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ASM 2021 Team
Module 2
Nutrition & Metabolism
Previous Exams
February 2015
Essay Questions
Mitochondrial
MalateDehydrogenase
Lactate Dehydrogenase
NAD+
NADH+H+
Pyruvate Carboxylase
ATP ADP + Pi
Biotin
H2CO3
NADH+H+
NAD+
Transport across
mitochondrial
membrane
Cytosolic
MalateDehydrogenase
NAD+
NADH+H+
Phosphoenolpyruvate Carboxykinase
GDPGTP CO2
Mg2+
‫الرحيم‬‫الرحمن‬‫اهلل‬‫بسم‬
Q1: Demonstrate the following biochemical conversions, mention enzymes
and coenzymes used in the reactions. (12 marks)
a- From Lactate to Phosphoenolpyruvate .
Oxaloacetate (in
Mitochondria)PyruvateLactate
Malate (in Mitochondria)Malate (in Cytosol)
Oxaloacetate (in Cytosol) Phosphoenolpyruvate
b- From Acetyl CoA to Mevalonate.
Acetyl CoA Acetyl CoA
Acetoacetyl CoA
Thiolase
CoASH
HMG CoA Synthase
Acetyl CoA
CoASH
H2O
β-Hydroxy-β-Methyl Glutaryl CoA (HMG CoA)
HMG CoA Reductase
2 NADPH + 2H+
CoASH
Mevalonate
Ornithine Transcarbamoylase
PiCarbamoyl
Phosphate
(CAP)
ATP
AMP + PPi
Aspartate
Mg2+
Fumarate
3-phosphoglycerate Dehydrogenase
NAD+
NADH+H+
Transaminase
Glutamat
e
α-ketoglutrate
PLP
H2O
Pi
Phosphatase
c- From Carbamoyl phosphate to Arginine.
d- From 3-Phosphoglycerate to Serine.
Ornithine
Argininosuccinate synthetase
Citrulline Argininosuccinate
Argininosuccinase
Arginine
3-Phosphoglycerate 3-phosphohydroxy pyruvate
β-PhosphoserineSerine
Transamidinase (in Kidney)
OrnithineArginine
PLP
MethylTransferase(inLiver)
SAM
SAH
ATP
ADP
Creatine Kinase (in Muscles)
Mg2+
e- From Glycine to Creatine Phosphate.
Glycine Guanido-acetate
CreatineCreatine Phosphate
Q2: Mention the biochemical effect of deficiency of each the following:-
(5 marks)
a- Glucose - 6 - phosphate dehydrogenase.
Favism
b- Galactose - 1 - phosphate uridyl transferase .
Galactosemia
c- Fatty acid α-hydroxylase.
Refsum’s Disease
d- Cystathionine Synthase.
Homocystinuria
e- P-hydroxy phenyl pyruvate hydroxylase.
Neonatal Tyrosinemia
Q3: Answer the questions about the following diagrams:-
I. (4 marks) Fatty Acid
Fatty Acyl CoA
C
Acetyl CoA + FattyAcyl CoA (-2C)
D
E
F
G
A
B (membrane carrier)
ATP
AMP + PPi
H2O
I/a- Write the detailed reaction A and E. (2 marks)
A:
E:
I/b- Mention the scientific name of B and C . (1 marks)
B: Carnitine (β-hydroxy-ϒ-trimethylammonium butyrate)
C: Fatty Acyl CoA
I/c- Mention the Coenzymes in the reaction D and G . (1 marks)
D: FAD
G: CoASH
II. (4 marks)
II/a- write the scientific name of compounds labeled from A to J (2.5 marks)
A: S-Adenosyl Methionine (SAM) F: Vitamin B 12
B: Methyl Transferase G: Tetrahydrofolate (THFA)
C: S-Adenosyl Homocysteine (SAH) H: Methionine
D: Spontaneously I: L-Met. Adenosyl transferase
E: Homocysteine
Acyl CoA Synthetase
Fatty Acid Acyl CoA
Enoyl CoA Hydratase
Enoyl CoA β-Hydroxy Acyl CoA
B
H2O
H+
F
CO2
II/b- Mention the function of this pathway (0.5 marks)
Recycling of Methionine and formation of S-Adenosyl Methionine which acts as a methyl donor.
