BCH3702 - UNISA
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Question 2 [32]
2.1. Illustrate how ATP is generated in glycolysis. (10)
ATP (adenosine triphosphate) is generated during the process of glycolysis, which is the initial step in the
breakdown of glucose to produce energy in the form of ATP. The overall process of glycolysis occurs in the
cytoplasm of cells and can be divided into two main phases: the energy investment phase and the energy
payoff phase. Here is a step-by-step illustration of how ATP is generated in glycolysis:
1. Glucose Activation: The process begins with the activation of glucose, which requires the input of
energy in the form of two ATP molecules. Glucose is phosphorylated by the enzyme hexokinase,
using two ATP molecules, to form glucose-6-phosphate.
2. Glucose Conversion: Glucose-6-phosphate is then converted into fructose-6-phosphate through a
series of enzymatic reactions.
3. Energy Investment Phase: In this phase, fructose-6-phosphate is further phosphorylated by the
enzyme phosphofructokinase using one ATP molecule. This step converts fructose-6-phosphate
into fructose-1,6-bisphosphate.
4. Fructose-1,6-bisphosphate Cleavage: Fructose-1,6-bisphosphate is cleaved into two three-carbon
molecules called glyceraldehyde-3-phosphate (G3P) and dihydroxyacetone phosphate (DHAP).
5. Isomerization: DHAP is converted into another molecule of G3P through an isomerization reaction.
6. Energy Payoff Phase: Each G3P molecule undergoes a series of reactions that result in the
generation of ATP and NADH, which is a high-energy electron carrier.
a. G3P Oxidation: G3P is oxidized by the removal of hydrogen atoms, and NAD+ (nicotinamide
adenine dinucleotide) is reduced to form NADH. The energy released during this oxidation is used
to synthesize ATP through substrate-level phosphorylation. This process occurs twice for each
glucose molecule.
b. ATP Synthesis: For each G3P molecule, a high-energy phosphate group is transferred to ADP
(adenosine diphosphate), resulting in the synthesis of ATP. This reaction is catalyzed by the enzyme
phosphoglycerate kinase.
7. Pyruvate Formation: The final step of glycolysis involves the conversion of the remaining G3P
molecules into pyruvate. This step generates two molecules of pyruvate per glucose molecule.
Overall, during glycolysis, a net gain of two ATP molecules is generated through substrate-level
phosphorylation (step 6b), along with two NADH molecules. These ATP molecules serve as a direct source
of energy for cellular processes.
2.2. Create an illustration, and discuss in detail, the pathological condition that results from excessive
fructose consumption. (10)
Pathological condition resulting from excessive fructose consumption:
, BCH3702 - UNISA
Excessive consumption of fructose, especially in the form of high-fructose corn syrup (HFCS) found in many
processed foods and sugary beverages, can lead to a pathological condition known as fructose
malabsorption or fructose intolerance. Fructose malabsorption occurs when the small intestine is unable
to effectively absorb and process fructose, leading to a range of digestive symptoms and potential long-
term health complications.
When excessive amounts of fructose are consumed, the small intestine's capacity to absorb fructose can
be overwhelmed, resulting in the following mechanisms and consequences:
1. Impaired Fructose Absorption: The intestine normally absorbs fructose through a specific carrier
protein called GLUT5. However, in fructose malabsorption, the transport system becomes
saturated, and excess fructose remains in the intestinal lumen.
2. Osmotic Effect: The unabsorbed fructose in the intestine attracts water, leading to an osmotic
effect. This can result in symptoms like diarrhea, bloating, abdominal pain, and flatulence.
3. Bacterial Fermentation: The unabsorbed fructose is fermented by bacteria in the large intestine,
leading to the production of short-chain fatty acids and gases, such as hydrogen, methane, and
carbon dioxide. These fermentation byproducts can contribute to additional symptoms like
bloating, gas, and discomfort.
4. Altered Gut Microbiota: The fermentation of fructose by gut bacteria can also lead to changes in
the composition of the gut microbiota. This imbalance in the gut flora may have broader
implications for overall gut health and immune function.
5. Metabolic Effects: Excessive fructose consumption can also contribute to metabolic dysregulation.
Fructose is metabolized primarily in the liver, where it can be converted into triglycerides, leading
to increased fat accumulation and potentially contributing to non-alcoholic fatty liver disease
(NAFLD). Furthermore, fructose consumption can disrupt insulin signaling, contributing to insulin
resistance and potentially increasing the risk of developing type 2 diabetes.
