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Biochem > Fatty Acid Oxidation And Ketogenesis > Flashcards

Fatty Acid Oxidation And Ketogenesis Flashcards

1
Q

Too many fatty acids in blood stream

A

Can be dangerous

So liver oxidizes them into acetyl CoA

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2
Q

From acetyl CoA —>

A

Make ketone bodies

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3
Q

Ketone bodies are only produced when

A
  1. Low insulin

2. A lot of fatty aid oxidation is going on

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4
Q

When

A
  1. Overnight fast
  2. Endurance exercise
  3. Stress (epi)
  4. Low carb diets (alternative fuel)
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5
Q

What triggers breakdown of TG and release of FA from adipose tissue?

A

Glucagon or epinephrine

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6
Q

Triacylglycerol —> glycerol + 3 fatty acids

Requires?

A

3 different lipases- each cut off one fatty acid

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7
Q

3 lipases required

A
  1. ATGL
  2. HS lipase
  3. MAG lipase
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8
Q

Process of cleaving off 3 fatty acids

A

In glucagon/epi signaling cascade cAMP activates PKA —> PKA phosphorylates perilipin to activate it —> perilipin restructures lipid droplet to make TG accessible —> perilipin also interacts with ATGL which cleaves off first FA (TAG —> DAG) —> PKA also activates HS lipase by phosphorylating it —> HS lipase cleaves off second FA (DAG —> MAG) —> MAP lipase cleaves off third fatty acid (MAG —> glycerol + 3 FA)

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9
Q

Long chain fatty acids

A
  • Hydrophobic

- Can be toxic at high concentrations because hydrophobic interactions in proteins are disrupted

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10
Q

How are fatty acids transported to tissues?

A

Albumin

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11
Q

Albumin

A
  • Can bind multiple FA b/c has hydrophobic pocket

- Delivers FA to lipid transfer protein at plasma membrane which brings FA into cell

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12
Q

Fatty acids must be degraded by removal of

A

2-C units

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13
Q

Fatty acid oxidation occurs in

A

Mitochondrira

  • FA are transported in by lipid transfer protein after albumin delivers them
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14
Q

2-C unit is released as ________

A

Acetyl-CoA

NOT free acetate

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15
Q

Activation step of FA oxidation

A
  • Only needs to happen once

Requires CoA (SH group) and ATP (make thioester bond)

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16
Q

Activation Step

Where?
Driven by?

A

Free fatty acid + HS-CoA + ATP —> Acyl-CoA + AMP + PPi

  • Occurs at OMM
  • Driven by hydrolysis of PPi
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17
Q

Activated fatty acids can?

A

Cross the OMM

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18
Q

Why have to add a CoA to free fatty acid?

A

Need to attach a carnitine molecule to the FA so that it can be transported across the IMM

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19
Q

Transport across IMM

A

Acyl-CoA + carnitine acyl-carnitine + HS-CoA

Enzyme: carnitine acyltransferase I

Attach carnitine to Activated FA —> CoA comes off and releases energy because break thioester bond

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20
Q

_______ carries acyl carnitine across IMM into matrix

A

Translocase

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21
Q

Carnitine acyltransferase II

A

Add CoA back to FA in the matrix —> acyl- CoA

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22
Q

What happens to carnitine after add CoA in matrix?

A

Recycle carnitine back out via translocase for use again

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23
Q

Beta-Oxidation Total Reaction

A

Palmitoyl CoA (16-C) + 7 FAD + 7 NAD+ + 7 H2O + 7 CoA —>

8 acetyl CoA + 7 FADH2 + 7 NADH + 7 H+

24
Q

Summary of mechanism chemistry

A

Single bond —> double bond —> alcohol —> ketone

25
Q

Step 1

A

Convert single bond between alpha and beta carbons to a double bond

  • Oxidation / reduction

C-C oxidized to C=C
FAD is reduced to FADH2 —> 1.5 ATP

26
Q

Step 2

A

Add water molecule to double bond —> double bond becomes an alcohol

27
Q

Step 3

A

Convert alcohol into a ketone

-OH —> C=O
NAD+ reduced to NADH —> 2.5 ATP

28
Q

Step 4

A

Acetyl CoA is split off and attach CoA to beta carbon of chain that has now been shortened by 2 carbons

