

15.

Assertion: GLUT-4 mediated glucose uptake decreases in insulin deficiency.
Reason: GLUT-4 is an insulin-dependent glucose transporter.

✅ Answer: A

Match-the-Following Questions

16. Match the enzyme with its pathway.

• Column I Column II

• P. PFK-1 1. HMP shunt

• Q. G6PD 2. Glycolysis

• R. Citrate synthase 3. TCA cycle

• S. Glycogen phosphorylase 4. Glycogenolysis

Options:
A. P-2, Q-1, R-3, S-4
B. P-1, Q-2, R-4, S-3
C. P-3, Q-2, R-1, S-4
D. P-2, Q-4, R-3, S-1

Answer: A

17. Match the hormone with its action.

• Column I Column II

• P. Insulin 1. Glycogenolysis

• Q. Glucagon 2. Glucose uptake

• R. Cortisol 3. Gluconeogenesis

• S. Epinephrine 4. Lipolysis

Options:
A. P-2, Q-3, R-4, S-1
B. P-3, Q-2, R-1, S-4
C. P-2, Q-1, R-3, S-4
D. P-4, Q-2, R-3, S-1

Answer: A

18. Match the transporter with its tissue.

• Column I Column II

• P. GLUT-1 1. Liver

• Q. GLUT-2 2. Brain

• R. GLUT-3 3. RBC

• S. GLUT-4 4. Skeletal muscle

Options:
A. P-3, Q-1, R-2, S-4
B. P-2, Q-3, R-1, S-4
C. P-1, Q-2, R-3, S-4
D. P-3, Q-4, R-2, S-1

Answer: A

19. Match the disease with the enzyme deficiency.

• Column I Column II

• P. Von Gierke disease 1. Muscle glycogen phosphorylase

• Q. McArdle disease 2. Acid maltase

• R. Pompe disease 3. Glucose-6-phosphatase

• S. Cori disease 4. Debranching enzyme

Answer: P-3, Q-1, R-2, S-4

20. Match the metabolite with its regulatory role.

• Column I Column II

• P. AMP 1. Activates pyruvate carboxylase

• Q. Citrate 2. Activates PFK-1

• R. Acetyl-CoA 3. Inhibits PFK-1

• S. ATP 4. Inhibits glycolysis

Answer: P-2, Q-3, R-1, S-4

21. Match the tissue with its preferred fuel during prolonged starvation.

• Column I Column II

• P. Brain 1. Fatty acids

• Q. RBC 2. Ketone bodies

• R. Cardiac muscle 3. Glucose

• S. Liver 4. Fatty acids and ketone synthesis

Answer: P-2, Q-3, R-1, S-4

22. Match the pathway with its principal function.

• Column IColumn II

• P. Glycolysis 1. NADPH production

• Q. HMP shunt 2. ATP production

• R. Gluconeogenesis 3. Blood glucose maintenance

• S. Glycogenesis 4. Glucose storage

Answer: P-2, Q-1, R-3, S-4

23. Match the hormone with the metabolic state.

• Column I Column II

• P. Insulin 1. Prolonged fasting

• Q. Glucagon 2. Fed state

• R. Cortisol 3. Stress response

• S. Growth hormone 4. Starvation adaptation

Answer: P-2, Q-1, R-3, S-4

24. Match the enzyme with its inhibitor.

• Column I Column II

• P. PFK-1 1. ATP

• Q. Pyruvate kinase 2. Alanine

• R. Glycogen synthase 3. Glucagon

• S. Acetyl-CoA carboxylase 4. Palmitoyl-CoA

Answer: P-1, Q-2, R-3, S-4

25. Match the substrate with gluconeogenic potential.

• Column I Column II

• P. Lactate 1. Cori cycle

• Q. Alanine 2. Glucose-alanine cycle

• R. Glycerol 3. Triglyceride breakdown

• S. Propionate 4. Odd-chain fatty acids

Answer: P-1, Q-2, R-3, S-4

26. Match the metabolic condition with the predominant pathway.

• Column I Column II

• P. Fed state 1. Ketogenesis

• Q. Overnight fast 2. Glycogenesis

• R. Starvation 3. Glycogenolysis

• S. Uncontrolled diabetes 4. Excess ketone production

Answer: P-2, Q-3, R-1, S-4

27. Match the organ with its major metabolic role.

• Column I Column II

• P. Liver 1. Glucose utilization only

• Q. Muscle 2. Blood glucose maintenance

• R. Adipose tissue 3. Fat storage

• S. Brain 4. Major glucose consumer

Answer: P-2, Q-1, R-3, S-4

28. Match the compound with its significance.

• Column I Column II

• P. NADPH 1. Reductive biosynthesis

• Q. FADH₂ 2. Electron transport chain

• R. ATP 3. Universal energy currency

• S. GTP 4. Protein synthesis and TCA cycle

Answer: P-1, Q-2, R-3, S-4

29. Match the diabetes complication with mechanism.

• Column I Column II

• P. Ketoacidosis 1. Excess ketogenesis

• Q. Polyuria 2. Osmotic diuresis

• R. Polyphagia 3. Cellular glucose deprivation

• S. Weight loss 4. Increased lipolysis

✅ Answer: P-1, Q-2, R-3, S-4

30. Match the pathway with cellular location.

• Column I Column II

• P. Glycolysis 1. Cytosol

• Q. TCA cycle 2. Mitochondrial matrix

• R. β-Oxidation 3. Mitochondria

• S. HMP shunt 4. Cytosol

Answer: P-1, Q-2, R-3, S-4

Remember these facts.

• PFK-1 is the rate-limiting enzyme of glycolysis.

• Fructose-1,6-bisphosphatase is the rate-limiting enzyme of gluconeogenesis.

• G6PD is the rate-limiting enzyme of the HMP shunt.

• GLUT-4 is insulin-dependent.

• Brain uses ketone bodies during starvation but never fatty acids.

• RBCs depend entirely on glycolysis and the HMP shunt due to the absence of mitochondria.

• Diabetic ketoacidosis is a hallmark of Type 1 diabetes mellitus.

• Glycogen phosphorylase = Rate-limiting enzyme of glycogenolysis.

• Glycogen synthase = Rate-limiting enzyme of glycogenesis

• Insulin: storage hormone; glucagon: mobilisation hormone.

• The brain uses glucose in fasting and ketone bodies in starvation.

• RBCs depend entirely on glycolysis and the HMP shunt because they lack mitochondria.

• Diabetic ketoacidosis is common in Type 1 diabetes mellitus.

• GLUT-4 is the favourite target of questions.

Dr Alok Singh.