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DMD 5242 > Lipids, Beta Oxidation, lipid syntesis (complete) > Flashcards

Lipids, Beta Oxidation, lipid syntesis (complete) Flashcards

1
Q

What are some biological functions of lipids

A
  1. STORAGE OF ENERGY
  2. Insulation
  3. Water repellant
  4. Buoyancy
  5. MEMBRANE STRUCTURE
  6. cofactors for enzymes
  7. SIGNALING MOLECULES
  8. Pigments
  9. Antioxidants
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2
Q

What makes Lipids effecient at storing energy

A
  1. they are reduced compounds (lots of available energy)

2. their hydrophobic nature (Good for tight packing)

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3
Q

What role do lipids play in membrane structure

A

they are the main structure of cell membranes

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4
Q

What signaling molecules are made of lipids

A
  1. paracrine hormones
  2. steroid hormones
  3. Growth factors
  4. Vitamins A + D
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5
Q

What determines if a fatty acid is an Omega 3 (or Omega 6) fatty acid

A

Omega 3 fatty acids are fatty acids that have a double bond that begins on the third Carbon counting from the back of the fatty acid.
(Omega 6 are fatty acids that have a double bond that begins on the 6th carbon from the back)

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6
Q

Do humans Synthesize omega 3 fatty acids

A

nope

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7
Q

Do humans need omega 3 fatty acids

A

yes

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8
Q

is omega 3 an essential nutrient

A

yes

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9
Q

How is the solubility of a fatty acid affected by its chain length

A

the longer the chain the less soluble it becomes

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10
Q

how is the melting point of a fatty acid affected by its chain length

A

the longer the chain the higher the melting point

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11
Q

how is the melting point of a fatty acid affected by the number of double bond it has

A

the more double bonds a fatty acid has the lower the melting point

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12
Q

Which type of fatty acid will be the least soluble

A

a long one

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13
Q

which type of fatty acid will have the highest melting point

A

the longest fatty acid with the least number of double bonds

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14
Q

Which type of fatty acid will have the lowest melting point

A

a short fatty acid with many double bonds

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15
Q

What is a saturated fatty acid

A

a fatty acid without double bonds

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16
Q

what is an unsaturated fatty acid

A

a fatty acid with double bonds

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17
Q

What is a monounsaturated fatty acid

A

a fatty acid with one double bond

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18
Q

what is a polyunsaturated fatty acid

A

a fatty acid with multiple double bonds

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19
Q

What are the steps in naming a fatty acid

A

A:B (DeltaC,C,C) D-C- Name
A = Number of carbons in the fatty acid
B = The Number of double bonds in the fatty acid
C = The different Carbon #’s that start a double bond
D = whether the C double bond is cis or trans

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20
Q

18:1 (Delta 9) cis-9- (NAME)

how many carbons does this fatty acid have

A

18

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21
Q

18:1 (Delta 9) cis-9- (NAME)

how many double bonds does this fatty acid have

A

1

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22
Q

18:1 (Delta 9) cis-9- (NAME)

where does the double bond of this fatty acid begin

A

the 9th carbon

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23
Q

18:1 (Delta 9) cis-9- (NAME)

is the double bond in this fatty acid cis or trans

A

cis

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24
Q

Which type of bond is more common in natural unsaturated fats

A

Cis

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25
Q

What does the Cis double bond lead to in the fatty acid chain

A

a kink in the chain

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26
Q

Which fats pack and stack better: unsaturated or saturated fats

A

saturated fats

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27
Q

why don’t unsaturated fats pack and stack as well as saturated fats

A

because their double bond puts a kink in the chain

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28
Q

Which type of fatty acids have a higher melting point: saturated or unsaturated fatty acids

A

saturated fats

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29
Q

why do saturated fats have a higher melting point than unsaturated fats

A

because saturated fatty acids are straight and stack better, so the have greater van der waal forces between them, making them harder to pull apart.

