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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
What happens to the propionyl CoA produced in odd chain B-oxidation?
broken down into methylmalonyl CoA by propionyl CoA carboxylase -->then methylmalonyl CoA mutase makes it into succinyl CoA (goes into TCA [anaplerotic]
26
what happens in Very long chain FA degradation
>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
What happens in branched chain FA degradation?
broken down in peroxisomes like with long chain oxidation
28
Where do branched chain FA's come from?
animals cant synthesize them | present in plants-->therefore we get them in our diet
29
w-oxidation (omega) happens when....
there is a disruption in B-oxidation pathways & FAs may b metabolized on the ER
30
What happens in w-oxidation?
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
ketone bodies are synthesized how?
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
Can the brain use FA as fuel? why or why not?
the brain can't use FA because it can't cross blood-brain barrier liver cleaves glycogen & releases glucose in blood (for brain)
33
where are ketone bodies made?
liver (hepatocytes do not consume much ATP)
34
What side products does synthesis of ketone bodies produce?
lots of NADH+ & H+ drive TCA cycle backwards (oxaloacetate converts to malate) increased acetyl CoA then goes into ketone body synthesis
35
ketoacidosis is what?
depression of blood pH by excessive ketone body production | caused by starvation or diabetes
36
where do all rxns of tca cycle happen?
in mitochondrial matrix
37
what is the key rate limiting step in TCA cycle?
isocitrate dehydrogenase | *ADP activates, ATP inhibits
38
1st step of TCA
oxaloacetate + acetyl CoA --> citrate | *catalyzed by citrate synthase
39
2nd step of TCA
citrate-->aconitate --> isocitrate | *aconitase catalyzes this 2step isomerization
40
3rd step in TCA
isocitrate -->a-ketoglutarate * NAD+ is used-->makes NADH & * *catalyzed by isocitrate dehydrogenase
41
4th step in TCA
a-ketoglutarate ---> succinyl CoA * needs CoASH & NAD+ to go in, NADH & CO2 come out * catalyzed by a-ketogluarate dehydrogenase
42
5th step in TCA
succinyl COA --> succinate * GDP & PI go in, get GTP & CoASH out * *catalyzed by sucinate thiokinase
43
6th step in TCA
succinate --> fumarate * FAD goes in, FADH2 comes out * **succinate dehydrogenase catalyzes rxn * ** " " part of ETC that makes proton grasdient
44
7th step in TCA
funarate --> Malate * put H2O in * *catalyzed by fumarate hydratase
45
8th step in TCA
malate to oxaloacetate * put NAD+ in, get NADH out * *catalyzed by malate dehydrogenase
46
TCA is amphibolic, explain...
catabolic: TCA cycle reduces NAD+ & FAD to make ATP via ETC anabolic: TCA intermediates are feedstock for otheer biosynthetic pathways
47
what other bisynthetic pathways are enhanced from the TCA cycle in the fed state?
* 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
what other bisynthetic pathways are enhanced from the TCA cycle in the fasting state?
glucose comes from malate | AA synthesis comes from oxaloacetate
49
myoadenylate deaminase deficiency
*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
what is the goal of the ETC?
to pump protons against conc. gradient to set up an energy difference
51
complex I of ETC
NADH dehydrogenase | *loses energy but NADH recovers it & pulls 4 protons into intermembrane space
52
COenzyme Q
lipid soluble & is in inner mito membrane * can accept one e- to = semiquinone * 2nd e- = dihydroquinol
53
complex II of ETC
cytochrome B c1 complex | CoQH2 comes from complex I
54
Complex III of ETC
Cytochrome c oxidase
55
what is the problem with incomplete reduction of O2?
it forms free radicals, sometimes very reactive like superoxide & hydrogen peroxide =bad news bears
56
adaptive thermogenesis process
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
inner mito membrane powers transport via what mechanisms?
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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