II/c- Explain the importance of cofactor F in this reaction (1 marks)
B12 in this reaction acts as a carrier of CH3.
First, the methyl group is transferred from CH3-THFA to cobalamin to form Methylcobalamin.
Then it is transported to Homocysteine to form Methionine.
III. (3 marks)
III/a- Mention the name of compounds labeled from A to F (1.5 marks)
A: Glucose - phosphate dehydrogenase (G6PD) F: NADPH+H+
B: NADP+
C: 6-phophoglucono-δ-lactone
D: 6-phosphogluconate
E: 6-phosphogluconate dehydrogenase
Glucose-6-Phosphate
C
A
Glucose-6-Phosphate
D
Ribulose - - Phosphate
E
III/b- Enumerate the functions of the products of this pathway. (1.5 marks)
Ribulose - 5 - Phosphate:
- Enter in the non oxidative branch of Hexose monophosphate shunt to produce Glucose.
- Isomerization into Ribose - 5 - phosphate to synthesize Nucleosides, Nucleotides and
subsequently DNA and RNA.
NADPH+H+
:
- Protection of RBCs and removal of H2O2
- Reductive synthesis of Lipids.
- Production of Energy in the Electron Transport Chain.
CO2:
- Synthesis of Purines and Pyrimidines.
- CO2 fixation reactions.
Q4: Explain the biochemical mechanism of each of the following. (3 marks)
a- Ketosis.
It occurs during prolonged fasting or uncontrolled diabetes. In absence of Glucose, OAA in
liver is utilized in gluconeogenesis instead of condensation with Acetyl CoA to form Citrate.
Excess Acetyl CoA lead to stimulate Ketogenesis. Ketone bodies is formed and accumulated in
blood and urine (Ketonemia & Ketonuria) with acetone odour in breath and acetone bodies in
urine.
Accumulation of Ketone bodies in blood leads to depletion of Alkali reserves in the blood
(buffering system) which leads to ketoacidosis and subsequently, comma that may be
exaggerated to death.
b- Hormonal Regulation of Glycogenolysis.
The Key Enzyme is Glycogen Phosphorylase
Insulin inhibits the Glycogen Phosphorylase by dephosphorylation.
Glucagon stimulates the Glycogen Phosphorylase by phosphorylation.(In liver only, not in
muscles because muscles has no receptors for Glucagon).
Epinephrine stimulates the Glycogen Phosphorylase by phosphorylation.(In liver and muscles).
c- Symptoms of Phenylketonuria
- Mental Retardation.
- Eczema of Skin.
- Mousy odour of urine.
- Hypopigmentation (fair skin and blue eyes)
- Increased plasma phenylketonuria (more than 20gm/dl).
Q5: Compare between Phosphagen system and aerobic system that supply
energy for muscle contraction during exercise. (2 marks)
System Phosphagen Aerobic System
Duration of Contraction 8-10 sec Unlimited as long as
nutrient lasts
Source Breakdown of ATP and
Creatine Phosphate
Aerobic Oxidation of
macronutrients
Speed Most rapid The slowest
Q6: Discuss the role of adipose tissue in regulation of food intake. (2 marks)
When the amount of fat in adipose tissue is increased, Adipocytes secretes a hormone
called Leptin. Leptin crosses the Blood Brain Barrier and bind to receptor in hypothalamus to
cause:
- Decrease of production of Appetite stimulators. (e.g.neuropeptide Y)
- Decrease of Insulin secretion which decrease energy storage (e.g. Lipogenesis)
- Increase of production of substances that decrease food intake.
