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Biochemistry > Block 2 Glycolysis > Flashcards

Block 2 Glycolysis Flashcards

1
Q

Where does glycolysis occur, and what are its major products?

A

In the cytosol; ATP and pyruvate

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2
Q

What are the 2 phases of glycolysis?

A

1: preparative phase; 2: ATP-generating phase

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3
Q

What happens in the preparative phase of glycolysis?

A

Glucose is P by ATP and cleaved into 2 triose phosphates

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4
Q

What happens in the ATP-generating phase of glycolysis?

A

Triose phosphate oxidized by NAD+ and P by Pi. The phosphates are rearranged into high energy bonds so they can form ATP.

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5
Q

What is the net yield of glycolysis?

A

1 mole glucose -> 2 mol ATP, 2 NADH, 2 pyruvate

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6
Q

What are the irreversible reactions of glycolysis?

A

Glucose -> G-6P by gluco/hexokinase; F-6P -> F-1,6-bisP by PFK-1; phosphoenolpyruvate -> pyruvate by pyruvate kinase

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7
Q

What is hexo/glucokinase?

A

Convert glucose to glucose-6-phosphate. *Irreversible.

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8
Q

How does glucose-6-phosphate affect hexo/glucokinase?

A

Inhibits hexokinase, no effect on glucokinase

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9
Q

What is phosphoglucose isomerase?

A

Converts G-6P to open chain form, then open chain F-6P, then fructose-6-P

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10
Q

What is PFK-1?

A

Converts F-6P + ATP to F-1,6-BP + ADP + H+. *Irreversible, key allosterically regulated enzyme

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11
Q

What is aldolase A?

A

Converts F-1,6-BP to dihydroxyacetone-P or glyceraldehyde-3-P

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12
Q

What is triose phosphate isomerase?

A

Converts between dihydroxyacetone-P and glyceraldehyde-3-P

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13
Q

What is glyceraldehyde-3-phosphate dehydrogenase?

A

Catalyzes conversion of GA-3-P to 1,3-BP-glycerate

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14
Q

What is 3-phosphoglycerate kinase?

A

Converts 1,3-BPG to 3-PG. *Substrate level P

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15
Q

What is phosphoglyceromutase?

A

Converts 3-PG to 2-PG

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16
Q

What is enolase?

A

Converts 2-PG to phosphoenolpyruvate

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17
Q

What is pyruvate kinase?

A

Converts phosphoenolpyruvate to pyruvate. *Irreversible, substrate level P

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18
Q

What is arsenate (AsO4 3-)?

A

Similar to P in structure and reactivity, can replace P in attack of thioester intermediate; uncouples oxidation and phosphorylation by forming acyl arsenate. *Potent poison b/c resembles phosphate!

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19
Q

How does NADH get reoxidized to NAD+ to be recycled in glycolytic pathway?

A

1) e- transported back into mito by glycerol-3-P or malate-aspartate shuttle & passed to O2 in ETC
2) Lactate DH

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20
Q

What is anaerobic glycolysis?

A

NADH from glycolysis re-oxidized in cytosol by reducing pyruvate to lactate with LDH

21
Q

Why are pyruvate levels lower in the blood than lactate?

A

Equilibrium for LDH favors lactate

22
Q

What tissues depend on anaerobic glycolysis for ATP?

A

RBC, lymphocytes, leukocytes, kidney medulla, eye, skeletal muscles

23
Q

What determines the ratio of glucose oxidized to CO2 vs. anaerobic glycolysis?

A

Mitochondrial oxidative capacity and O2 supply to tissue

24
Q

What is the Cori cycle?

A

Lactate produced by exercising muscle, RBCs, etc. converted to glucose by gluconeogenic pathway in liver

25
Q

What pathway do fructose-6P, glucose-6P, and glyceraldehyde-3P feed into?

A

Become ribose-5P in pentose pathway, which provides ribose and deoxyribose for nucleotides

26
Q

What amino acids can 3-phosphoglycerate help make?