It's important to note that fructose malabsorption is different from hereditary fructose intolerance, which
is a rare genetic disorder caused by a deficiency in the enzyme aldolase B, responsible for metabolizing
fructose. Hereditary fructose intolerance can result in severe symptoms and can be life-threatening if not
properly managed.
2.3. Discuss in detail how the pyruvate complex is regulated. (7)
Regulation of the pyruvate complex:
The pyruvate complex refers to a group of enzymes that play a crucial role in the conversion of pyruvate,
a product of glycolysis, into acetyl-CoA, which enters the citric acid cycle (also known as the Krebs cycle)
for further energy production. The pyruvate complex is regulated through several mechanisms to maintain
an appropriate balance between pyruvate metabolism and energy needs within the cell. Here are the key
regulatory aspects:
1. Substrate Availability: The first level of regulation occurs through the availability of substrates.
Pyruvate is produced as a result of glycolysis, and the rate of pyruvate formation is influenced by
, BCH3702 - UNISA
the activity of glycolytic enzymes and glucose availability. Factors that affect glycolysis, such as
glucose levels and hormonal regulation, indirectly influence the pyruvate complex's activity.
2. Pyruvate Dehydrogenase (PDH) Kinase: PDH kinase is an enzyme that phosphorylates and
inactivates the pyruvate dehydrogenase complex (PDC). When PDH kinase is active, it leads to the
phosphorylation of PDC, reducing its activity. This phosphorylation inhibits the conversion of
pyruvate into acetyl-CoA, thereby regulating the flux of pyruvate. PDH Phosphatase: In contrast to
PDH kinase, PDH phosphatase is an enzyme that dephosphorylates and activates the pyruvate
dehydrogenase complex. When PDH phosphatase is active, it removes the phosphate group from
PDC, promoting its activity and allowing the conversion of pyruvate to acetyl-CoA.
3. Allosteric Regulation: The activity of the pyruvate complex is also regulated by allosteric effectors.
One of the key allosteric regulators is acetyl-CoA itself. When the concentration of acetyl-CoA is
high, it inhibits the activity of the pyruvate complex, preventing further conversion of pyruvate
into acetyl-CoA. This mechanism helps to regulate the production of acetyl-CoA according to the
cellular energy status.
4. Feedback Inhibition: The pyruvate complex can be regulated by feedback inhibition. High levels of
NADH, an indicator of abundant energy supply, can inhibit the complex. NADH acts as a feedback
inhibitor, reducing the activity of the pyruvate complex and slowing down the conversion of
pyruvate to acetyl-CoA.
5. Hormonal Regulation: Hormones such as insulin and glucagon can also modulate the activity of
the pyruvate complex. Insulin promotes the dephosphorylation and activation of the complex,
facilitating the conversion of pyruvate to acetyl-CoA for energy production. Glucagon, on the other
hand, inhibits the pyruvate complex, favoring alternative pathways for glucose metabolism, such
as gluconeogenesis.
The regulation of the pyruvate complex is crucial for maintaining metabolic homeostasis and ensuring
the efficient utilization of glucose-derived pyruvate. It allows for the coordination of energy production
with the cellular demands and the availability of substrates, ensuring a balanced supply of acetyl-CoA
for the citric acid cycle.
2.4. Explain how glucose-6-phosphate dehydrogenase provides an evolutionary advantage in some
circumstances. Include an example to substantiate your
Glucose-6-phosphate dehydrogenase (G6PD) evolutionary advantage:
Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme involved in the pentose phosphate pathway, a
metabolic pathway that generates reducing equivalents in the form of NADPH and produces ribose-5-
phosphate for nucleotide synthesis. G6PD deficiency is a genetic condition that affects the activity of this
enzyme and is most commonly found in populations with a history of malaria exposure. Here's how G6PD
provides an evolutionary advantage:
1. Protection against Malaria: G6PD deficiency offers protection against malaria, a parasitic disease
transmitted by mosquitoes. The Plasmodium parasite responsible for malaria relies on the
availability of reactive oxygen species (ROS) to survive and replicate within red blood cells. G6PD
@scienceratutors
, BCH3702 - UNISA
Question 2 [32]
2.1. Illustrate how ATP is generated in glycolysis. (10)
ATP (adenosine triphosphate) is generated during the process of glycolysis, which is the initial step in the
breakdown of glucose to produce energy in the form of ATP. The overall process of glycolysis occurs in the
cytoplasm of cells and can be divided into two main phases: the energy investment phase and the energy
payoff phase. Here is a step-by-step illustration of how ATP is generated in glycolysis:
1. Glucose Activation: The process begins with the activation of glucose, which requires the input of
energy in the form of two ATP molecules. Glucose is phosphorylated by the enzyme hexokinase,
using two ATP molecules, to form glucose-6-phosphate.