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30
Q

What is a trans fatty acid

A

unsaturated fatty acids that are partially dehydrogenated. this gives it a trans double bond instead of a cis double bond

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31
Q

what does a trans double bond do to the fatty acid

A

makes it more extended (less kinked) which gives it a higher melting point

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32
Q

why are trans fats made

A

it increases the shelf life

it has a higher melting point (solid at room temp)

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33
Q

What is the problem with trans fats

A

consuming them increases the risk of cardiovascular disease

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34
Q

What does the basis of lipid classification come from

A

the structure and function of the lipid

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35
Q

Do all lipids contain fatty acids

A

nope

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36
Q

What is an example of lipids that don’t have fatty acids

A

cholesterol

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37
Q

What are the two different classifications of lipids that DO have fatty acids

A

storage lipids and membrane lipids

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38
Q

What is the name for the type of lipids that are storage lipids

A

triacylglycerols

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39
Q

What are the different categories of membrane lipids

A
  1. phospholipids
  2. glycolipids
  3. archaebacterial ether lipids
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40
Q

What is the structure of triacylglcerols

A

a glycerol bound to three fatty acids

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41
Q

Are triacylglycerols polar or nonpolar

A

nonpolar

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42
Q

Why do fats carry more energy per carbon than polysaccharides

A

because they are more reduced

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43
Q

Which is for quick delivery of energy? fatty acids or polysaccharides

A

polysaccharides

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44
Q

What makes up glycerophospholipids

A
  1. Glycerol (3 binding sites)
  2. Two attached Fatty acids bound to glycerol
  3. a phosphate that can have an alcohol added to it
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45
Q

What kind of fatty acid is usually added to the C2 of a glycerophospholipid

A

a UNsaturated fatty acid

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46
Q

A glycerophospholipid usually has two fatty acids (C2 usually has an unsaturated fatty acid), what else is bound to it

A

a phosphate group

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47
Q

what is usually added to the phosphate group of a glycerophospholipid

A

an alcohol

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48
Q

What is the name for substituent groups added onto the glycerol that aren’t fatty acids

A

head groups

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49
Q

Where is phosphatidylcholine used

A

it is the major component of most eukaryotic cell membranes

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50
Q

What is phosphatidylcholine

A

a glycerophospholipid with a choline as the head group

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51
Q

What is phosphatidylethanolamine

A

a glycerophospholipid that has ethanolamine (C2,N,H3) as the head group

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52
Q

Is plasmalogen an ether lipid?

A

yes

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53
Q

what is the structure of plasmalogen like in comparison to phosphatidylethanolamine

A

plasmalogen is the vinyl ether analog of phosphatidylethanolamine. The glycerol has an ether attached to one of it’s carbons as opposed to an ester like normal

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54
Q

Where is plasmalogen commonly found

A

heart tissue of vertebrates

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55
Q

how well is the function of plasmalogen understood

A

it is not well understood.

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56
Q

how easily is plasmalogen cleaved

A

not very easily, it is resistant to cleavage by common enzymes, but a few specific lipases can

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57
Q

What MAY be some possible functions of plasmalogen

A
  1. increase membrane rigidity
  2. source of signaling lipids
  3. antioxidants
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58
Q

What is the difference between sphingolipids and glycerophospholipids

A

the backbone of sphingolipids isn’t glycerol, its sphingosine

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59
Q

What are the main differences between sphingosine and glycerol

A
  1. sphingosine only has two spots where things can bind (it has a long-chain amino alcohol instead of a third space for binding)
  2. the fatty acid is joined by amide linkage, not ester linkage
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60
Q

What king of fat is sphingomyelin

A

a sphingolipid

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61
Q

What is the structure of sphingomylin like

A
  1. a sphingosine
  2. amide linked fatty acid
  3. phosphocholine head group
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62
Q

