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Biochemistry-Exam 2 > FA Metabolism > Flashcards

FA Metabolism Flashcards

0
Q

CM and VLDL upon delivering their FA stores become?

A

LDL

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1
Q

What is the process of LPL?

A

Lipoprotein lipase. Cleaves all three FA at tissue site. Glycerol is free to dissolve.

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2
Q

How quickly do glucose stores exhaust during exercise?

A

Roughly 40 min

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3
Q

What is the preferred storage form of energy in the body?

A

Triglycerides

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4
Q

What is the process of FA degredation?

A

Beta oxidation

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5
Q

Where does beta oxidation occur?

A

Inner Mitochondrial matrix

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6
Q

T or F: The more oxidized a carbon, the less energy it stores

A

T (reduced carbons are the most energetic

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7
Q

What are FA ultimately metabolized to?

A

Acetyl CoA

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8
Q

Glycerol is metabolized to?

A

First to dihydroxyacetone phosphate, then dihydroxyacetone phosphpate (DHAP) to glucose and acetyl CoA

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9
Q

Where is glycerol broken down?

A

Liver and kidneys

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10
Q

What is the one exception to FA transport regarding CM?

A

Serum albumin can transport FA from adipose to tissues (muscle)

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11
Q

Acyl CoA is made from?

A

FA taking 2 ATP

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12
Q

What is the regulated step of beta oxidation?

A

Carnitine Palmitoyl Shuttle

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13
Q

T or F: Energy is required for the carnitine palmitoyl shuttle

A

F (passive)

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14
Q

What two enzymes and where are they located are critical to the carnitine palmitoyl shuttle?

A

Acyl CoA is transported into intermembrane space of mitochondria by carnitine palmitoyl tranfersase I (CPS I). Then made into Fatty acyl carnitine which is transported CPS II into MM where is is remade into fatty acyl CoA and Carnitine is recylced

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15
Q

Per two carbons of a FA, what is made?

A

NADH, FADH2, and 1 Acetyl CoA

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16
Q

When there are 4 carbons left in acyl CoA, what is produced in Beta oxidation?

A

2 Acetyl CoA

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17
Q

Carnitine is associated with what enzyme in FA oxidation?

A

CPS II

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18
Q

Where is CPS I located?

A

Outer mitochondrial membrane

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19
Q

Where is CPS II located?

A

Inner mitochondrial membrane

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20
Q

How are odd chain fatty acids digested?

A

When 3 carbons left, biotin and B12 make 4 carbon succinyl CoA from carbon dioxide

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21
Q

How are double bonds oxidized in FA?

A

Enzymes exist to isomerize the the molecule into the trans intermediate, lose 1 ATP though in the move

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22
Q

Mutations in double bond isomerases would cause?

A

Lack of beta oxidation in unsaturated FA

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23
Q

What is the yield from a 12:0 FA energetically?

A

5 FADH2, 5 NAD, and 6 acetyl CoA giving 97 ATP minus 2 ATP for acyl CoA synthesis

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24
Q

Fat is roughly what times more efficient in storing energy per weight as glucose?

A

2.5

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25
Q

What is Zellweger syndrome?

A

No functional peroxisome leading to defect in FA>26 carbon oxidation and alpha oxidation. You see lots of long FA in blood clinically

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26
Q

What is Refsum syndrome?

A

Defect in degradation or methyl branched FA leading to accumulation of phytanic acid

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27
Q

What bodies are produced when starving or on a low carb diet?

A

Ketone bodies

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28
Q

Describe what happens metabolically when low carb diet?

A

Depletion of glucose stores via gluconeogenesis meaning that oxaloacetate is depleted. Accumulate Acetyl CoA from FA degredation. Acetyl CoA is converted to ketone bodies. All takes place in liver

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29
Q

What are the two major ketone bodies?

A

Acetoacetate and beta-hydroxybutyrate (also known as 3-hydroxybutyrate)

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30
Q

Acetoacetate is converted into?

