Exam 1 Flashcards
2009
The ΔG’º for hydrolysis of ATP is -30.5 kJ/mole. The ΔG’º for hydrolysis of PEP is -61.9 kJ/mole. The ΔG’º for the following reaction is:
PEP + ADP ⇔ Pyruvate + ATP
- -92.4 kJ
- +31.4 kJ
- -31.4 kJ
- +92.4 kJ
- cannot be determined from data provided
-31.4 kJ
( -61.9 - (-30.5) = -31.4 )
2009
For A ⇔ B, ΔG’º is negative.
- The rate of reaction of B to A is increased
- The rate of reaction of B to A is decreased
- The rate of reaction of B to A is dependent on the magnitude of ΔG’º
- The rate of reaction is not influenced by the sign of magnitude of ΔG’º
- There is no reaction at all in either direction becase it is at equilibrium
The rate of reaction is not influenced by the sign of magnitude of ΔG’º
2009
ln K (K equilibrium constant) is equal to
- RT ΔG’º
- RT ΔG’º
- ΔG’º/RT
- ΔG’º/RT
- ΔG’ºT/R
- ΔG’º/RT
( ΔG’º = -RT ln K)
2009
ΔG’º (under cellular conditions) for ATP hydrolysis is -50 kJ/mole and 4000 kJ our caloric intake (in 24 hours) is used for synthesis ATP. The amount of ATP formed by a human in 24 hours is (MW ATP ≈ 500)
- ≈ 6g
- 80g
- 0
- -40 Kg
- ATP is only hydrolized
-40 Kg

2009
In glycolysis ATP synthesis is catalyzed by
- 6-phosphofructo-1 kinase
- hexokinase
- phosphoglycerate kinase
- glyceraldehyde 3-phosphate dehydrogenase
- none of the above
phosphoglycerate kinase
2009
The irreversible reactions of glycolysis include that catalyzed by
- phosphoglycerate kinase
- fructose biphosphate aldolase
- 6-phosphofructo-1-kinase
- glyceraldehyde 3-phosphate dehygrogenase
- phosphoglucose isomerase
6-phosphofructo-1-kinase
2009
6-Phosphofructo-1-kinase activity can be decreased by all of the following EXCEPT
- low pH
- AMP
- decreased concentration of fructose 2,6-bisphosphate
- ATP at high concentrations
- citrate
AMP
2009
Which of the following supports gluconeogenesis?
- lysine degradation
- leucine degradation
- acetyl CoA + oxaloacetate + H2O ⇔ citrate + CoA
- pyruvate + ATP + HCO3 ⇔ oxaloacetate + ADP + Pi + H+
- α-ketoglutarate + aspartate ⇔ glutamate + oxaloacetate
pyruvate + ATP + HCO3 ⇔ oxaloacetate + ADP + Pi + H+
2009
In the Cori Cyle
- glucose is converted to pyruvate/lactate in anaerobic (i.e. red blood cells) tissues, and this pyruvate/lactate return to the liver, where it is converted to glucose
- nitrogen from alanine must be converted to urea, increasing the amount of energy required to drive the process
- only tissues with aerobic metabolism (i.e. mitochondria and O2) are involved
- the same amount of ATP is used in the liver to synthesize glucose as it is released during glycolysis, leading to no net efect on whole-body energy balance
- a three-carbon compound arising from glycolysis is converted to glucose at the expense of energy from fatty acid oxidation
glucose is converted to pyruvate/lactate in anaerobic (i.e. red blood cells) tissues, and this pyruvate/lactate return to the liver, where it is converted to glucose
2009
Gluconeogenic enzymes include all of the following EXCEPT
- phosphoenolpyruvate carboxykinase
- pyruvate carboxylase
- fructose 1,6-bisphosphatase
- phosphogucmutase
- glucose 6-phosphatase
phosphogucmutase
(only in glycolysis)
2009
Phospho-dephospho regulation of, 6-phosphofructo-2-kinase, and pyruvate kinase is an important regulatory mechanism in
- skeletal muscle
- liver
- intestine
- erythrocytes
- brain
liver
(where glycolysis occurs)
2009
Phosphorylation-dephosphorylation and allosteric activation of enzymes play roles in stimulating glycogen degradation. All of the following result in enzyme activation EXCEPT
- Phosphorylation of Phosphorylase kinase
- Phosphorylation of protein kinase A
- binding of AMP to Phosphorylase b
- Phosphorylation of Phosphorylase
- dePhosphorylation of glycogen synthase
Phosphorylation of protein kinase A
2009
Glucose 6-phosphatase, which is deficient in Von Glerke’s disease, is necessary for the production of blood glucose from
- fructose
- galactose
- amino acid carbon chains
- liver glycogen
- all of the above
all of the above
2009
