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FOM > FOMweek2 > Flashcards

FOMweek2 Flashcards

1
Q

Double bonds in FA’s do what to the melting point?

A

decrease the melting point

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2
Q

Double bonds in FA’s do what to the melting point?

A

decrease the melting point

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3
Q

saturated FA’s are in what phase at room temp?

A

solid

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4
Q

3 essential unsaturated FA’s gained through our diet?

A

arachachidonic acid, linoleic, linolenic

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5
Q

precursor for FA’s

A

acyl CoA

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6
Q

where does long chain FAs take place?

A

mito matrix

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7
Q

How does palmitoylCoA cross the inner mito matrix (impermeable)?

A

carnitine shuttle using enzyme carnitine:palmitoyl transferase 1 (CPT 1)

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8
Q

What is the major regulator of FA catabolism (and how does it regulate it)?

A

CPT I is major regulator of FA catabolism

  • CPT I is in outer mito membrane
  • inhibited by malonyl CoA (inhibitted by AMP & activated by insulin)
  • fatty acyl CoA & carnitine bind to make fatty acylcarnitine [and CoA] that can be transported across inner mito membrane
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9
Q

CPT II deficiency symptoms

A

adults: muscle pain, weakness, & myoglobinuria after prolonged exercise/fasting
neonatal/infant: irritable, FTT, often fatal

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10
Q

4 steps in B-oxidation of long chain FA’s

A

Oxidation
Hydration
Oxidation
Carbon-Carbon bond cleavage

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11
Q

Main goal for B-oxidation

A

make acetyl-CoA for TCA cycle

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12
Q

3 essential unsaturated FA’s gained through our diet?

A

arachachidonic acid, linoleic, linolenic

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13
Q

which FAs yield less usefule energy?

A

unsaturated fats yield less useful energy

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14
Q

where does long chain FAs take place?

A

mito matrix

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15
Q

How does palmitoylCoA cross the inner mito matrix (impermeable)?

A

carnitine shuttle using enzyme carnitine:palmitoyl transferase 1 (CPT 1)

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16
Q

What is the major regulator of FA catabolism (and how does it regulate it)?

A

CPT I is major regulator of FA catabolism

  • CPT I is in outer mito membrane
  • inhibited by malonyl CoA (inhibitted by AMP & activated by insulin)
  • fatty acyl CoA & carnitine bind to make fatty acylcarnitine [and CoA] that can be transported across inner mito membrane
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17
Q

What happens in branched chain FA degradation?

A

broken down in peroxisomes like with long chain oxidation

1st) a-C is oxidized to CO2
2nd) B-oxidation occurs, alternately releasing propionyl CoA & acetyl CoA

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18
Q

4 steps in B-oxidation of long chain FA’s

A

Oxidation
Hydration
Oxidation
Carbon-Carbon bond cleavage

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19
Q

How many carbons of FA chain are oxidized per cycle?

A

2 carbons

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20
Q

how do you diagnose CPT deficiencies?

A

Diagnose: lipid profile

CPTII see increase in FA acylcanritine, CPTI has increase in COA & decrease in carnitine

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21
Q

Main goal for B-oxidation

A

make acetyl-CoA for TCA cycle

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22
Q

MCAD- medum chain acyl CoA dehydrogenase deficiency

A

faulty acyl-CoA dehydrogenase, so can’t break down Acyl-CoA into trans-delta2-enoyl-CoA

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23
Q

what can enoyl-CoA hydratase work on?

A

only accepts substrates that have trans-double bonds (most dietary fats have cis bonds)

24
Q

what happens in odd chain length FA B-oxidation?

A

B-oxidation goes on normally until 5 C chain is left

–>then thiolase makes 1 acetyl CoA & 1 propionyl CoA

25
Q

What happens to the propionyl CoA produced in odd chain B-oxidation?

A

broken down into methylmalonyl CoA by propionyl CoA carboxylase
–>then methylmalonyl CoA mutase makes it into succinyl CoA (goes into TCA [anaplerotic]

26
Q

what happens in Very long chain FA degradation

A

> 22 C chains are degraded by peroxisomes simlarly to B-oxidation (but not in mitochondria)
1st step rxn donates e- to O2 not FAD–>makes h20
b-oxidation continues until chain is 4-6 C long & then are transferred via carnitine into mitochondria for complete b-oxidation

27
Q

What happens in branched chain FA degradation?

A

broken down in peroxisomes like with long chain oxidation

28
Q

Where do branched chain FA’s come from?

A

animals cant synthesize them

present in plants–>therefore we get them in our diet

29
Q

w-oxidation (omega) happens when….

A

there is a disruption in B-oxidation pathways & FAs may b metabolized on the ER

30
Q

What happens in w-oxidation?

