Lecture 20 Fatty acid Metabolism, response to starvation Flashcards

(55 cards)

1
Q

on average how many KG of fat does a 70KG person have and how many Kcal is that

A

15kg and 141kcal

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2
Q

Do you have a lot of glycogen?

A

no

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3
Q

what does your liver make and gallbladder store to emulsify fats

A

Cholic acid (bile salts)

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4
Q

What is cholic acid

A

a bile salt that is made by you liver release into small intestine to break down fats

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5
Q

After releasing bile salts and emulsifying what do the fats turn into in your small intestine

A

mixed micelles

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6
Q

What enzymes digest lipids in your small intestines

A

lipases (enzymes that digest lipids)

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7
Q

What do lipases digest your triglycerols into and why is this important

A

glycerol and three fatty acids dur bc triglycerols cannot cross the membrane but the two smaller things can (so they can get into your lymphatic system and your circulatory system)

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8
Q

what is the primary transporter of triglycerols in your circulatory systems

A

Chylomicron

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9
Q

what is chylomicron

A

the primary transporter of triglycerols in your circulatory systems

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10
Q

what happens after glycerol and fatty acids cross your intestinal mucosa

A

they are reassembled into triglycerols and given to chylomicron to carry through the circulatory system

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11
Q

is there a reversible reaction form TGAs to free fatty acids

A

yes

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12
Q

how does the TGA cross the membrane

A

by breaking them down into free fatty acids and glycerol

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13
Q

how do lipases attack TAG

A

by attacking each ester bond individually forming three reactions so the TAG–>DAG—>MAG— >FA+ glycerol

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14
Q

do different lipases target each ester bond in a TAG

A

yes

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15
Q

how does glycerol enter central metabolism

A

through G3P (glycolysis)

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16
Q

What are the general steps of prep for B oxidation

A
  1. activate fatty acid by shoving a CoA on it
  2. transport that into the mitochondria via the carnitine carrier system
  3. beta oxidation
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17
Q

where does activation step of fatty acids happen

A

in the cytoplasm

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18
Q

how much ATP does beta oxidation activation take

A

2 ATP

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19
Q

purpose of carnitine pathway

A

to get your activated fatty acids into the mitochondria so they can be beta oxidized

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20
Q

steps of the carnitine pathway

A
  1. transfer the activated fatty acyl coA onto a molecule called carnitine by taking off its CoA, that is then able to pass through the outer mtocontral membrane. (by using Carnitine Acyltransferase 1)
  2. the whole thing then moves into the matrix bc carnitine has a special transporter form the intermembrane space into the matrix
  3. Once in the matrix, you replace the carnitine again with coenzyme A (where it goes on its merry way) by using Carnitine Acyltransferase II
    ta da!
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21
Q

does the carnitine pathway consume energy, does it go with is concentratioin gradiet

A

no, it goes with with concentration gradient

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22
Q

how you you shit off FA degradation

A

shut off the carnitine pathway

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23
Q

general steps of Beta oxidation and when is what produced

A

1.(acetyl CoA dehydrogenase) dehydrogenation (produce FADH2)

  1. Hydration (has to be tras bond) (enoyl CoA hydratase) (shove on OH)
  2. dehydrogenation (Beta hydroxyacyl-CoA dehydrogenase) (turn OH into carbonyl group) (produce NADH)
  3. Thiolytic cleavage (thiolase)
24
Q

What is beta oxidation like? (in terms of mechanisms)

A

Amino acid degradation and citric acid cycle

25
another name for FAD
flavin cofactor
26
besides initial activation, where does the other ATP get used in the activation step of beta oxidation
putting back together the 2 inorganic phosphates that you broke apart after using the ATP
27
Overall how many ATPs does it take to activate B oxidation
2
28
balance sheet for one turn of the citric acid cycle if you start with one acetyl coa
A acetyl-CoA= 3 NADH + 1 FADH2 + 1 ATP (ie 10 ATPS)
29
practice beta oxidation with regular 16 C chain (how many ATP???)
106net
30
what are the two variations of the beta oxidations and how do we get around them
1. if you have an unsaturated bond you don't have to do the initial dehydrogenation (making of trans double bond) so you subtract an FADH2 from every double bond you have (+you also might have to isomerize it into a trans but that does not affect energy) 2. Odd chain fatty acid chains= at the end of oxidation you are left with a three carbon thing which you carboxylase using cofactor biotin and an ATP and HCO- (propionyl CoA Carboxylase) then you do some mutase reactions to form SUCCINYL CoA which can go into the citric acid cycle where it can generate 1 FADH2 and one NADH - so if you have uneven thing treat it as if it were even then at the end SUBTRACT 1 MORE ATP and ADD 1 NADH AND 1 FADH
31
what is special about vitamin B12 and what's another name for it
Methylcobalamin and it can do radical chemistry which enables now enzyme mechanisms (make a tricyclic energetically unstable thing)
32
where does normal fatty acid degradation take place?
in the mitochondria
33
where does degradation of branched chain fatty acids and FA over =or more than 22C long (in humans and in plants)
in humans: Peroxisome In plants: Glyoxysome
34
what scenario would you degrade FA in the peroxisome (or glyoxysome in plants) instead of the mitochondria?
if its branched or 22 or more C long
35
where does FA biosynthesis happen
cytoplasm
36
when beginning to synthesize FA what molecule do you mix with acetyl CoA to start adding carbons
Malonyl-Coa! is made by mixing Acetyl-Co2 and Cox
37
what enzyme performs FA synthesis and what is special about it
Fatty Acyl synthetase (big polypeptide that has different domains that do different steps) special bc its is doing substrate channeling!!
38
Steps of FA biosynthesis
1. Activation (Acetyl CoA +Co2 --> Malonyl CoA) using cofactor Biotin (the regulated step) 2. IDK IF I NEED TO KNOW THIS
39
what cofactor is used for carboxylation
biotin
40
what cofactor is used for decarboxylations
TPP
41
What are the pros and cons of a multifunctional protein
pro: substrate channeling, correct stoichiometry, no need to encode binding surface con: no change for modularity (can't use it for other stuff)
42
What is your system doing at time =0 since eating
release insulin
43
why can't your brain use fatty acids as energy efficiently? (4 reasons)
1. hard to transfer them across the blood/ brain barrier 2. the ATP generation linked to beta oxidation demands more oxygen than glucose, which is risking neurons to become hypoxic 3. Beta oxidation leads to superoxides and other types of oxygen radicals which will damage the brain due to severe oxidative stress. 4. Also the rate of ATP generation is just overall slower than glucose
44
What happens at t=2 hours since eating
drop insulin increase glucagon start breakdown glycogen
45
What happens at t=4 hours since eating
glycogen is gone so start mobilizing FA for liver and muscle
46
What happens at t >12 hours since eating
Formation of ketone bodies created to replenish glucose
47
most common ketone body
Acetoacetate
48
what is acetoacetate
a ketone body that feeds your brain when glucose is gone
49
What does your brain do when it has no glucose
makes ketone bodies
50
3 types of ketone bodies
Acetone, Acetoacetate, D-B-hydroxybutyrate
51
The 2 uses of formed Acetyl CoA:
1. citric acid cycle 2. converted to ketone bodies
51
Where do ketone bodies come from?
liver and Acetyl coa
52
Tell me about the synthesis of ketone bodies
last 5 min of starvation lecture HELP
53
where is glucose coming from after you run out of everything
proteins from your muscle then your organs
54
can you live with no glucose in your body
NO