Glucose labeled at C-1 is incubated with glycolytic enzymes and necessary cofactors. The pyruvate CH3COCOO- that is formed will be labeled at
- C-1
- C-2
- C-3
- All C atoms
- At none of the C atoms
C-3
2009
Removal of a glucose residue from glycogen (by phosphorylase) and passing it thorugh glycolysis to 2 pyruvates yields _____ ATP
- 1
- 2
- 3
- 4
- None
3
2009
Glucose labeled at C-3 is allowed to undergo fermentation to ethanol CH3CH2OH and CO2. The label will show in
- Ethanol at C-1 only
- Ethanol at C-2 only
- CO2 only
- Both A and C
- Both B and C
CO2 only
2009
The conversion of 1 mol of fructose 1,6-biphosphate to 2 mol of pyruvate by the glycolytic pathway results in a net formation of:
- 2 mol of NADH and 2 mol of ATP
- 1 mol of NADH and 1 mol of ATP
- 2 mol of NADH and 4 mol of ATP
- 1 mol of NAD+ and 2 mol of ATP
- 2 mol of NAD+ and 4 mol of ATP
2 mol of NADH and 4 mol of ATP
2009
Which of the following statements is true of muscle glycogen phosphorylase?
- It removes glucose residues from the reducing ends of the glycoen chains
- It exists in an active (a) form and an inactive (b) form that is allosterically regulated by AMP
- It degrades glycogen to form glucose 6-phosphate
- It catalyzes phosphorolysis of the α(1→6) bonds at the branch points of glycogen
- It degrades glycogen to glucose
It exists in an active (a) form and an inactive (b) form that is allosterically regulated by AMP
2009
Which of these enzymes is a control point, regulated by the cell’s energy supply?
- Phosphofructokinase-1
- Glycogen phosphorylase
- Pyruvate kinase
- All of the above are control points
- None of the above is a control point
All of the above are control points
2009
The main function of the pentose phosphate pathway is to
- Supply pentoses and NADPH
- Give the cell an alternate pathway should glycolysis fail
- Supply NADH
- Provide a mechanism for the utilization of the carbon skeletons of excess amino acids
- Supply energy
Supply pentoses and NADPH
2009
Which of the following describes fatty acid transport into the mitochondrial matrix?
- It is the rate-limiting step in fatty acid oxidation
- It is regulated by malonyl-CoA
- The cytosolic and matrix pools of CoA are distince and separate
- Once fatty acyl groups have entered the matrix, they are committed to oxidation to acetyl-CoA
- All of the above are true
All of the above are true
2009
Fatty acid synthase of mammalian cells
- uses a four-step sequence to lengthen a growing fatty acyl chain by one carbon
- contains ACP, which carries acyl groups attached through thioester linkages
- requires chemical energy in just one form, the reducing power of NADPH
- is activated by glucagon and epinephrine
- is activated by palmitoyl CoA, the principal product of fatty acid synthesis
contains ACP, which carries acyl groups attached through thioester linkages
2009
How are fatty acid oxidation and synthesis controlled so that futile cycling (when two opposing reactions/pathways occurring in the same location and at the same time, one forming an energy-rich compound, the other consuming an energy-rich compound) does not occur?
- A - they occur in different cellular compartments
- B - they employ different electron carriers
- C - the product of the first oxidation reaction inhibits the rate-limiting step of biosynthesis
- A and B
- A, B, and C
A and B
2009
In mammmalian cells, fatty acid synthesis occurs in the cytosol. The beginning subsrate for this series of reaction is acetyl-CoA, which is formed in the mitochondrial matrix. How does the acetyl-CoA move from matrix to cytosol?
- Acetyl-CoA reacts with oxaloacetate and leaves the matrix as citrate via the citrate transporter
- Acetyl-CoA combines with bicarbonate and is transported out of the matrix as pyruvate
- There is a specific transport protein for acetyl-CoA
- Acetyl-CoA is a nonpolar molecule and can diffuse across all membranse
- Inner and outer mitochondrial membranes are freely permeable to Acetyl-CoA due to the presence of transmembrane pore or channels.
Acetyl-CoA reacts with oxaloacetate and leaves the matrix as citrate via the citrate transporter