A

Beta-hydroxybutyrate via a dehydrogenase and into acetone sponateously.

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31
Q

Where are ketone bodies formed?

A

Liver

32
Q

Acetoacetate is made into?

A

2 acetyl CoA via a CoA transferase and thiolase which can undergo TCA in brain, kidney, heart and so on (oxaloacetate is not depleted in these tissues)

33
Q

What are some examples of physiological ketosis?

A

late pregnancy,neonatal period, high fat diet, starvation, extreme exercise

34
Q

Describe the pathway of pathological ketosis?

A

cells cannot absorb glucose, liver does gluconeogenesis > oxaloacetate goes down and Beta oxidation goes up leading to high ketone bodies. Acidosis and loss of fluid/minerals occurs

35
Q

What is hypoketotic hypoglycemia?

A

A symptom of starvation due to inefficient use of FA as primary energy source. Cant make ketone bodies

36
Q

Brain fuel?

A

Glucose, no beta oxidation, ketone bodies in starvation

37
Q

Muscle fuel?

A

Glucose, FA, ketone bodies, large glycogen storage, beta oxidation in resting muscle, and little TCA with glucose due to cori cycle

38
Q

Heart fuel?

A

No glycogen, almost exclusively aerobic, FA and ketone bodies, doesn’t really use glucose

39
Q

Adipose tissue fuel?

A

Glucose, FA, needs glucose to make glycerol, typical storage of 135000 kcal

40
Q

Kidney fuel?

A

Glucose, FA, ketone bodies, uses about 10 percent of total oxygen, very important for gluconeogenesis

41
Q

Liver fuel?

A

Smaller glycogen storage, doesn’t use glucose/FA/ or ketone bodies but makes glucose from alanine, lactate, or pyruvate. Glycolysis to get building blocks for biosynthesis, energy from alpha-keto acids (AA degredation), under starvation can use beta oxidation

42
Q

Where does FA synthesis take place?

A

Liver and adipose (mostly in liver). Synthesis from acetyl CoA and Malonyl CoA IN THE CYTOSOL

43
Q

Where does FA synthesis take place in the cell?

A

The cytosol

44
Q

Describe the in/out of formation of palmitic acid (16:0) from a FA synthesis.

A

8 Acetyl CoA (from glucose or AA) + 14 NADPH + 14 H+ + 7ATP gives one Palmitic acid

45
Q

Where does NADPH for FA synthesis come from?

A

Pentose phosphate pathway or Malic enzyme

46
Q

What protein is responsible for facilitating FA synthesis?

A

Acyl Carrier Protein (ACP)

47
Q

T or F: A FA being synthesized is attached to CoA

A

F (attached to ACP instead)

48
Q

What is the most regulated step for FA synthesis?

A

Isocitrate to Alpha-ketoglutarate in TCA. Regulation of isocitrate dehydrogenase.

49
Q

When do you make FA?

A

High fat high carb diet. Done in abundance of ATP. You don’t make fat from fat; you make it from carbohydrates

50
Q

What regulates isocitrate dehydrogenase?

A

ATP and NADH inhibit the enzyme (well fed state)

51
Q

What happens when isocitrate dehydrogenase is inhibited?

A

Citrate is exported from the mitochondria to the cytosol via the citrate shuttle

52
Q

Describe the citrate shuttle?

A

Citrate into the cytosol from the MM, where it is taken to oxaloacetate and then to malate and then to pyruvate and back into the MM. (Produces an Acetyl CoA NADPH and consumes NADH)

53
Q

Malate enzyme regenerates what?

A

NADPH

54
Q

Citrate lysase catalyzes?

A

Citrate to oxaloacetate releasing acetyl CoA

55
Q

What is required to make Malonyl CoA from Acetyl CoA?