2. Glucose Conversion: Glucose-6-phosphate is then converted into fructose-6-phosphate through a
series of enzymatic reactions.
3. Energy Investment Phase: In this phase, fructose-6-phosphate is further phosphorylated by the
enzyme phosphofructokinase using one ATP molecule. This step converts fructose-6-phosphate
into fructose-1,6-bisphosphate.
4. Fructose-1,6-bisphosphate Cleavage: Fructose-1,6-bisphosphate is cleaved into two three-carbon
molecules called glyceraldehyde-3-phosphate (G3P) and dihydroxyacetone phosphate (DHAP).
5. Isomerization: DHAP is converted into another molecule of G3P through an isomerization reaction.
6. Energy Payoff Phase: Each G3P molecule undergoes a series of reactions that result in the
generation of ATP and NADH, which is a high-energy electron carrier.
a. G3P Oxidation: G3P is oxidized by the removal of hydrogen atoms, and NAD+ (nicotinamide
adenine dinucleotide) is reduced to form NADH. The energy released during this oxidation is used
to synthesize ATP through substrate-level phosphorylation. This process occurs twice for each
glucose molecule.
b. ATP Synthesis: For each G3P molecule, a high-energy phosphate group is transferred to ADP
(adenosine diphosphate), resulting in the synthesis of ATP. This reaction is catalyzed by the enzyme
phosphoglycerate kinase.
7. Pyruvate Formation: The final step of glycolysis involves the conversion of the remaining G3P
molecules into pyruvate. This step generates two molecules of pyruvate per glucose molecule.
Overall, during glycolysis, a net gain of two ATP molecules is generated through substrate-level
phosphorylation (step 6b), along with two NADH molecules. These ATP molecules serve as a direct source
of energy for cellular processes.
2.2. Create an illustration, and discuss in detail, the pathological condition that results from excessive
fructose consumption. (10)
Pathological condition resulting from excessive fructose consumption:
, BCH3702 - UNISA
Excessive consumption of fructose, especially in the form of high-fructose corn syrup (HFCS) found in many
processed foods and sugary beverages, can lead to a pathological condition known as fructose
malabsorption or fructose intolerance. Fructose malabsorption occurs when the small intestine is unable
to effectively absorb and process fructose, leading to a range of digestive symptoms and potential long-
term health complications.
When excessive amounts of fructose are consumed, the small intestine's capacity to absorb fructose can
be overwhelmed, resulting in the following mechanisms and consequences:
1. Impaired Fructose Absorption: The intestine normally absorbs fructose through a specific carrier
protein called GLUT5. However, in fructose malabsorption, the transport system becomes
saturated, and excess fructose remains in the intestinal lumen.
2. Osmotic Effect: The unabsorbed fructose in the intestine attracts water, leading to an osmotic
effect. This can result in symptoms like diarrhea, bloating, abdominal pain, and flatulence.
3. Bacterial Fermentation: The unabsorbed fructose is fermented by bacteria in the large intestine,
leading to the production of short-chain fatty acids and gases, such as hydrogen, methane, and
carbon dioxide. These fermentation byproducts can contribute to additional symptoms like
bloating, gas, and discomfort.
4. Altered Gut Microbiota: The fermentation of fructose by gut bacteria can also lead to changes in
the composition of the gut microbiota. This imbalance in the gut flora may have broader
implications for overall gut health and immune function.
5. Metabolic Effects: Excessive fructose consumption can also contribute to metabolic dysregulation.
Fructose is metabolized primarily in the liver, where it can be converted into triglycerides, leading
to increased fat accumulation and potentially contributing to non-alcoholic fatty liver disease
(NAFLD). Furthermore, fructose consumption can disrupt insulin signaling, contributing to insulin
resistance and potentially increasing the risk of developing type 2 diabetes.
