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MBOD Block 4 > Khan Fatty Acid Oxidation > Flashcards

Khan Fatty Acid Oxidation Flashcards

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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?
25
58. What are the enzymes that reversibly transport FA‐CoA and Fa‐Carnitine in the mt.?
58. 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
59. Is there a shuttle for FA‐CoA?
59. If there was, why are we talking about all this carnitine transport business
27
60. What is the first step of β‐oxidation
60. AcylCoA DH takes 2e‐ out into FADH2 from saturated FA, oxidizes alpha‐beta carbon bond to alkene
28
61. What is the second step of β‐oxidation
61. Hydration via enoy CoA hydratase
29
62. Describe the action of glucagon on lipolysis
62. Glucagon receptorGsACcAMP via ATPPKAhormone sensitive lipase and perilipins phosphorylateddegradation of TAG
30
63. What is the third step of β‐oxidation?
63. B‐hydroxyacylCoA DH , oxidizes hydroxyl to ketone & produces NADH
31
64. What is the fourth step of β‐oxidation?
64. β‐ketothiolase (cleaves terminal Acyl‐CoA), reverse claisen condensation, thioester attached to ketone of beta carbon is good for nucleophilic attack
32
65. How many rounds of β‐oxidation to completely breakdown oleate?
8
33
66. How many rounds of β‐oxidation to completely breakdown palmitate?
7
34
67. What is similarity between CAC and β‐oxidation?
67. Hydration, and oxidation of metabolites to produce FADH2 and NADH
35
68. Where is AcylCoA synthetase located?
68. Bound to outer mt. membrane
36
69. Why can short and medium chain FA enter mt but not long chains?
69. ...large ones are biggercan’t diffuse..recall the pores acoss mt are membrane are selective for size
37
70. Why is the AcylCoA synthetase rx irreversible?
70. 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
71. How does free carnitine return across the membrane?
Translocase
39
72. What inhibits CPT1?
72. malonyl coA a FA synthesis precursor
40
73. What is the logic of CPT1/2?
73. 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
74. What is the regulated step of FA oxidation?
74. 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
75. How are electrons transferred from FADH to ETC?
75. ETFCoQETC via a series of semiquinones,etc.
43
76. How many ATP’s are generated by oxidation of a saturated 16 C FA?
76. 7FADH2x1.5,7NADHx2.5,8AcetylCoAx10,‐2ATP=106ATP
44
77. How many ATP’s are generated by oxidation of a saturated 22 C FA?
148
45
78. How many ATP’s are generated by oxidation of a saturated 49 C FA?
337
46
79. How many ATP’s are generated by oxidation of a saturated 109 C FA?
757so how do I get these #? Use the formula 2(N‐2)+5N‐2 for any saturated FA where N = # of carbons
47
80. How many ATP’s are generated by oxidation of palmitate (d16:9)?
80. 102 (loss of first round and usage of NADPH)
48
81. What is the major control of FA oxidation?
Availability of FA
49
82. What enzyme does insulin stimulate in FA synthesis?
82. ACC (Acetyl CoA carboxylase)
50
83. What is different in oxidation of unsaturated FA?
83. 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
84. What is different in oxidation of odd chain FA?
84. 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
85. What vitamin does methylmalonyl coa mutase require?
85. B12 (corrin ring structure)
53
86. What is the 1st step of peroxisome oxidation of FA?
86. AcylCoa DH (makes FADH2 and peroxide)
54
87. What step is diff. in peroxisomal oxidation of FA? How many times is oxidation repeated?
87. 1st step, until chain is 6‐10C’s ong and can be transported to mt. where oxidation is completed
55
88. What type of oxidation is used in peroxisome? What disease is correlated with a defect in this?
88. Alpha oxidation, Refsun’s disease
56
89. Where does omega‐oxidation take place?
ER
57
90. What is the most common sort of deficiencies in FA oxidation?
90. Oxidation of MCAD’s: treatment is to avoid fasting, eat meals with less fat to control lipolysis and decrease dependence on ketones
58
91. What is the energy diff. in peroxisomal oxidation of FA?
91. 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)

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