Lecture 19: Glycolysis Flashcards

1
Q

Catabolism

A

-BREAKDOWN fuels into energy
-usually coupled with reducing equivalents of NADH

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2
Q

How is energy generated in mammals

A

-oxidation of carbon compounds to CO2 and H2O using O2
-release ATP and NADH

-start with reduced carbon end with oxidized carbon

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3
Q

Anabolism

A

-BIOSYNTHESIS from smaller molecules
-REQUIRES energy from ATP or NADPH

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4
Q

NADH form

A

reduced

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5
Q

NADPH vs NADH

A

-NADPH mostly used for ANABOLISM

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6
Q

Regulation of metabolism

A

-feedback or feedforward control at:
-rate-limiting step
-commitment step

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7
Q

rate-limiting step

A

slowest in pathway

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8
Q

commitment step

A

first irreversible step unique to pathway

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9
Q

irreversible steps usually involve

A

-high energy substrates
-ex: ATP

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10
Q

Futile Cycles

A

-formed by irreversible reactions in opposite directions
-activation of both wastes energy

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11
Q

Use of a futile cycle in the liver

A

-between glucose and glucose 1-phosphate as a buffer to maintain blood glucose levels

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12
Q

To minimize energy loss of a futile cycle:

A

reactions only in one direction should be active at a given time
-gycolysis vs gluconeogenesis

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13
Q

Types of regulation of metabolism

A

-transcriptional (slow)
-protein degradation (slow)
-allosteric regulation (fast)
-post-translational modification (fast)
-compartmentation (fast)

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14
Q

Slow regulation of metabolism

A

-transcriptional/translational (induce genes)
-protein degradation (ubiquitin-proteasome or lysosomal proteolysis)

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15
Q

Fast regulation of metabolism

A

-allosteric regulation (activators/inhibitors)
-post-translational modifications (phosphorylation)
-compartmentation (shuttling substrates to compartments for reactions)

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16
Q

Compartmentation

A

-shuttling substrates to compartment for reactions
-fatty acid biosynthesis in cytosol
-oxidation in the mitochondria

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17
Q

Difference in metabolism between organs

A

-utilize dif metabolic pathways
-organs must cooperate to optimize phsyiological responses

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18
Q

Point of No return of Metabolism

A

-pyruvate (C3) to acetyl CoA (C2)

19
Q

Glycolysis overview

A

Glucose to fructose 1,6 to 2 glyceraldhyde 3-phosphate to 2 pyruvate
-cytosol
-harvest 2 ATP and 2 NADH

20
Q

1st reaction in glycolysis

A

Glucose + 2 ATP –> fructose 1,6 bisphosphate + 2 ADP

21
Q

2nd reaction in glycolysis

A

fructose 1,6 bisphosphate ((C6) –> 2 glycaeraldehyde 3-phosphate (C3)

22
Q

3rd reaction in glycolysis

A

2 G3P + 4 ADP + 2 NAD+ —> 2 pyruvate + 4 ATP + 2NADH

-net gain: 2 ATP and 2 NADH

23
Q

Priming reaction of glycolysis

A
  1. Glucose + ATP = G6P +ADP (hexokinase)
  2. G6P –> F6P (reversible)
  3. F6P + ATP = F1,6B +ADP (6-phosphofructo1Kinase)
24
Q

Regulation of priming reactions

A

-insulin increases # of glucose transporters on cell membrane (EXCEPT LIVER)
-G6P inhibits G6P production (hexokinase)

25
Q

Regulation of hexokinase

A

-inhibited by G6P

26
Q

regulation of 6-phosphofructokinase

A

-activated by AMP, fructose2,6
-inhibited by ATP, citrate, H+

27
Q

Reactions coupled with ATP hydrolysis

A

-typically irreverdible

28
Q

G6p

A

-also used in glycogen synthesis and pentose phosphate pathway

*inhibiting this would inhibit other process other than glycolysis

29
Q

Commitment step of glycolysis

A

-production of fructose1,6B

*target this one instead to stop glycolysis

30
Q

AMP

A

-signal used by cells to sense energy status
- AMP much much lower than ADP and then ATP in cells

31
Q

small decrease in ATP leads to

A

significant increase in AMP

32
Q

AMP-activated protein kinase (AMPK)

A

-critical role in cellular energy homeostasis

33
Q

Adenylate kinase reaction

A

2 ADP <-> ATP + AMP

34
Q

Keq

A

[ATP][AMP]/[ADP]^2

=1

35
Q

Regulation of glycolysis at Splitting steps

A

F1,6P all the way to phosphoenolpyruvate are unregulated
-enzymes keep them at equilibrium
-reversible

36
Q

Regulation of pyruvate kinase

A

-activated by F1,6B
-inhibited by ATP and alanine

-pyruvate is also used to make alanine

37
Q

Pyruvate

A

-product of glycolysis
-transported to mitochondria to be turned into acteyl CoA (oxidative decarboxylation)
-can be used to make glucose through gluconeogenesis
-can also make alanine and lactate

38
Q

Glycogen

A

-excess glucose stored in liver and muscles
-synthesis and breakdown regulated
-used by liver to regulate blood glucose levels

39
Q

Glycogen synthesis

A
  1. G6P –> G1P
  2. G1P +UTP <–> Glycogen + UDP

-inhibited again by G6P (inhibts hexokinase)

40
Q

Fructose

A

-does not increase blood insulin
-different metabolism
-same splitting enzyme (aldolase B)
-+glucose=sucrose

41
Q

Fructose metabolism

A
  1. fructose + ATP –> F1P + ADP
    (fructokinase)
  2. F1P + ATP –> 2 G3P + ADP
    (aldolase B)
42
Q

Excess fructose

A

-accumulates F1P in liver cells
-depletes ATP and phosphate which may cause liver damage

43
Q

Aldolase B

A

breaks 6 carbon to 3 carbon

44
Q

Which of the following CANNOT be a carbon source for gluconeogenesis?

-pyruvate
-lactate
-alanine
-acetyl CoA

A

acetyl CoA