GLYCOLYSIS Flashcards
what is glycolysis
- Glycolysis is the major enzymic pathway for the utilisation of carbohydrates, particularly glucose, that produces energy in the form of adenosine triphosphate (ATP)
- BREAK DOWN of GLUCOSE
- catabolism
what is the end product of glycolysis
pyruvate
Where does glycolysis occur
- solute cytoplasm (cytosol) of all cells
what are the pathways of pyruvate in aerobic and anaerobic glycolysis
- In the presence of oxygen (aerobic conditions): Pyruvate can be converted to acetyl CoA via pyruvate dehydrogenase
- In the absence of oxygen (anaerobic conditions): Pyruvate is converted to lactate via lactate dehydrogenase
what is the main process of glycolysis
breaking C6 into to 2 C3 intermediates
- C6 phase = investment phase
- C3 = yield phase
why is it called the investment phase
- hexokinase uses 1 ATP
phosphofructokinase uses 1ATP
= -2ATP
Why is it called the yeild phase
- Phosphoglycerate kinase = + 1ATP
- phosphoglycerate mutase = +1ATP
both occur twice, once in each 3C substrate = +4ATP
How much ATP is yielded in total during glycolysis
-2 + 4 = +2ATP
how is glycolysis regulated
Regulatory steps:
1. Physiologically irreversible:
Hexokinase, PKF1 and pyruvate kinase don’t reverse (these are the ones to learn, don’t learn other ones)
- Allosterically regulated
Why is hexokinase irriversible? explain what glucokinase is
- phosphorylates glucose, now impermeable to cell wall so can’t get back out
- controlled allosterically by its product
- can be called glucokinase in liver of humans which is needed because hexokinase can’t deal with the volume of sugar coming into the liver -> does same thing but faster and in first order (dependent on glucose conc)
what are the irriversible steps of glycolysis
- hexokinase
- PFK1
- pyruvate kinase (last step)
Why is PFK1 irreversible? how is it regulated
- adding phosphate -> anchored again
Inhibition:
- Allosteric: ATP, citrate, H+
- ATP - enough energy = slow down
- H+ - sprinting decreases glycolysis
Stimulation:
- Allosteric: Frutose 2,6-biphosphate,
- AMP
What does Fructose 2,6 bisphosphate do to PFK1
- stimulates PFK1
- fructose is produced by PFK2 to activate PFK1
how is pyruvate kinase regulated
Inhibition
- Allosteric: ATP and alanine
- Covalent: Glucagon (via cAMP-depentant protein kinase)
Stimulation:
- Allosteric: Fructose 1,6-biphosphate (feed forward control)
- The activity is also regulated by covalent modulation through glucagon which leads to phosphorylation and subsequent inhibition of pyruvate kinase
differences between hexokinase and glucokinase
- Hexokinase is inhibited allosterically by its product, glucose 6-P. Glucokinase is not regulated by G 6-P but is specific for glucose.
- Hexokinase is non-specific but prefers glucose to other hexoses. Glucokinase is specific for glucose.
- Hexokinase Km is 20 μM; glucokinase Km is 12 mM.
- Glucokinase concentration is regulated by the amount of carbohydrate in the non-rurnmant diet -> first order
What is the final electron recpetor of anaerobic glycolysis?
lactate -> made by converting pyruvate with lactate dehydrogenase enzyme (reversible) if no O2
- this recycles NADH into NAD+
What is the final electron acceptor of aerobic glycolysis
- oxygen
What happens to pyruvate in aerobic conditions
pyruvate converted to Acetyl coA via pyruvate dehydrogenase (irriversible) in mitochondria
what happens to pyruvate dehydrogenase during starvation?
- want to turn this off during starvation so glucose is conserved -> if its active, irreversibly turns pyruvate into acetyl coA -> inhibited by fatty acids producing acetyl coA when starving because fat is mobilised into fatty acids
- also regulated covalently by adding P via
how is Pyruvate dehydrogenase regulated
- End product inhibition -> inhibited by fatty acids producing acetyl coA when starving because fat is mobilised into fatty acids
also regulated covalently by adding P via
covalent modulation:
- PDH kinase inhibits -> activated by high acetyl coA (fatty acids cause increase from fa mobilisation), NADH also produced by fatty acid breakdown from fat
- PDH phosphatase activates -> insulin produced when high levels of glucose, causes phosphate to be removed from Pyruvate dehydrogenase so TCA cycle can begin
- calcium released during contraction, need more energy so increases TCA