- Increase of sympathetic activity to increase metabolic rate expenditure
. ...‫هللا‬ ‫بحمد‬ ‫تم‬...

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  • 1. ASM 2021 Team Module 2 Nutrition & Metabolism Previous Exams February 2015 Essay Questions
  • 2. Mitochondrial MalateDehydrogenase Lactate Dehydrogenase NAD+ NADH+H+ Pyruvate Carboxylase ATP ADP + Pi Biotin H2CO3 NADH+H+ NAD+ Transport across mitochondrial membrane Cytosolic MalateDehydrogenase NAD+ NADH+H+ Phosphoenolpyruvate Carboxykinase GDPGTP CO2 Mg2+ ‫الرحيم‬‫الرحمن‬‫اهلل‬‫بسم‬ Q1: Demonstrate the following biochemical conversions, mention enzymes and coenzymes used in the reactions. (12 marks) a- From Lactate to Phosphoenolpyruvate . Oxaloacetate (in Mitochondria)PyruvateLactate Malate (in Mitochondria)Malate (in Cytosol) Oxaloacetate (in Cytosol) Phosphoenolpyruvate
  • 3. b- From Acetyl CoA to Mevalonate. Acetyl CoA Acetyl CoA Acetoacetyl CoA Thiolase CoASH HMG CoA Synthase Acetyl CoA CoASH H2O β-Hydroxy-β-Methyl Glutaryl CoA (HMG CoA) HMG CoA Reductase 2 NADPH + 2H+ CoASH Mevalonate
  • 4. Ornithine Transcarbamoylase PiCarbamoyl Phosphate (CAP) ATP AMP + PPi Aspartate Mg2+ Fumarate 3-phosphoglycerate Dehydrogenase NAD+ NADH+H+ Transaminase Glutamat e α-ketoglutrate PLP H2O Pi Phosphatase c- From Carbamoyl phosphate to Arginine. d- From 3-Phosphoglycerate to Serine. Ornithine Argininosuccinate synthetase Citrulline Argininosuccinate Argininosuccinase Arginine 3-Phosphoglycerate 3-phosphohydroxy pyruvate β-PhosphoserineSerine
  • 5. Transamidinase (in Kidney) OrnithineArginine PLP MethylTransferase(inLiver) SAM SAH ATP ADP Creatine Kinase (in Muscles) Mg2+ e- From Glycine to Creatine Phosphate. Glycine Guanido-acetate CreatineCreatine Phosphate
  • 6. Q2: Mention the biochemical effect of deficiency of each the following:- (5 marks) a- Glucose - 6 - phosphate dehydrogenase. Favism b- Galactose - 1 - phosphate uridyl transferase . Galactosemia c- Fatty acid α-hydroxylase. Refsum’s Disease d- Cystathionine Synthase. Homocystinuria e- P-hydroxy phenyl pyruvate hydroxylase. Neonatal Tyrosinemia Q3: Answer the questions about the following diagrams:- I. (4 marks) Fatty Acid Fatty Acyl CoA C Acetyl CoA + FattyAcyl CoA (-2C) D E F G A B (membrane carrier)
  • 7. ATP AMP + PPi H2O I/a- Write the detailed reaction A and E. (2 marks) A: E: I/b- Mention the scientific name of B and C . (1 marks) B: Carnitine (β-hydroxy-ϒ-trimethylammonium butyrate) C: Fatty Acyl CoA I/c- Mention the Coenzymes in the reaction D and G . (1 marks) D: FAD G: CoASH II. (4 marks) II/a- write the scientific name of compounds labeled from A to J (2.5 marks) A: S-Adenosyl Methionine (SAM) F: Vitamin B 12 B: Methyl Transferase G: Tetrahydrofolate (THFA) C: S-Adenosyl Homocysteine (SAH) H: Methionine D: Spontaneously I: L-Met. Adenosyl transferase E: Homocysteine Acyl CoA Synthetase Fatty Acid Acyl CoA Enoyl CoA Hydratase Enoyl CoA β-Hydroxy Acyl CoA
