Energy Metabolism II Flashcards

1
Q

Where in the cell does pyruvate oxidation take place

A

Mitochondria

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2
Q

Where in the mitochondria does electron transfer/oxidative phosphorylation take place?

A

Inner membrane

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3
Q

where in the mitochondria does the TCA cycle and fatty acid oxidation take place?

A

matrix

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4
Q

How does pyruvate get into the matrix of the mitochondria

A

through symporter that couples it with H+ movement down it’s gradient

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5
Q

pyruvate dehydrogenase

A

converts pyruvate to acetyl CoA and Co2 through oxidative decarboxylation

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6
Q

what does pyruvate dehydrogenase require to function

A

5 cofactors (mainly B vitamin derived)

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7
Q

Regulation of pyruvate dehydrogenase

A

under hormonal control and feedback regulation

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8
Q

Beriberi

A
  • deficiency in thiamin (B1)
  • decreased ability to oxidize pyruvate
  • leads to high blood pyruvate and lactate
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9
Q

arsenic poisoining

A
  • inactivates pyruvate dehydrogenase

- arsenate=robs cells of ability to make ATP

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10
Q

Acetaldehyde

A
  • metabolic product from alcohol
  • can get a lot from excessive alcohol consumption
  • inhibits pyruvate dehydrogenase
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11
Q

TCA cycle (kreb’s, citric acid)

A
  • starting substance is acetyl-coA (2 carbons)
  • 2 carbons leave as CO2
  • generates 4 pairs of electrons, one GTP that are fed into the electron transport chain to generate ATP
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12
Q

succinate dehydrogenase

A

only enzyme in TCA cycle that is embedded in mitochondrial inner membrane, the rest are in the matrix

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13
Q

substrate level phosphorylation of GTP

A

at one step in TCA cycle; when GTP is generate directly from a reaction, not indirectly

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14
Q

oxaloacetate

A

what is combined with acetyl coA at the beginning of the TCA cycle to make citrate
-can limit flux through pathway by limiting it

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15
Q

TCA intermediates can be used for what?

A

can be used for biosynthesis of amino acids, glucose, fatty acids, cholesterol, and porphyrins

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16
Q

pyruvate carboxylase

A
  • generates oxaloacetate from pyruvate

- helps replenish TCA intermediate supply

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17
Q

If NAD+ level is high, what does that do to the flux of the TCA cycle

A

Increases it because you want to create NADH for electron transport chain

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18
Q

If ADP level is high, what does that do to the flux of the TCA cycle

A

Increases it so you can get NADH and put that into electron transport chain

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19
Q

what is the ultimate acceptor of electrons in electron transport chain?

A

oxygen

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20
Q

Flavin mono nucleotide

A

carries two electrons

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21
Q

coenzyme Q

A
  • carries up to two electrons
  • very hydrophobic so stays in mitochondrial membrane
  • collects electrons from complex 1 (NADH) but can also collect straight from FAD (just generates slightly less ATP
22
Q

cytochromes

A

-can carry only 1 electron

23
Q

iron-sulfur proteins

A

allow use of electrons outside the mitochondrial matrix

24
Q

complex I

A
  • electrons from NADH reduce it and in the process it pumps 4 protons into outside matrix
  • can only accept from NADH not FAD
  • passes electrons to CoQ
25
Q

complex III

A
  • takes electrons from CoQ

- passes electrons to cyt c

26
Q

complex IV

A
  • cyt c binds to it and it oxidizes it, pulling electrons off of it and putting them on oxygen which gets reduced to water
  • in the process pumps 2 protons into inter membrane space
27
Q

Inhibitors of complex IV

A
  • azide, carbon monoxide, cyanide

- bind to complex IV at higher affinity than oxygen and poison it so it can’t work at all

28
Q

How does ATP synthase generate ATP?

A
  • uses energy from proton moving down proton gradient to cause conformational changes that release ATP
  • more positive in intermembrane space, more negative in the matrix
29
Q

ATP translocators

A
  • move ATP from mitochondria to other parts of the cell
  • ADP/ATP exchange (ATP is more negative so it wants to go to the more positive inner membrane space so the two switch)
  • phosphate translocase (symporter) allows phosphate to flow in with proton (uses energy from proton moving down gradient)
  • phosphate and ADP combine to make ATP that can flow out through ADP/ATP exchange
30
Q

What happens to electron transport chain when there is no oxygen

A

basically stops

31
Q

The electron transport chain is an example of:

A

oxidative phosphorylation

32
Q

Dinitrophenol (DNP)

A
  • provides another path for protons to cross the membrane
  • uncouples oxidative phosphorylation in an uncontrolled way; collapses the proton gradient so you lose proton motive force and ATP synthesis halts
33
Q

UCP/thermogenin

A
  • uncouples oxidative phosphorylation in a controlled way
  • in mitochondria of brown fat (where there is a high content of mitochondria)
  • ATP is not generated and instead the movement of protons down their gradient generates heat
34
Q

gluconeogenesis

A
  • biosynthesis of glucose
  • occurs mainly in liver (also in kidney)
  • occurs during fasting (especially after depletion of glycogen), when it is the sole glucose source
  • requires carbon source and energy source
35
Q

carbon source for gluconeogenesis

A

carbon skeletons from amino acids

36
Q

energy source for gluconeogenesis

A

from fatty acid oxidation

37
Q

metformin

A

inhibits gluconeogenesis

-used for type II diabetes

38
Q

three irreversible steps of glycolysis that must be bypassed in gluconeogenesis

A
  • hexokinase
  • phosphofructokinase (PFK-1)
  • pyruvate kinase
39
Q

how is pyruvate kinase bypassed

A

through conversion of pyruvate to oxaloacetate (shuttled out of mitochondria) then to PEP

40
Q

carbon sources for gluconeogenesis

A
  • lactate from muscles or RBCs (converted to pyruvate by lactate dehydrogenase)
  • fructose and galactose
  • glucogenic amino acids from diet or muscle breakdown
  • glycerol from triglyceride breakdown
41
Q

crucial entry point for gluconeogenesis

A

oxaloacetate

42
Q

pyruvate carboxylase

A

converts pyruvate to oxaloacetate

43
Q

cori cycle

A

converts lactate to glucose in the liver

44
Q

glucose-alanine cycle

A

converts alanine to glucose in the liver (through pyruvate)

45
Q

major carbon source for gluconeogenesis during fasting

A

amino acids from muscle breakdown

46
Q

glucose-6-phosphatase

A
  • converts glucose-6-phosphate back to glucose so it can diffuse into the blood
  • only liver and kidney have it
47
Q

von Gierke disease

A

glucose-6-phosphatase deficiency

-patients with this need to be constantly fed some form of glucose

48
Q

PEP carboxykinase

A

converts oxaloacetate to PEP

-committed step in gluconeogenesis from pyruvate/lactate

49
Q

Fructose 2,6 bisphosphate (F26BP) regulatory function

A
  • activates glycolysis
  • inhibits gluconeogenesis
  • concentrations high in fed state, low in fasting state
50
Q

PFK-2

A

synthesizes F26BP

  • activated by insulin
  • will stimulate glycolysis
51
Q

FBPase-2

A

breaks down F26BP to Fructose-6-phosphate

  • activated by glucagon
  • stimulates gluconeogenesis