A

cytochrome p450 oxidizes the w-terminal C to a carboxyl–>dicarboxyl FA
both carboxyl ends are then broken into medium chain dicarboxyls to b used by other tissues or excreted in urine

31
Q

ketone bodies are synthesized how?

A

in fasting, decreased insulin/glucagon ratio stimulates lipase to free FA’s from TAGs stored in adipose
free FA travel to energy needing tissues & undergo b-oxidation to =energy (in heart & skeletal muscle)

32
Q

Can the brain use FA as fuel? why or why not?

A

the brain can’t use FA because it can’t cross blood-brain barrier
liver cleaves glycogen & releases glucose in blood (for brain)

33
Q

where are ketone bodies made?

A

liver (hepatocytes do not consume much ATP)

34
Q

What side products does synthesis of ketone bodies produce?

A

lots of NADH+ & H+ drive TCA cycle backwards (oxaloacetate converts to malate)
increased acetyl CoA then goes into ketone body synthesis

35
Q

ketoacidosis is what?

A

depression of blood pH by excessive ketone body production

caused by starvation or diabetes

36
Q

where do all rxns of tca cycle happen?

A

in mitochondrial matrix

37
Q

what is the key rate limiting step in TCA cycle?

A

isocitrate dehydrogenase

*ADP activates, ATP inhibits

38
Q

1st step of TCA

A

oxaloacetate + acetyl CoA –> citrate

*catalyzed by citrate synthase

39
Q

2nd step of TCA

A

citrate–>aconitate –> isocitrate

*aconitase catalyzes this 2step isomerization

40
Q

3rd step in TCA

A

isocitrate –>a-ketoglutarate

  • NAD+ is used–>makes NADH &
  • *catalyzed by isocitrate dehydrogenase
41
Q

4th step in TCA

A

a-ketoglutarate —> succinyl CoA

  • needs CoASH & NAD+ to go in, NADH & CO2 come out
  • catalyzed by a-ketogluarate dehydrogenase
42
Q

5th step in TCA

A

succinyl COA –> succinate

  • GDP & PI go in, get GTP & CoASH out
  • *catalyzed by sucinate thiokinase
43
Q

6th step in TCA

A

succinate –> fumarate

  • FAD goes in, FADH2 comes out
  • **succinate dehydrogenase catalyzes rxn
  • ** “ “ part of ETC that makes proton grasdient
44
Q

7th step in TCA

A

funarate –> Malate

  • put H2O in
  • *catalyzed by fumarate hydratase
45
Q

8th step in TCA

A

malate to oxaloacetate

  • put NAD+ in, get NADH out
  • *catalyzed by malate dehydrogenase
46
Q

TCA is amphibolic, explain…

A

catabolic: TCA cycle reduces NAD+ & FAD to make ATP via ETC
anabolic: TCA intermediates are feedstock for otheer biosynthetic pathways

47
Q

what other bisynthetic pathways are enhanced from the TCA cycle in the fed state?

A
  • FA synthesis comes from citrate
  • *a-ketoglutarate makes glutamate and then GABA
  • **odd chain FA make succinyl CoA (from succinate) that goes towards heme synthesis
48
Q

what other bisynthetic pathways are enhanced from the TCA cycle in the fasting state?

A

glucose comes from malate

AA synthesis comes from oxaloacetate

49
Q

myoadenylate deaminase deficiency

A

*muscle pain
*weakness when exercising
no increase in blood NH4+ after exercise
no AMPD1 in muscle biopsy
**caused by mutations in muscle specific AMPD1 isoform of AMP deaminase =inactive enzyme

50
Q

what is the goal of the ETC?

A

to pump protons against conc. gradient to set up an energy difference

51
Q

complex I of ETC

A

NADH dehydrogenase

*loses energy but NADH recovers it & pulls 4 protons into intermembrane space

52
Q

COenzyme Q

A

lipid soluble & is in inner mito membrane

  • can accept one e- to = semiquinone
  • 2nd e- = dihydroquinol
53
Q

complex II of ETC

A

cytochrome B c1 complex

CoQH2 comes from complex I

54
Q

Complex III of ETC

A

Cytochrome c oxidase

55
Q

what is the problem with incomplete reduction of O2?

A

it forms free radicals, sometimes very reactive like superoxide & hydrogen peroxide
=bad news bears

56
Q

adaptive thermogenesis process

A

norepinephrine is released & activates lipase

  • froms free FA from TAG in brown fat cells
  • *proton channel: thermogenin is activated (UCP1)
  • **fat can b used for heat separately from ATP consumption
57
Q

inner mito membrane powers transport via what mechanisms?

A

electrochemical gradient: matric=x side of membrane is negatively charged compared to intermembrane space side
pH gradient: H+ is lower in matrix than intermembrane space

FOM (6 decks)

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