Flashcards in 5. Energy Production - Carbohydrates (b) Deck (29)
How do high NADH levels regulate glycolysis?
They signal high energy levels so there is product inhibition of step 6, which inhibits glycolysis.
Activator or inhibitor binds at another site.
What are the two ways in which enzymes can be inhibited?
Allostery and covalent modification.
What are the key steps affected by allosteric regulation in glycolysis?
1, 3 and 10.
How is step 1 of glycolysis regulated?
By the enzymes hexokinase. It has decreased action if glucose 6-phosphate are too high due to product inhibition.
How is step 3 of glycolysis regulated?
By the enzyme phosphofructokinase-1. In the muscles, it has decreased action, and therefore inhibits glycolysis, if the ATP:AMP ratio is high. In the liver, it has increase action, and therefore stimulates glycolysis, if there is a high insulin: glucagon ratio.
How is step 10 of glycolysis regulated?
By the enzyme pyruvate kinase. It is stimulated by a high insulin: glucagon ratio.
How could product inhibition of step 6 of glycolysis occur?
If there was no NAD+ regenerated and lots of NADH produced.
What two ways can NAD+ be regenerated?
In stage four of metabolism or by lactate dehydrogenase.
How can lactate be utilised?
NAD+ + lactate -> NADH + H+ + pyruvate.
What can raise lactate levels?
Strenuous exercise, shock or congestive heart disease.
Why does hyperlactaemia not have any affect on the blood pH but lactic acidosis does?
Because hyperlactaemia means the levels of lactate (2-5mM) are below the renal threshold, whereas with lactic acidosis, the levels of lactate (>5mM) are above the renal threshold so lowers pH.
What is the cause of fructosuria?
Absence of fructokinase.
What is the cause of fructose intolerance?
Absence of aldolase. This means fructose 1-P accumulates in the liver causing liver damage.
How can fructose intolerance be treated?
Remove fructose from the diet.
Describe the outline of fructose metabolism.
Describe the outline of galactose metabolism.
| galactose-1-P uridyl transferase
What is the incidence of galactosaemia?
What are the two causes of galactosaemia?
Galactokinase deficiency (rare) or galactose-1-P uridyl transferase deficiency (common).
What accumulates as a result of a galactokinase deficiency?
What accumulates as a result of a galactose-1-P uridyl transferase deficiency?
Galactose and galactose-1-P.
What problems arise from an accumulation of galactose?
It enters another pathway:
Galactose + NADPH --> galactitol + NADP+
This leads to depletion of NADPH stores, meaning free sulphydryl groups on proteins aren't maintained. Inappropriate disulphide bond formation occurs which means there is loss of structural and functional integrity of proteins that depend on free -SH groups so cataracts form.
What problems arise form an accumulation of galactose-1-P?
It affects the liver, kidney and brain.
How is galactosaemia treated?
Remove lactose from the diet.
What are the two stages of the pentode phosphate pathway?
Oxidative decarboxylation and rearrangement to glycolytic intermediates.
What does the rate of the pentose phosphate pathway depend on?
The NADP+:NADPH ratio at G6P dehydrogenase.
What are the two key roles of NADH?
Biosynthetic reducing power and maintaining free -SH groups on certain proteins to prevent oxidation.
What are the implications of a glucose-6-phosphate deficiency?
The pentode phosphate pathway will be inhibited so there is a reduced amount of NADPH so free -SH groups aren't always maintained which could lead to cataracts.