Where do we find sphingomyelin

A

in the myelin sheath that surrounds some nerve cells

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63
Q

Why do fats carry less water than polysaccharides

A

because they are non-polar

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64
Q

When do we use glycogen and glucose as energy sources

A

in short term energy needs, with a quick delivery

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65
Q

Are fats for long term storage or short

A

long term

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66
Q

is the delivery of fats into energy fast or slow

A

it is a slow delivery

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67
Q

Where is cholesterol synthesized or obtained from food

68
Q

from what do many hormones come

69
Q

What are the steps of digestion of dietary fatty acids from arrival in the intestines to arrival at the tissues

A
  1. Bile salts emulsify dietary fats in the small intestine
  2. lipases degrade triacylglycerides
  3. break down products are taken up by the intestinal mucosa and converted into triacylglycerols
  4. Triacyglycerols, apolipoproteins, and cholesterol are packaged as chylomicrons
  5. chylomicrons move through the lymph and blood to the tissues
  6. in the capillary lipoprotein lipase converts triacylglycerols into glycerol and fatty acids
  7. Fatty acids enter cells and are either used for fuel, or saved as storage
70
Q

What initially emulsifies fats in the small intestine

A

bile salts

71
Q

what happens to triacyglycerides in the intestine

A

they are degraded by lipases

72
Q

what happens to the degraded triacyglycerides that are degraded in the intestine once they are moved into the intestinal mucosa

A

they are reconverted into triacyglycerols

73
Q

What is a chylomicron, and what is its function

A

it is a ball of fats essentially, with phospholipids making an outer membrane, triacyglycerols and other fatty acids in the middle. and apolipoproteins helping stabilize it.
its function is a sort of transport vesicle for fats through the blood

74
Q

What happens to triacyglycerols in the capillaries

A

they are broken down by lipoprotein lipase into fatty acids and glycerol so they can enter cells

75
Q

what happens to the fatty acids and glycerol upon arriving at the cell

A

they are either used for energy or stored

76
Q

What hormone stimulate the breakdown of fats

A

epinepherine and glucagon

77
Q

what is the difference in signals sent to the fats by epinepherine and glucagon

A

epinepherine says “we need energy now”

glucagon says “we are out of glucose”

78
Q

What is the process by which glucagon stimulates the mobilization of stored triacyglycerols

A
  1. glucagon binds to the receptor
  2. adenylate cyclase is activated
  3. Adenylate cyclase produces cAMP
  4. cAMP activates PKA
  5. PKA activates Hormone sensitive lipase and phosphorylates perilipin
  6. Phosphorylated perilipin causes CGI to move to ATGL
  7. ATGL takes triaccylglylcerols and converts them into diacyglycerols
  8. Hormone sensitive lipase takes Diacyglycerols and converts them into monoacyglycerols
  9. MGL takes monoacyglycerols and cleaves them into glycerol and a fatty acid
  10. Fatty acids move to the blood and are transported by serum albumin
  11. They enter cells through fatty acid transporters
  12. Then begin beta oxidation
79
Q

What are the steps of mobilization of fats from glucagon binding to its receptor, to the first fatty acid chain being removed

A
  1. glucaon binds to the receptor, activating adenylate cyclase
  2. adenylate cyclase produces cAMP
  3. cAMP activates PKA
  4. PKA phosphorylates perilipin, and Hormone sensitive lipase (HSL)
  5. Perilipin releases CGI which goes and binds to ATGL
  6. ATGL begins to break down triacylglycerols
80
Q

What does ATGL stand for

A

adipose triacylglycerol lipase

81
Q

what are the steps of fat mobilization from the activation of ATGL by CGI to beta oxidation

A
  1. ATGL breaks down triacylglycerols to diacylglycerols
  2. HSL breaksdown diacyglycerols into monoacyglycerols
  3. MGL breaks down monoacyglycerols into glycerol and a fatty acid
  4. fatty acids are transported in the blood by serum albumin
  5. fatty acids leave the blood through fatty acid transporters
  6. in the cell they undergo beta oxidation
82
Q

