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MBOD Block 4 > Khan Fatty Acid Oxidation > Flashcards

Khan Fatty Acid Oxidation Flashcards

1
Q
  1. Are fatty acids a source of energy for all tissues?
A

No

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2
Q
  1. How much energy does oxidation of fat yield?
A

9kcal/g

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3
Q
  1. What are fats largely ingested as?
A

TAG

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4
Q
  1. What pathway oxidizes FA?
A

B-Oxidation

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5
Q
  1. How are FA transported?
A

Bound to serum albumin

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6
Q
  1. What are some examples of saturated fA?
A
  1. palmitate (16C), stearate (18C), arachidate (20C)
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7
Q
  1. What are some examples of monounsaturated FA?
A
  1. palmitoleate, oleate (18C)
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8
Q
  1. What are some examples of polyunsaturated FA (PUFA)?
A
  1. linoleic, linolenic, arachidonic
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9
Q
  1. What bond is cleaved in beta‐oxidation?
A
  1. α‐β bond (by standard organic chemistry nomenclature convention)
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10
Q
  1. What FA can humans not synthesize, thus require in diet?
A
  1. ω‐3,ω‐6
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11
Q
  1. Does glucagon stimulate FA synthesis?
A
  1. no, it stimulates lipolysis
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12
Q
  1. Describe hepatic glycerol metabolism.
A
  1. Gycerol kinase phosphorylates glycerol to glycerol 3 phosphateG3P DHGNG
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13
Q
  1. What two hormones increase cAMP levels and in turn lipolysis (via PKA actions on Hormone
    sensitive lipase)?
A
  1. Glucagon, Epi
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14
Q
  1. What is an antilipolytic hormone?
A

Insulin

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15
Q
  1. What can lack of insulin in Type 1 diabetes lead to ( in terms of FA metabolism)?
A

Keto Acidosis

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16
Q
  1. What are long chain FA’s carried on in the blood?
A

Serum Albumin

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17
Q
  1. How is a FA transported across the mitochondrial membrane?
A
  1. Transport coupled to carnitine (which is mt. membrane soluble)
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18
Q
  1. What happens to FA in the mitochondria?
A
  1. Oxidizing environment, NAD is high relative to NADHrx. Favoring reducing equivalents
    favored and NADH/FADH2 produced for energy utilization via CAC,ETC, KB,etc.
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19
Q
  1. How are FA’s activated in order to form FA‐CoA
A
  1. FA‐CoA synthetase claves ATP to AMP (2 high energy bonds) to produce FA‐CoA and
    pyrophosphate (uses the energy from repulsion,entropy,resonance of ATP to form a high energy
    thioester bond, energy is conserve)
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20
Q
  1. How many high energy phosphate bonds are required just for activation of FA to FA‐CoA?
A

2

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21
Q
  1. What nucleotide is cleaved to activate FA?
A
  1. ATP to AMP.. if you miss this now you deserve to get it wrong
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22
Q
  1. What is the method of transport for short and medium chain FA’s into the mt.?
A

Diffusion

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23
Q
  1. What is the method of transport for long chain FA’s into the mt.?
A

Carnitine Transport

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24
Q
  1. Where are very long chain FA’s oxidized?
A

Peroxisome

25
Q
  1. What are the enzymes that reversibly transport FA‐CoA and Fa‐Carnitine in the mt.?
A
  1. Carnitine‐palmitoyl‐transferase 1 and 2 (CPT1,CPT2); CPT1 is on outer mt membrane, CPT2 is on inner membrane (reforms FA‐CoA and releases carnitine inside mt.)
26
Q
  1. Is there a shuttle for FA‐CoA?
A
  1. If there was, why are we talking about all this carnitine transport business
27
Q
  1. What is the first step of β‐oxidation
A
  1. AcylCoA DH takes 2e‐ out into FADH2 from saturated FA, oxidizes alpha‐beta carbon bond to
    alkene
28
Q
  1. What is the second step of β‐oxidation
A
  1. Hydration via enoy CoA hydratase
29
Q
  1. Describe the action of glucagon on lipolysis
A
  1. Glucagon receptorGsACcAMP via ATPPKAhormone sensitive lipase and perilipins
    phosphorylateddegradation of TAG
30
Q
  1. What is the third step of β‐oxidation?
A
  1. B‐hydroxyacylCoA DH , oxidizes hydroxyl to ketone & produces NADH
31
Q
  1. What is the fourth step of β‐oxidation?
A
  1. β‐ketothiolase (cleaves terminal Acyl‐CoA), reverse claisen condensation, thioester attached to
    ketone of beta carbon is good for nucleophilic attack
32
Q
  1. How many rounds of β‐oxidation to completely breakdown oleate?
33
Q
  1. How many rounds of β‐oxidation to completely breakdown palmitate?
34
Q
  1. What is similarity between CAC and β‐oxidation?
A
  1. Hydration, and oxidation of metabolites to produce FADH2 and NADH
35
Q
  1. Where is AcylCoA synthetase located?
A
  1. Bound to outer mt. membrane
36
Q
  1. Why can short and medium chain FA enter mt but not long chains?
A
  1. …large ones are biggercan’t diffuse..recall the pores acoss mt are membrane are selective for
    size
37
Q
  1. Why is the AcylCoA synthetase rx irreversible?
A
  1. Entropy, imagine trying to rearrange PPi to ATP with so very few PPi’s present (cleavage of PPi
    and the thioster bond is similar in free energy)
38
Q
  1. How does free carnitine return across the membrane?
A