  • 8. B H2O H+ F CO2 II/b- Mention the function of this pathway (0.5 marks) Recycling of Methionine and formation of S-Adenosyl Methionine which acts as a methyl donor. II/c- Explain the importance of cofactor F in this reaction (1 marks) B12 in this reaction acts as a carrier of CH3. First, the methyl group is transferred from CH3-THFA to cobalamin to form Methylcobalamin. Then it is transported to Homocysteine to form Methionine. III. (3 marks) III/a- Mention the name of compounds labeled from A to F (1.5 marks) A: Glucose - phosphate dehydrogenase (G6PD) F: NADPH+H+ B: NADP+ C: 6-phophoglucono-δ-lactone D: 6-phosphogluconate E: 6-phosphogluconate dehydrogenase Glucose-6-Phosphate C A Glucose-6-Phosphate D Ribulose - - Phosphate E
  • 9. III/b- Enumerate the functions of the products of this pathway. (1.5 marks) Ribulose - 5 - Phosphate: - Enter in the non oxidative branch of Hexose monophosphate shunt to produce Glucose. - Isomerization into Ribose - 5 - phosphate to synthesize Nucleosides, Nucleotides and subsequently DNA and RNA. NADPH+H+ : - Protection of RBCs and removal of H2O2 - Reductive synthesis of Lipids. - Production of Energy in the Electron Transport Chain. CO2: - Synthesis of Purines and Pyrimidines. - CO2 fixation reactions. Q4: Explain the biochemical mechanism of each of the following. (3 marks) a- Ketosis. It occurs during prolonged fasting or uncontrolled diabetes. In absence of Glucose, OAA in liver is utilized in gluconeogenesis instead of condensation with Acetyl CoA to form Citrate. Excess Acetyl CoA lead to stimulate Ketogenesis. Ketone bodies is formed and accumulated in blood and urine (Ketonemia & Ketonuria) with acetone odour in breath and acetone bodies in urine. Accumulation of Ketone bodies in blood leads to depletion of Alkali reserves in the blood (buffering system) which leads to ketoacidosis and subsequently, comma that may be exaggerated to death.
  • 10. b- Hormonal Regulation of Glycogenolysis. The Key Enzyme is Glycogen Phosphorylase Insulin inhibits the Glycogen Phosphorylase by dephosphorylation. Glucagon stimulates the Glycogen Phosphorylase by phosphorylation.(In liver only, not in muscles because muscles has no receptors for Glucagon). Epinephrine stimulates the Glycogen Phosphorylase by phosphorylation.(In liver and muscles). c- Symptoms of Phenylketonuria - Mental Retardation. - Eczema of Skin. - Mousy odour of urine. - Hypopigmentation (fair skin and blue eyes) - Increased plasma phenylketonuria (more than 20gm/dl). Q5: Compare between Phosphagen system and aerobic system that supply energy for muscle contraction during exercise. (2 marks) System Phosphagen Aerobic System Duration of Contraction 8-10 sec Unlimited as long as nutrient lasts Source Breakdown of ATP and Creatine Phosphate Aerobic Oxidation of macronutrients Speed Most rapid The slowest Q6: Discuss the role of adipose tissue in regulation of food intake. (2 marks) When the amount of fat in adipose tissue is increased, Adipocytes secretes a hormone called Leptin. Leptin crosses the Blood Brain Barrier and bind to receptor in hypothalamus to cause: - Decrease of production of Appetite stimulators. (e.g.neuropeptide Y) - Decrease of Insulin secretion which decrease energy storage (e.g. Lipogenesis) - Increase of production of substances that decrease food intake. - Increase of sympathetic activity to increase metabolic rate expenditure . ...‫هللا‬ ‫بحمد‬ ‫تم‬...