A

Biotin and ATP and CO2 to carboxylate acetyl CoA to Malonyl CoA

56
Q

T or F: CO2 is added to the carbon count in a FA

A

F (added to make Malonyl ACP but is released wheh combined with Acetyl ACP)

57
Q

What is the first step of FA synthesis?

A

Acetyl ACP and Malonyl ACP condense to make a chain

58
Q

Acetyl CoA Carboxylase makes?

A

Malonyl CoA from Acetyl CoA

59
Q

Excess alcohol consumption does what to metabolic pathways?

A

Ethanol to acetylaldehyde to acetate releasing NADH. Excess NADH pushes pyruvate to lactate and oxaloacetate to malate

60
Q

How are FA longer or shorter than 16 Carbons made?

A

Chain elongation

61
Q

Where does chain elongation occur?

A

ER membrane (mitochondria possible too)

62
Q

How does chain elongation occur?

A

Addition of 2 carbons at at time.

63
Q

What accepts carbons in chain elongation? Donates?

A

Acyl-CoA is donator to Malonyl-CoA to elongate (i.e. 16 is added to 2)

64
Q

T or F: Elongation works on both saturated and unsaturated acyl CoA

A

T

65
Q

Where are unsaturated FA made?

A

ER by desaturases

66
Q

For a 16:0 FA, what are the possible double bonds?

A

Del 9, 6, or 5

67
Q

T or F: Molecular oxygen is the hydrogen acceptor in synthesis of desaturated FA

A

T (NADH + H to NAD and 2 H2O)

68
Q

What is the limitation to desaturases in terms of position?

A

Cannot desaturate beyond C-9 or omega-7 in a 16:0 chain

69
Q

What are the essential FA?

A

Omega 6 and Omega 3 (del(9,12),18:2 and del (9,12,15), 18:3)

70
Q

In the presence of AMP what happens to acetyl CoA carboxylase?

A

AMPK is activated to phosphorylate the carboxylase and prevent malonyl CoA formation

71
Q

T or F: Acetyl CoA Carboxylase is phosphorylated to be inactivated

A

T

72
Q

What happens to AMPK in the presence of ATP?

A

Inhibited, preventing the inactivation of carboxylase therefore there is malonyl CoA formation

73
Q

Glucagon and epinephrine encourage Acetyl CoA carboxylase to?

A

Become inactive by inhibiting the activation of the Acetyl CoA carboxylase (do not make fat)

74
Q

Insulin encourages Acetyl CoA carboxylase to?

A

Become active and dephosphorylate and activate the Acetyl CoA carboxylase

75
Q

What are the two general categories of FA metabolism regulation?

A

Rapid: allosteric or covalent modification (AMPK for example on Acetyl CoA carboxylase)
Slow: Rate of synthesis (are enzymes present)

76
Q

Name the 5 lipogenic enzymes and their function

A

Acetyl CoA Carboxylase - Cytosol to make malonyl CoA in synth
FA synthase - Combine malonyl ACP and acetyl ACP in synth
Citrate lyase - NADPH transport in the citrate shuttle (Acetyl CoA in cytosol)
Malic Enzyme - NADPH transport in citrate shuttle (malate to pyruvate in the cytosol to make NADPH)
Dehydrogenase of PPP- Generate NADPH

77
Q 
Describe what happens to long term lipogenic enzymes:
High CHO diet
Up reg insulin
High Fat/Low CHO diet
Fasting
A

UP, UP, DOWN, DOWN

78
Q

Describe three instances of short term regulation of lipogenic enzymes

A

Isocitrate DH is inhibited by ATP
Cartinitine-Palmitoyl Translocase (CPS 1 basically) is inibited by malonyl CoA to prevent beta oxidation
Acetyl CoA carboxylase is inhibited by AMPK (it is phosphorylated), activated by citrate, inhibited by palmitoyl CoA
Hormones: Insulin activates, glucagon and epinephrine inactivate

Biochemistry-Exam 2 (14 decks)

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