Translocase

39
Q
  1. What inhibits CPT1?
A
  1. malonyl coA a FA synthesis precursor
40
Q
  1. What is the logic of CPT1/2?
A
  1. FA’s are carried via O‐acyl carnitine linkages which have an eq. constant near 1, due to orbital
    overlap bw C and O , usually this is not the case however it takes the place of the high energy due to thioeser bonds that have less overlap beteen S and C therefore less resonance stabilization and less energy than usual
41
Q
  1. What is the regulated step of FA oxidation?
A
  1. CPT1, entry into mt. recall cytosol and mt have diff. CoA pools (mt is used for ox, cyt. Is used for synthesiscompartmentalization once we move between pools we are more or less committed to the pathway).
42
Q
  1. How are electrons transferred from FADH to ETC?
A
  1. ETFCoQETC via a series of semiquinones,etc.
43
Q
  1. How many ATP’s are generated by oxidation of a saturated 16 C FA?
A
  1. 7FADH2x1.5,7NADHx2.5,8AcetylCoAx10,‐2ATP=106ATP
44
Q
  1. How many ATP’s are generated by oxidation of a saturated 22 C FA?
45
Q
  1. How many ATP’s are generated by oxidation of a saturated 49 C FA?
46
Q
  1. How many ATP’s are generated by oxidation of a saturated 109 C FA?
A

757so how do I get these #? Use the formula 2(N‐2)+5N‐2 for any saturated FA where N = # of
carbons

47
Q
  1. How many ATP’s are generated by oxidation of palmitate (d16:9)?
A
  1. 102 (loss of first round and usage of NADPH)
48
Q
  1. What is the major control of FA oxidation?
A

Availability of FA

49
Q
  1. What enzyme does insulin stimulate in FA synthesis?
A
  1. ACC (Acetyl CoA carboxylase)
50
Q
  1. What is different in oxidation of unsaturated FA?
A
  1. Isomerizes from cis unconjugated double bonds via enoylCoA isomerae to trans, ciscontinue
    beta oxreduce conjugated double bond via 2,4 dienoyl CoA reductase (uses NADPH) and
    produces trans d3 and is then isomerized into trans d2
51
Q
  1. What is different in oxidation of odd chain FA?
A
  1. Production of propionyl CoA upon terminal rx of beta oxpropionyl CoA carboxylase (uses
    1ATP for AMP) to produce methylmalony CoA via an epimerasemutase to produce succinyl CoArun it through TCA for 1 GTP, 1 FADH2 and 1 NADH (basically lose 2NADH from AKG DH,isocitrate DH)
52
Q
  1. What vitamin does methylmalonyl coa mutase require?
A
  1. B12 (corrin ring structure)
53
Q
  1. What is the 1st step of peroxisome oxidation of FA?
A
  1. AcylCoa DH (makes FADH2 and peroxide)
54
Q
  1. What step is diff. in peroxisomal oxidation of FA? How many times is oxidation repeated?
A
  1. 1st step, until chain is 6‐10C’s ong and can be transported to mt. where oxidation is completed
55
Q
  1. What type of oxidation is used in peroxisome? What disease is correlated with a defect in this?
A
  1. Alpha oxidation, Refsun’s disease
56
Q
  1. Where does omega‐oxidation take place?
57
Q
  1. What is the most common sort of deficiencies in FA oxidation?
A
  1. Oxidation of MCAD’s: treatment is to avoid fasting, eat meals with less fat to control lipolysis
    and decrease dependence on ketones
58
Q
  1. What is the energy diff. in peroxisomal oxidation of FA?
A
  1. Loss of energy from first step (still produces FADH but is not coupled to ETC since its not in mt,
    transfers e‐ instead to peroxide)

MBOD Block 4 (15 decks)

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