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WEEK 9:
Carbohydrates 2- glucose breakdown:
| Question | Answer |
|---|---|
| NAD+/ NADH are derivatives of | niacin |
| FAD/FADH2 are derivatives of | riboflavin |
| how many stages of glycolysis | 3 (phosphorylation, splitting/ cleavage, NADH and ATP production) |
| phase 1 glycolysis | phosphorylation: 2 phosphates are added to glucose using ATP |
| phase 2 glycolysis | splitting (cleavage):6-carbon glucose split into two 3-carbon molecules |
| phase 3 glycolysis | NADH and ATP production: NAH+ reduced to NADH, ADP phosphorylated to ATP (x2), and two molecules of pyruvate are made |
| phase 1 and 2 together is also called | energy investment phase |
| glucose -> | glucose 6-P -> fructose 6-P -> fructose 1,6-bis P |
| fructose 1,6-bisphosphate -> | glyceraldehyde 3-P (using the enzyme DHAP) |
| phase 3 of glycolysis is also called | energy generation phase |
| glyceraldehyde 3- P -> | 1,3-BPG (NADH made) -> 3-PG (ATP made)-> 2-PG -> PEP (ATP made)-> pyruvate |
| why cant NAD+ be made in anaerobic conditions eg exercise | NADH cannot be oxidised to regenerate NAD+ since this requires oxygen |
| how is NAD+ regenerated in anaerobic conditions | by conversion of pyruvate to lactate |
| link reaction | pyruvate -> acetyl CoA (-CO2 and make NADH) using PDH enzyme (pyruvate dehydrogenase) |
| beri beri (thiamine/vitamin B1 deficiency) | thiamine is a cofactor for pyruvate dehydrogenase (PDH) leading to damage to peripheral nervous system and weakened muscles; cardiovascular disorders which is more common in countries where polished rice is a big part of diet |
| mercury and arsenite poisoning | bind to enzyme E2 causing CNS pathologies |
| acetyl CoA + oxaloacetate -> | citrate + CoA |
| what catalyses the first step in TCA cycle | citrate synthase |
| isocitrate + NAD+ -> | a-ketoglutarate + NADH + CO2 |
| a- ketoglutarate + CoA + NAD+ -> | succinyl CoA + NADH + CO2 |
| succinyl CoA + Pi + GDP -> | succinate + CoA + GTP |
| succinate + FAD+ -> | fumarate + FADH2 using succinate dehydrogenase |
| malate + NAD+ -> | oxaloacetate + NADH |
| end products of TCA cycle (for each molecule of acetyl CoA oxidised) | 3 NADH , 1 FASH2, 2CO2 + 1GTP |
| pyruvate dehydrogenase | multi enzyme complex with vitamin derived cofactors, CO2 release and NADH formation, and tight regulatory control |
| control of glucose in glycolysis requires how many steps | 3 |
| control of glucose in link reaction requires how many steps | 1 |
| control of glucose in TCA cycle requires how many steps | 3 |
| high ATP conc / high citrate conc leads to what effect | inhibition (favouring glycogen synthesis) |
| high AMP conc or high G6P conc leads to what effect | activation |
| which part is the overall rate limiting step in glucose metabolism | link reaction (as it controls entry of glucose in to the TCA cycle) and is an irreversible reaction so PDH is very tightly regulated allosterically, covalently, and hormonally (insulin activates) |
| how can PDH be regulated tightly | allosterically, covalently, and hormonally |
| PDH is directly inhibited by | NADH and acetyl CoA |
| PDH is activated by | PDH phosphatase |
| PDH phosphatase is activated by | Ca2+ and insulin |
| PDH kinase deactivates | PDH |
| PDH kinase is activated by | ATP, acetyl CoA and NADH |
| PDH kinase is inhibited by | pyruvate |
| glycolysis is controlled largely by | regulating PFK |
| what products from the TCA cycle provide the most energy output | reduced cofactors |
| which of the following is not a mobile metabolic intermediate | FAD/FADH2 |