It's important to note that fructose malabsorption is different from hereditary fructose intolerance, which
is a rare genetic disorder caused by a deficiency in the enzyme aldolase B, responsible for metabolizing
fructose. Hereditary fructose intolerance can result in severe symptoms and can be life-threatening if not
properly managed.
2.3. Discuss in detail how the pyruvate complex is regulated. (7)
Regulation of the pyruvate complex:
The pyruvate complex refers to a group of enzymes that play a crucial role in the conversion of pyruvate,
a product of glycolysis, into acetyl-CoA, which enters the citric acid cycle (also known as the Krebs cycle)
for further energy production. The pyruvate complex is regulated through several mechanisms to maintain
an appropriate balance between pyruvate metabolism and energy needs within the cell. Here are the key
regulatory aspects:
1. Substrate Availability: The first level of regulation occurs through the availability of substrates.
Pyruvate is produced as a result of glycolysis, and the rate of pyruvate formation is influenced by
, BCH3702 - UNISA
the activity of glycolytic enzymes and glucose availability. Factors that affect glycolysis, such as
glucose levels and hormonal regulation, indirectly influence the pyruvate complex's activity.
2. Pyruvate Dehydrogenase (PDH) Kinase: PDH kinase is an enzyme that phosphorylates and
inactivates the pyruvate dehydrogenase complex (PDC). When PDH kinase is active, it leads to the
phosphorylation of PDC, reducing its activity. This phosphorylation inhibits the conversion of
pyruvate into acetyl-CoA, thereby regulating the flux of pyruvate. PDH Phosphatase: In contrast to
PDH kinase, PDH phosphatase is an enzyme that dephosphorylates and activates the pyruvate
dehydrogenase complex. When PDH phosphatase is active, it removes the phosphate group from
PDC, promoting its activity and allowing the conversion of pyruvate to acetyl-CoA.
3. Allosteric Regulation: The activity of the pyruvate complex is also regulated by allosteric effectors.
One of the key allosteric regulators is acetyl-CoA itself. When the concentration of acetyl-CoA is
high, it inhibits the activity of the pyruvate complex, preventing further conversion of pyruvate
into acetyl-CoA. This mechanism helps to regulate the production of acetyl-CoA according to the
cellular energy status.
4. Feedback Inhibition: The pyruvate complex can be regulated by feedback inhibition. High levels of
NADH, an indicator of abundant energy supply, can inhibit the complex. NADH acts as a feedback
inhibitor, reducing the activity of the pyruvate complex and slowing down the conversion of
pyruvate to acetyl-CoA.
5. Hormonal Regulation: Hormones such as insulin and glucagon can also modulate the activity of
the pyruvate complex. Insulin promotes the dephosphorylation and activation of the complex,
facilitating the conversion of pyruvate to acetyl-CoA for energy production. Glucagon, on the other
hand, inhibits the pyruvate complex, favoring alternative pathways for glucose metabolism, such
as gluconeogenesis.
The regulation of the pyruvate complex is crucial for maintaining metabolic homeostasis and ensuring
the efficient utilization of glucose-derived pyruvate. It allows for the coordination of energy production
with the cellular demands and the availability of substrates, ensuring a balanced supply of acetyl-CoA
for the citric acid cycle.
2.4. Explain how glucose-6-phosphate dehydrogenase provides an evolutionary advantage in some
circumstances. Include an example to substantiate your
Glucose-6-phosphate dehydrogenase (G6PD) evolutionary advantage:
Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme involved in the pentose phosphate pathway, a
metabolic pathway that generates reducing equivalents in the form of NADPH and produces ribose-5-
phosphate for nucleotide synthesis. G6PD deficiency is a genetic condition that affects the activity of this
enzyme and is most commonly found in populations with a history of malaria exposure. Here's how G6PD
provides an evolutionary advantage:
1. Protection against Malaria: G6PD deficiency offers protection against malaria, a parasitic disease
transmitted by mosquitoes. The Plasmodium parasite responsible for malaria relies on the
availability of reactive oxygen species (ROS) to survive and replicate within red blood cells. G6PD
