T2 L10: regulation and carbohydrate metabolism

Question 1

Where does gluconeogenesis occur?

Answer 1

In the liver and kidneys

Question 2

What are the 2 requirements for gluconeogenesis?

Answer 2

A source of carbon and a source of energy

Question 3

What are the sources of carbon for gluconeogenesis?

Answer 3

Lactate, amino acids or glycerol released from triglycerides by lipolysis in adipose tissue

Question 4

What is the energy source for gluconeogenesis?

Answer 4

Provided by the metabolism of fatty acids (beta-oxidation generates ATP)

Question 5

What is ammonia converted to in the liver?

Answer 5

Urea and then passed out of the bloodstream through urine

Question 6

What is fumarate converted to?

Answer 6

Into oxaloacetate in the cytoplasm

Question 7

What is the equation for the production of urea?

Answer 7

NH3 + CO2 + 2H2O + 3ATP + aspartate = urea + fumarate +2ADP + AMP + 2Pi + PPi

Question 8

Which molecules allosterically regulate PFK-1?

Answer 8

Subject to energy dependent allosteric regulation by ATP, AMP, H+, Fru-6-P, Fru-2,6-BP and Citrate

Question 9

What’s meant by allosteric regulation?

Answer 9

Regulation of enzymes by molecules present in the cell

Question 10

Why does ATP allosterically inhibit PFK-1?

Answer 10

Because it’s a sign of high energy levels in muscles.

Question 11

Why does AMP allosterically active PFK-1?

Answer 11

It’s a sign of low energy in muscles

Question 12

What is anoxia?

Answer 12

insufficient O2 supply

Question 13

Why does H+ allosterically inhibit PFK-1?

Answer 13

[H+] increases during anoxia or anaerobic respiration so it inhibits glycolysis to prevent the pH from falling too low and from damaging the cells

Question 14

What can overcome high [H+] in cardiac muscle so it continues beating?

Answer 14

High AMP levels. This results in cellular damage and angina but the heart can’t stop beating

Question 15

How does Fru-6-P allosterically control PFK-1?

Answer 15

Fru-6-P activates PFK-1 because it’s a sign of high glucose levels so glycolysis is stimulated to use up that glucose

Question 16

How does Fru-2,6-BP allosterically control PFK-1?

Answer 16

Fru-2,6-BP activates PFK-1 because it’s a sign of high glucose levels so glycolysis is activated to use up that glucose

Question 17

Which molecule is the most potent allosteric activator known in glucose metabolism?

Answer 17

Fru-2,6-BP

Question 18

Hoe does Citrate allosterically control PFK-1?

Answer 18

Citrate inhibits PFK-1. Its a sign of that there is more CoA that can be oxidised like in starvation so glucose is conserved

Question 19

Why do all cells have PFK-1, PFK-2, and F-2,6-BPase?

Answer 19

Because all cells require glucose

Question 20

Why do only liver and kidney cells have F-1,6-BPase?

Answer 20

Because that’s where gluconeogenesis takes place. F-1,6-BPase is an enzyme for gluconeogenesis

Question 21

What is fructose-2,6-phosphate synthesised from and using which enzyme?

Answer 21

From fructose-6-phosphate using PFK-2

Question 22

Which molecule is the most potent allosteric inhibitor of PFK-1?

Answer 22

Fructose-2,6-phosphate

Question 23

What does cAMPPK do?

Answer 23

It activates F-2,6-BPase and deactivates PFK-2

Question 24

Which 2 enzymes involved in glycolysis are attached and are the same molecule?

Answer 24

PFK-2 and F-2,6-BPase. Phosphorylation inhibits PFK-2 and stimulates F-2,6-BPase

Question 25

What does PFK-2 do?

Answer 25

Synthesises F-2,6-BP

Question 26

What stimulates gluconeogenesis in the short term?

Answer 26

Adrenaline and glucagon

Question 27

How is gluconeogenesis inhibited in the short-term?

Answer 27

Insulin

Question 28

What stimulates gluconeogenesis in the long term?

Answer 28

Glucagon, glucocorticosteroids, and thyroid hormones