Energy Production: Carbohydrate 2 Flashcards
(31 cards)
What are some important intermediates in glycolysis?
Glycerol phosphate which lays the foundation for biosynthesis for fats.
2,3-biphosphoglycerate which is produced in red blood cells and is an important regulator of haemoglobin O2 affinity. An increased level of 2,3-biphosphoglycerate decreases the affinity for O2 and promotes release.
Why is glycerol phosphate an important intermediate of glycolysis?
DHAP goes to glycerol phosphate with the oxidation of NADH.
Glycerol phosphate is important in synthesis of triglycerides and phospholipids
Where is DHAP converted into glycerol phosphate?
In adipose tissue and in the liver. This means that lipid synthesis in liver requires glycolysis.
What happens if all NAD+ is used up in glycolysis?
It stops because no more NADH can be produced.
Where does NAD+ regenerate then?
It is converted from NADH in stage 4 of metabolism (electron transport chain).
Why is this a problem in red blood cells?
Because of the red blood cells not having any mitochondria RBCs have no stage 3 and 4 and NAD+ is no regenerated by stage 4. Therefore NAD+ needs to be regenerated via some other route.
What other route of NAD+ regeneration do RBCs use?
Via lactate production. Lactate dehydrogenase also called LDH is used:
NADH+H+ + pyruvate -> NAD+ and lactate
Where is lactate produced?
In RBCs and skeletal muscle (skin, brain and GI)
Where can you find lactate?
It is released into the blood.
Where is lactate metabolised?
Usually by the liver and heart but also kidneys.
Why would lactate be produced from pyruvate in skeletal muscle instead of pyruvate going into acetyl CoA and then TCA cycle and electron transport chain?
Due to a lack of oxygen. Pyruvate is then converted into NAD+ and lactate so NAD+ can be used again in glycolysis.
Why is lactate metabolised in the liver and heart?
Heart as a use for energy.
Liver to form pyruvate again and there make more glucose from gluconeogenesis to transport it to the tissue again and use it for glycolysis.
What is an elevated level of plasma lactate concentration called?
Hyperlactaemia. This is at 2-5mM. There is no change in blood pH at this rate.
Lactic acidosis is an even more elevated level of concentration above 5mM. This is above the renal threshold so lactate levels stack up. This causes the blood pH to be lowered. This can be very troublesome as a lower pH means enzymes do not work properly.
Glucose is turned into G-6-P then G-3-P and then Pyruvate. Where does fructose, galactose, glycogen and lactate play part in that pathway?
Fructose is directly turned into G-3-P.
Galactose is first turned into G-1-P and then into G-6-P.
Glycogen is first turned into G-1-P and then into G-6-P.
Lactate is turned into Pyruvate.
Briefly outline the pathway of Fructose into G-3-P.
Fructose turns into fructose-1-P by fructokinase. Aldolase then converts fructose-1-P to glyceraldehyde and DHAP which are then converted into G-3-P.
How is fructose metabolism of clinical importance?
Essential fructosuria:
Fructokinase is missing.
Fructose intolerance:
Aldolase is missing.
What are some side effects of essential fructosuria?
The only side effect is fructose in the urine. Because fructokinase is missing fructose never undergoes it reaction to enter glycolysis. It just exits the body. There are no clinical signs.
What are some side effects of fructose intolerance?
This is a bit more serious because fructose has already started undergo the reaction to enter glycolysis. The fructokinase step is an irreversible step so there is now a build up of fructose-1-P in the liver. This can lead to liver damage.
Briefly outline the pathway of galactose into glucose-1-P.
Lactose is broken down into glucose and galactose. Galactose is then via galactosekinase converted into Galactose-1-P. Uridyl transferase then converts it into glucose-1-P.
There is another pathway for galactose than glucose-1-P. Which?
Galactose-1-P can turn into UDP-Galactose then UDP-Glucose and finally glycogen.
Galactose-1-P turns into UDP-galactose via UDP-galactose epimerase.
Which of these enzymes can cause galactosaemia?
Any of the three.
Galactokinase
Uridyl transferase
UDP-galacto epimerase
What is galactosaemia?
An inability to utilise galactose.
In galactokinase deficiency galactose will acculumulate
In transferase deficiency galactose and galactose-1-P will accumulate.
Why is galactosaemia a problem?
The accumulation of galactose means that it will enter another pathway. This pathway is that galactose turns into galactitol via aldose reductase and the oxidation of NADPH to NADP+.
What are the consequences of galactose being converted into galactitol?
NADPH is used up which should be used for biosynthesis. The release of the H+ also causes inappropriate disulphide bond formation. This causes loss of structural and functional integrity of some proteins that depend on free -SH groups like the lens of the eye.
This causes cataracts.
