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Human Function- Exam 4 Material > Fatty Acid Mobilization and Oxidation > Flashcards

Fatty Acid Mobilization and Oxidation Flashcards

1
Q

what is fatty acid utilization?

A

process of releasing FA from storage

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2
Q

what is lipolysis?

A

hydrolysis of FA from TAG in adipose

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3
Q

what is beta oxidation?

A

mitochondrial oxidation of FA to acetylCoA

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4
Q

which provides more energy glycogen or fatty acids?

A

fatty acids

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5
Q

when is serum FA low?

A

fed states

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6
Q

when is serum FA high?

A

stressed states (starvation, emotional)

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7
Q

where do TAGs come from?

A 
dietary TAG (chylomicrons)
liver TAG (VLDL)
glucose (de novo TAG synthesis)
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8
Q

what enzyme is used to remove TAGs from lipid droplets inside cells?

A

adipose triglyceride lipase

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9
Q

how are TAGs stored inside cells?

A

lipid droplets

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10
Q

what are lipid droplets surrounded by?

A

phospholipid layer

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11
Q

what is perilipin?

A

binds to CGI58 and prevents it from activating adipose triglyceride lipase

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12
Q

what is CG158?

A

activates adipose triglyceride lipase

inhibited by perilipin

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13
Q

what does adipose triglyceride lipase do?

A

first step of lipolysis- removal of a fatty acid from TAG, forms DAG

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14
Q

what does hormone sensitive lipase do?

A

removes second fatty acid from the DAG

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15
Q

what does monoacylglycerol lipase do?

A

removes last FA from MAG

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16
Q

what is the main stimulator of the starved state?

A

stress

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17
Q

what signals lipolysis?

A

epinepherine and sympathetic stimulation

very few glucagon receptors on adipose cells

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18
Q

what signal pathway does the starved state use?

A

cAMP/PKA

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19
Q

what does PKA do during the starved state?

A

phophorylates perilipin- it releases CGI58

phophorylates hormone sensitive lipase

20
Q

what is the rate determining step of lipolysis?

A

phophorylation of hormone sensitive lipase

21
Q

what is the main inhibitor of lipolysis?

A

insulin- don’t need to mobilize TAGs if in fed state

22
Q

what does insulin do?

A

dephosphorylates hormone sensitive lipase (via phosphatase)

decreases cAMP

23
Q

how does FA travel in the blood?

A

bound to albumin

24
Q

how many FAs can albumin hold?

A

8

25
Q

what are the 2 things that can happen to fatty acids once inside a cell?

A
  • bound by fatty acid binding protein to store

- converted to FA acyl CoA by acyl-CoA synthetase

26
Q

what type of chains enter mitochondria?

A

short/medium chains (less than 18)

27
Q

what type of chains go to peroxisomes?

A

long chain (greater than 18)

28
Q

how do fatty acyl-CoAs get into mitochondria

A
  1. cross outer membrane freely
  2. converted to fatty acylcarnitine by carnitine palmitoyltransferase (adds free carnitine and takes off the CoA)
  3. carnitine acylcarnitine trnaslocase brings it into the matrix and kicks a carnitine into the inner membrane space
  4. CPTII converts the fatty acyl carnitine back to fatty acyl CoA
29
Q

how many pools of CoA are in the mitochondria?

A

2- inner membrane space and matrix

30
Q

how is CPT regulated?

A

inhibited by malonyl CoA from acetyl CoA carboxylase during fed state- sends FAs to be stored

31
Q

what are the steps of mitochondrial beta oxidation of fatty acids?

A
  1. dehydrogenation via acetylCoA dehydrogenase (FAD part of electron transport chain)
  2. hydration
  3. dehydrogenation- NAD
  4. cleavage
32
Q

what are symptoms of acetylCoA dehydrogenase deficiency?

A

muscle weakness
lack of ketones (no acetyl CoA)
acyl carinitines in urine

33
Q

how do long chain fatty acids enter the peroxisome?

A

ABC proteins

34
Q

what are the steps of peroxisome beta oxidation

A
  1. dehydrogenation linked to catalase
  2. hydration
  3. dehydrogenation
  4. cleavage
35
Q

why is catalase necessary in the first step of peroxisome beta oxidation?

A

no electron transport chain to take the reducing equivalents from FAD
FAD gives them to O2, forming hydrogen peroxide
catalase oxidizes H2O2 to O2 and H2O

36
Q

how far does the peroxisome oxidize FA chains?

A

down to 8-10 FAs so they can get into the mitochondria

37
Q

what is peroxisome proliferation used for?

A

deal with high serum TAG presence
increase number of peroxisomes to deal with excess long chain fatty acids
results in decreased VLDL in blood

38
Q

what are 3 fates of FA in liver?

A

beta oxidation
peroxisome oxidation
resynthesis of TAGs

39
Q

what is left after complete oxidation of odd chain fatty acids?

A

propinoyl CoA (used as a substrate for gluconeogenesis)

40
Q

what are the enzymes of odd chain fatty acid oxidation?

A

propionyl CoA carboxylase
racemase
methylmalonyl-CoA mutase

41
Q

how are odd chain fatty acids oxidized?

A

beta oxidation down to propinoyl
then propionyl CoA carboxylase
racemase
methylmalonyl-CoA mutase

42
Q

what does propionyl CoA carboxylase do?

A

turns propionyl CoA to methylmalonyl CoA

43
Q

what does racemes do?

A

switches form of methylmalonyl CoA

44
Q

what does methylmalonl-CoA mutase do?

A

turns methylmalonyl CoA to succinyl CoA (succinyl CoA enters TCA cycle)
requires biotin to add a carbon via HCO3-

45
Q

how can odd chain fatty acid oxidation help in acylCoA dehydrogenase deficiencies?

A

give patients odd chain fatty acids so they can be processed this way to avoid the missing dehydrogenase
-enhances gluconeogenesis with anapleurotic reactions

Human Function- Exam 4 Material (25 decks)

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