Bob's 3

Question 1

Name two important intermediates of glycolysis?

Answer 1

Glycerol phosphate which is used in triglyceride and phospholipid synthesis. Also 2-3 bisphosphoglycerate which is used to regulate haemoglobin O2 affinity.

Question 2

What would cause glycolysis to stop?

Answer 2

Low NAD+ levels.

Question 3

When is NAD+ regenerated from NADH?

Answer 3

Stage 4 of metabolism

Question 4

Why do we need another route to regenerate NADH?

Answer 4

NADH regeneration happens in stage 4 of metabolism which doesn’t occur in RBC’s for example. Stage 4 of metabolism also requires oxygen which isn’t always available in certain tissues like muscles.

Question 5

What two ways do we have of regenerating NADH?

Answer 5

Stage 4 metabolism or using lactate dehydrogenase.

Question 6

When do you get lactate production?

Answer 6

When there isn’t enough oxygen and when metabolism is under stress for example in a fuel overload.
Also during pathological situations like shock and congestive heart disease and during strenuous exercise.

Question 7

What happens in the lactate dehydrogenase reaction?

Answer 7

Pyruvate and NADH are converted to lactate and NAD+.

Question 8

When lactate is produced in the body where is it metabolised?

Answer 8

In the liver and heart which always have a steady oxygen supply. Here the reaction reverses so lactate and NAD+ become pyruvate and NADH.

Question 9

What is the difference between hyperlactaemia and lactic acidosis?

Answer 9

Hyperlactaemia is where you have a high lactate of between 2-5 mM, however this is below renal threshold and can be managed to prevent blood pH from decreasing. Lactic acidosis on the other hand is where the concentration is greater than 5mM and above renal threshold so blood pH is lowered. This along with a low pH IS A CLINICAL MARKER OF A CRITICALLY ILL PATIENT.

Question 10

Name two clinical problems associated with fructose metabolism?

Answer 10

Essential fructosuria- missing fructokinase enzyme, fructose not metabolised and simply passes through body and gives no clinical problem.

Fructose intolerance- no aldolase enzyme so fructose-1-P accumulates and damages liver, prevent by removing fructose from the body.

Question 11

What is lactose made from?

Answer 11

Galactose and glucose

Question 12

What are the two fates of galactose in the diet?

Answer 12

Will either go through glycolysis or become glycogen

Question 13

What is a galactose build u in the diet called?

Answer 13

Galactosaemia

Question 14

What happens to galactose in galactosaemia?

Answer 14

Galactose will be converted to galactitol using NADPH and the H+ ions released can cause disulphide bonds to form between proteins and cataracts of the eye can result.

Question 15

What is galactitol?

Answer 15

The substance formed from galactose if

Question 16

Where do fructose and galactose enter glycolysis?

Answer 16

Early on before pyruvate formation

Question 17

What is the purpose of the penthouse phosphate pathway?

Answer 17

It synthesises 5 carbon sugars for DNA and RNA, nucleotides, coenzymes and produces NADPH. It occurs when we are well fed.

Question 18

What controls whether pentose phosphate pathway will occur?

Answer 18

High NADPH to NAD+ ratio at g6p dehydrogenase

Question 19

Where does the penthouse phosphate pathway begin and what enzyme starts it?

Answer 19

With glucose-6-P and glucose-6-p dehydrogenase.

Question 20

What is NADPH used for?

Answer 20

Fatty acid biosynthesis,steroid biosynthesis, glutathione (GSH) regeneration

Question 21

What makes penthouse phosphate pathway unidirectional?

Answer 21

The step which involves the loss of a CO2 molecule.

Question 22

Functions of pentose phosphate pathway?

Answer 22

Make NADPH which retains free SH groups on proteins and prevents disulphide bond formation.

Biosynthetic reducing power for lipid synthesis, steroid synthesis etc.

C5 sugars for DNA and RNA

Question 23

What happens with glucose 6 phosphate dehydrogenase deficiency?

Answer 23

pentose phosphate pathway wont run resulting in disulphide bond formation in lens of eye and cataracts. Consequences similar to that of galactosaemia.