Acetyl CoA goes through TCA cycle
C=(n-2) goes back and cycle is repeated 7 time

29
Q

Get ____ ATP per cycle

A

14

30
Q

Complete oxidation of 1 palmitic acid yields

A

108 total ATP

106 net ATP (2 used in activation step)

31
Q

Large energy yield is due to

A

Highly reduced state of carbon in fatty acids

32
Q

Complete oxidation of one glucose yields

A

80 ATP

33
Q

Regulation of fatty acid oxidation is linked to

A

ETC and how rapidly NAD+ and FAD can be regenerated

34
Q

Carnitine acyltransferase I regulation

Result:

A

Negative allosteric modifier: Malonyl CoA (made by acetyl CoA carboxylase in fed state)

Result: FA do not get into mitochondria in fed state

35
Q

____ control rate of O2 consumption (rate of ETC)

A

ADP

High ADP = speed up ETC
Low ADP (high ATP) = slow down ETC
36
Q

Because ATP is utilized in gluconeogenesis…

A

ADP levels rise —> ETC speeds up —> FAD and NAD+ regenerated —> fatty acid oxidation increases

37
Q

NADH and FADH2

A

Negative allosteric modifiers

38
Q

Ketogenesis occurs in

A

Liver

39
Q

What happens during ketogenesis

A

Ketone bodies are synthesized from acetyl CoA

—> generating an alternative fuel source to glucose

40
Q

Advantages of ketone bodies (2)

A
  1. Water soluble

2. Reduces burden on liver to continue gluconeogenesis at a high rate

41
Q

Every tissue except ____________ can use FA for energy

A

RBC and brain

42
Q

Liver ________ ketone bodies but cannot ________

A

Liver synthesizes ketone bodies but cannot oxidize them because lack CoA transferase

43
Q

Step 1 ketogenesis

A

Condense 2 acetyl CoA together —> acetoacetyl CoA + CoA

44
Q

Step 2 ketogenesis

A

Acetoacetyl CoA + acetyl CoA + H2O —> HMG-CoA + CoA

If have insulin…HMG-CoA used by HMG-CoA reductase to make metholonate
If have no insulin…

45
Q

Step 3 ketogenesis

A

HMG-CoA —> Acetoacetate + CoA

46
Q

Step 4 ketogenesis

A

Depending on NAD+/NADH …

Form D-3-hydroxybutyrate or acetone

47
Q

3 ketone bodies

Which predominates?

A
  • Acetoacetate
  • Acetone
  • D-3-hydroxybutryrate (predominates)
48
Q

Ketone bodies do not rise significantly in blood until

A

2-3 days of starvation

49
Q

Advantage of ketone bodies

A

Glucose and muscle sparing

Reduces burden on liver for gluconeogenesis —> don’t have to breakdown as much muscle protein

50
Q

Conditions that increase KB synthesis and oxidation

A
  1. Length of fasting (>3 days)
  2. Low carb diets
  3. Untreated type 1 diabetes
  4. Chronic alcoholism
51
Q

Untreated Type 1 diabetes vs. Type 2 diabetes

A

Untreated type 1 diabetes leads to diabetic ketoacidosis

Type 2 diabetics do not show ketoacidosis

52
Q

Chronic alcoholism leads to

A

Alcohol induced ketoacidosis

53
Q

Oxidation of KB- step 1

A

D-3-hydroxybutyrate + NAD+ —> Acetoacetate + NADH + H+

54
Q

Oxidation of KB- step 2

A

Acetoacetate + succinyl CoA —> acetoacetyl CoA + succinate

Succinyl CoA is from TCA cycle

55
Q

Oxidation of KB- step 3

A

Acetoacetyl-CoA + CoA —> 2 acetyl CoA

Go into TCA cycle

56
Q

Oxidation of KB can be done by

A

Most tissues - Requires mitochondria

Not RBC or liver

Biochem (15 decks)

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