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Biochemistry > Lecture 28/29: Lipid metabolism > Flashcards

Lecture 28/29: Lipid metabolism Flashcards

1
Q

Major step in phase one of FA synthesis

A

Cytosolic entry of Acetyl CoA

Its made in the mitochondrial matrix but needed in cytoplasm

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2
Q

Major step in phase two of FA synthesis

A

Generation of Malonyl CoA
Acetyl CoA is carboxylated to malonyl CoA- Most important substrate in FA synthesis
Rate limiting step

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3
Q

Major step in phase three of FA synthesis

A

FA chain formation

Fatty acid synthase catalyzes 7 reactions that incorporate Acetyl CoA and Malonyl CoA into Palmitate

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4
Q

Steps in transport of Acetyl CoA from mitochondria to cytoplasm

A
  • Acetyl CoA + Oxaloacetate makes Citrate
  • Transport of citrate from mitochondria to cytosol
  • Citrate converted back to Acetyl CoA and OAA (citrate lyase catalyzes)
  • Acetyl CoA used in FA syntheses, OAA reduced to malate
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5
Q

Two mechanisms for regeneration of OAA after it is reduced to malate in cytosol

A
  • Malate transported back into mitochondria via malate/a-ketoglutarate transporter, then oxidized to OAA by malate dehydrogenase
  • Cytosolic malate converted to pyruvate which is transported to mitochondria and carboxylated to OAA by pyruvate carboxylase
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6
Q

Acetyl CoA carboxylase (ACC)

A

Catalyzes Acetyl CoA–>Malonyl CoA

  • Adds CO2 to Acetyl CoA
  • Rate limiting step in FA synthesis
  • Uses ATP and Biotin
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7
Q

ACC structural forms and active state

A

Dimeric- inactive

Polymeric- active

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8
Q

How does Malonyl CoA help regulate FA pathway

A

Inhibits Carnitine Acyltransferase (Rate limiting enzyme in FA degradation)
Prevents FA synthesis and degradation from occurring simultaneously

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9
Q

What substrates are required for palmitate synthesis

A

1 Acetyl CoA
7 Malonyl CoA
14 NADPH
14 H+

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10
Q

What are the substrates for the initial reaction to begin forming palmitate

A

1 Acetyl CoA
1 Malonyl CoA
2 NADPH
Then 1 Malonyl CoA and 2 NADPH are added 6x more

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11
Q

ATP citrate lyase function/regulation

A

Converts Citrate to Acetyl CoA and OAA
Stimulated by phosphorylation
Gene expression induced by glucose/insulin and counteracted by PUFAs (polyunsaturated fatty acids) and Leptin

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12
Q

Allosteric regulation of ACC (Acetyl CoA Carboxylase)

A 
\+ Citrate
\+ Insulin
- Glucagon
- High AMP levels
- Epinephrine
- PUFA
- Long chain fatty acids (palmitate)
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13
Q

Phosphorylation/activation state of ACC- what molecules regulate using what enzymes

A 
Inactivated by phosphorylation
Insulin + via activation of PP
Epi - via PKA
Glucagon - via PKA
AMP - via AMP kinase
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14
Q

Gene expression of ACC is upregulated via

A

High carb/low fat diet

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15
Q

Presence of phosphorylated sugars has what effect on Fatty acid synthase (FAS)

A

Increased activity

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16
Q

Induction/repression of transcription of FAS is affected by

A 
Insulin/glucocorticoid hormones ++
High carb/low fat ++
High fat diet --
Starvation --
High PUFA --
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17
Q

Where is palmitate converted into longer chain

A

Smooth ER or mitochondria

18
Q

Fatty acid synthesis occurs primarily where, but also

A

Primarily in liver

Also in adipose tissue, brain, kidneys, lactating mammary glands

19
Q

When palmitate is converted into a longer chain, what molecules donate carbons in the SER vs the Mitochondrial pathway of palmitate elongation

A

SER- Malonyl CoA is carbon donor

Mitochondria- Acetyl CoA is carbon donor

20
Q

T or F: Brain cells need longer chain fatty acids

A

True, Palmitate is lengthened 2 carbons at a time, using NADPH as reducing power

21
Q

T or F: FA with double bond beyond carbon 11-12 cannot be synthesized

A

False

FA with double bond beyond carbon 9 and 10 cannot be synthesized

22
Q

Where does introduction of double bonds (desaturation) occur for fatty acids

A

In the smooth ER, using NADH or NADPH and oxygen, catalyzed by Acyl CoA Desaturases

23
Q

Can humans synthesize Omega 3 and Omega 6 fatty acids

A

No, they must be incorporated into diet

24
Q

What is used to make arachidonic, docosahexanoic and eicosapentanoic acid

A

Linoleic acid

25
Q

Human desaturases cannot introduce unsaturation beyond

A

C9 and the methyl (omega) end

26
Q

What is the precursor for prostaglandins

A

Arachidonate

27
Q

Insulin effect on TAG breakdown

A

Insulin activates its receptor (RTK) which activates PP1
PP1 dephosphorylates and inactivates HSL
This inhibits breakdown of DAGs

28
Q

How do perilipins regulate lipolysis

A

They coat lipid droplets and control physical access to lipid breakdown enzymes

29
Q

Regulation of perilipins

A

Perilipins are phosphorylated by PKA which then allows association with HSL which promotes lipolysis

30
Q

What is the effect of overexpression of Perilipin 1

A

Inhibition of lipolysis

31
Q

Phase I of fatty acid breakdown

A

Fatty acid activation in cytosol (traps FA in cell)
FA-Albumin–> FA-CoA by Acyl-CoA synthetase
Can then pass through outer mito-membrane which is not permeable to regular FA

32
Q

Phase II of fatty acid breakdown

A

Beta-Oxidation in mitochondrial matrix

FA-CoA –> Acetyl CoA

33
Q

What must occur for FA-CoA to pass through mitochondrial inner membrane

A

Mitochondrial inner membrane is not permeable to FA-CoA

It is converted to FA-Carnitine, passes into matrix, and converted back to FA-CoA

34
Q

Carnitine Acyltransferase I

A

Converts Acyl CoA to Acyl Carnitine for transport into mitochondrial matrix

  • Rate limiting enzyme
  • Inhibited by Malonyl CoA
35
Q

Four steps of B-oxidation

A

Oxidation
Hydration
Oxidation
Thiolysis

36
Q

ACAD

A

Acyl CoA dehydrogenase
Step 1 oxidation
Oxidizes B-carbon to produce FADH2

37
Q

Enoyl CoA hydratase

A

Step 2 Hydration

Saturates the alkene with water to form B-hydroxyl acyl CoA

38
Q

Beta hydroxy acyl CoA dehydrogenase

A

Step 3 Oxidation

Oxidizes carbon to form ketoacyl CoA and NADH

39
Q

Acyl CoA acyl transferase or ketothiolase

A

Step 4 Thiolysis

Attaches sulfur of CoA to ketone formed from cleavage of acetyl CoA from fatty acyl chain

40
Q

Net ATP produced by B-oxidation of palmitic acid

A

129

41
Q

What happens to excess unused Acetyl CoA

A

Enters TCA cycle and combines with OAA -> citrate
If you are starving, OAA will be low and Acetyl CoA will not be able to enter TCA cycle
In this case it is converted to Ketone bodies which are used for energy during fasting or starvation

Biochemistry (20 decks)

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