Metabolism V

Question 1

How to ATP synthase inhibitors poison the ETC?

Answer 1

Directly inhibit mitochondrial ATPsynthase causing an increased proton gradient. ATP cant be produced because electron transport stops alltogether (p.102)

Question 2

Name one ATP synthase inhibitor.

Answer 2

Oligomycin (p.102)

Question 3

How to ATP uncoupling agents poison the ETC?

Answer 3

Increase the permeability of the membrane causing a decreased proton gradient and increased oxygen consumption. ATP synthesis stops but electron transport continues and heat is produced (p.102)

Question 4

Give three examples of an ETC uncoupling agent.

Answer 4

2,4-DNP, aspirin (fevers often accompany asprin overdose), thermogenin in brown fat (p.102)

Question 5

Name the four irreversible enzymes in gluconeogenesis.

Answer 5

Pyruvate carboxylase, PEP carboxykinase, Fructose 1,6-bisphosphatase, Glucose-6-phosphatase (p.102)

Question 6

What reaction is catalyzed by pyruvate carboxylase and where does the reaction occur?

Answer 6

Pyruvate –> oxaloacetate. Reaction occurs in the mitochondria (p.102)

Question 7

What reaction is catalyzed by PEP carboxykinase and where does the reaction occur?

Answer 7

Oxaloacetate –> Phosphoenolpyruvate. Reaction occurs in the cytosol (p.102)

Question 8

What reaction is catalyzed by Fructose-1,6-bisphosphatase and where does the reaction occur?

Answer 8

Fructose-1-6-bisphosphate –> fructose-6-P. Reaction occurs in the cytosol (p.102)

Question 9

What reaction is catalyzed by Glucose-6-phosphatase and where does the reaction occur?

Answer 9

Glucose 6-Phosphate –> Glucose. Reaction occurs in the ER (p.102)

Question 10

What two cofactors are required by Pyruvate carboxylase?

Answer 10

Biotin, ATP (p.102)

Question 11

What cofactor is required by PEP carboxykinase?

Answer 11

GTP (p.102)

Question 12

What activates Pyruvate carboxylase?

Answer 12

Acetyl CoA (p.102)

Question 13

Where does gluconeogenesis primarily occur?

Answer 13

In the liver; enzymes also found in the kidney and intestinal epithelium (p.102)

Question 14

What results from a deficiency of the key gluconeogenic enzymes?

Answer 14

Hypoglycemia (p.102)

Question 15

Why can’t muscle participate in gluconeogenesis?

Answer 15

Muscles lack glucose-6-phosphatase (p.102)

Question 16

What is the product of odd chain fatty acids during metabolism?

Answer 16

Produces propionyl CoA which can directly enter the TCA cycle as succinyl CoA to undergo gluconeogeneis and serve as a source of glucose (p.102)

Question 17

Why can’t even chain fatty acids produce glucose?

Answer 17

Because they yield two acetyl coA equivalents and no propionyl coA (p.102)

Question 18

What are the products of the HMP shunt (pentose phosphate pathway)?

Answer 18

Provides a source of NADPH from abundantly available glucose-6-phosphate. Also provides ribose for nucleotide synthesis and glycolytic intermediates (p.103)

Question 19

What is NADPH used for in metabolism?

Answer 19

NADPH is required for reductive reactions including glutathione reduction inside RBCs (p.103

Question 20

How can the two phases of the pentose phosphate pathway be classified?

Answer 20

Oxidative and nonoxidative (p.103)

Question 21

Where does the HMP shunt occur?

Answer 21

In the cytoplasm (p.103)

Question 22

How much ATP is used and produced in the HMP shunt?

Answer 22

No ATP is used or produced (p.103)

Question 23

In what tissues does the HMP shunt occur?

Answer 23

Lactating mammary glands, liver, adrenal cortex (sites of fatty acid or steroid synthesis), RBCs (p.103)

Question 24

Describe the oxidative reaction in the HMP shunt.

Answer 24

Glucose-6-phosphate is converted to 2NADPH and Ribulose-5-P by glucose-6-P dehydrogenase. This is the rate limiting step (p.103)

Question 25

Is the oxidative reaction of the HMP shunt reversible or irreversible?

Answer 25

Irreversible (p.103)