A

Serine, cysteine, glycine

27
Q

What amino acid can pyruvate be converted to? What can it become in the liver?

A

Alanine, when transaminated. In liver, pyruvate/AcCoA is a substrate for FA biosynthesis

28
Q

What can dihydroxyacetone phosphate become?

A

Glycerol-3P, backbone of TAGs and PLs

29
Q

What is 2,3-BPG?

A

A detour from glycolytic pathway; an intermediate between 1,3-BPG and 3-PG

30
Q

Why does glycolysis need to be regulated?

A

So rate of ATP generation matches rate of utilization

31
Q

What are the activators and inhibitors of PFK?

A

Activator: AMP, F-6P-BP
Inhibitor: ATP, citrate

32
Q

How does AMP activate PFK?

A

Binds allosteric site, induces conformational change to increase affinity for F-6P (separate binding site from F-2,3-bisP)

33
Q

How is hexokinase regulated?

A

Decreased flux through PFK increases G-6P levels and inhibit hexokinase

34
Q

How does the pentose phosphate pathway influence the activity of hexokinase?

A

G-6P can be converted to glycogen and enter PPP, so the rate of use of G-6P can influence its inhibition of hexokinase

35
Q

How is glucokinase regulated?

A

Insulin increases synthesis of GK. GKRP in nucleus binds to inhibit GK in absence of glucose. High F-6P increases GK-GKRP, but glucose inhibits this interaction.

36
Q

How does F-2,6-bisP affect PFK-1?

A

Mediates effects of insulin and glucagon. Increase in ins/gluc ratio increases levels, which activate PFK-1

37
Q

How does pyruvate kinase regulate glycolysis?

A

Increase in glucagon/decrease in ins/gluc ratio during fasting activates PKA, PK-P = inactive. Increase in insulin or ratio after high carb meal activates phosphatase and activates PK.

38
Q

What are three ways to regulate pyruvate kinase?

A

Insulin/glucagon ratio and activation of kinase/phosphatase; feed forward fructose-1,6-BP activation (liver); allosteric regulators ATP, alanine inhibit with gluconeogenesis is active

39
Q

What is the Pasteur effect?

A

In aerobic conditions/increased respiration, levels of citrate and ATP increase, which inhibit PFK-1 (both) and PK (ATP)

40
Q

What are the most common inherited enzyme deficiencies of glycolysis?

A

95% patients - pyruvate kinase; 4% - phosphoglucose isomerase

41
Q

Where are PL and hexokinase deficiencies expressed?

A

Erythrocytes only

42
Q

Where is triose phosphate isomerase deficiency seen?

A

Erythrocytes, leukocytes, muscle, CNS

43
Q

What condition do most patients with glycolytic enzyme deficiency exhibit, and how are severe cases treated?

A

Hemolytic anemia; severe hemolysis treated with folic acid supplements

44
Q

How does a PK deficiency lead to hemolytic anemia?

A

Decrease in enzyme = decrease in glycolysis rate = decreased ATP -> instability of PM of RBCs -> phagocytosis by macrophages in spleen

45
Q

What is lactic acidosis?

A

Accumulation of LA in blood due to increased rate of production vs. metabolism, decreasing pH below 7.2

46
Q

What deficiencies may lead to lactic acidosis?

A

Impaired ox of pyr by PDH (B1 def), TCA cycle, inability to re-ox NADH efficiently, pry carboxylase, exercise, MI

47
Q

How does excessive NADH lead to lactic acidosis?

A

Drives lactate DH reaction in the direction of lactate

48
Q

How does an MI cause lactic acidosis?

A

Absence of O2 for OXPHOS decreases ATP levels, increases AMP, activating PFK-1. Increase ATP, low O2 -> lactate, lower pH, inhibits PFK-1, inhibiting ATP generation

49
Q

What is the ATP yield from aerobic/complete oxidation and anaerobic glycolysis of glucose?

A

Aerobic: 30-32 moles ATP/mole glucose
Anaerobic: 2 moles ATP

Biochemistry (17 decks)

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