What is MGL

A

monoacylglycerol lipase

83
Q

what happens to the glycerol that is cleaved off of the monoacyglycerol by MGL

A

in the cell it is converted into an intermediate of glycolysis and is used to produce ATP

84
Q

What is the enzyme that begins the conversion of glycerol into glyceraldehyde-3-phosphate (intermediate in glycolysis)

A

glycerol kinase (this step uses ATP)

85
Q

What is the first step of breaking down fatty acids. This happens once it enters the cell

A

it is converted into fatty acyl-CoA

86
Q

Why are fatty acids converted into fatty acyl-CoA upon entering the cell

A

So they can be transported into the mitochondria

87
Q

why do the fatty acids need to get into the mitochondria of cells

A

because that is where beta oxidation occurs

88
Q

how does the process of converting fatty acids into fatty acyl-CoA work

A
  1. Fatty acid adds an AMP from ATP and becomes more reactive

2. CoA comes and replaces the AMP

89
Q

Can fatty acids diffuse freely across the mitochondrial membrane

A

Yes, if they are short (12 carbons or less_)

No, if they are long (most free fatty acids)

90
Q

if longer fatty acids can’t diffuse across the mitochondrial membrane then how do they enter the mitochondria

A

through the acyl-carnitine/carnitine transporter

91
Q

how does the acyl-carnitine/carnitine transporter work

A
  1. fatty acyl-CoA has the acyl-CoA replaced by carnitine
    (carnitine acyltransferase 1 does this)
  2. Fatty-carnitine moves through the carnitine transporter into the mitochondria
  3. Fatty-carnitine has the carnitine replaced by acyl-CoA (done by carnitine acyltransferase 2)
  4. carnitine leaves to do the process again
92
Q

what happens to the fatty acyl-CoA in the mitochondria

A

it goes through beta-oxidation

93
Q

what are the steps of beta-oxidation

A
  1. trans double bond is formed between alpha and beta carbons (creates FADH)
  2. Water adds to the double bond and creates an alcohol off of the Beta carbon
  3. NAD+ steals the H and electrons from the alcohol creating a carbonyl at the beta carbon (makes NADH)
  4. Thiolase uses CoA-SH and replaces the two carbon end with CoA
  5. this results in the loss of 2 carbons (Acetyl-CoA) and a new CoA end to the fatty acid
94
Q

What is the Structure of FADH like

A

a three six-carbon ring molecule

95
Q

for each step of beta oxidation how many NADH, FADH, and Acetyl=CoA do you get

A

1- FADH
1- NADH
1- Acetyl-CoA (except you get 2 acetyl-CoA on the last round)

96
Q

What happens to the NADH and FADH produced in beta oxidation

A

they go to the ETS to create ATP

97
Q

What happens to the Acteyl-CoA produced in beta oxidation

A

it goes through the Citrate cycle to make ATP, NADH, and FADH

98
Q

What kind of double bond is formed in beta oxidation when FAD+ comes in and becomes NADH creating a double bond

99
Q

can the cell easily handle cis double bonds

100
Q

how does the cell handle and breakdown monounsaturated fatty acids

A

it uses an isomerase to convert cis double bonds to trans double bonds

101
Q

how does the cell handle and breakdown polyunsaturated fatty acids

A

it uses isomerase to convert the cis double bond at carbon 2 to a trans double bond, and it uses a reductase to reduce all the other cis double bonds

102
Q

what is the step by step process of breaking down a polyunsaturated fatty acid

A
  1. beta oxidation takes off carbons in two carbon segments until the cis double bond is found at the Beta (3rd) carbon
  2. Isomerase moves the bond to convert the cis double bond into a trans double bond (just like after the first step of regular beta oxidation)
  3. last three steps of beta oxidation occur, and the first step of the next beta oxidation (FADH made)
  4. there is now a trans double bond at beta carbon, and the next cis double bond is one carbon away
  5. reductase takes these two double bondos, and reduces them into a single double bond in between where the old double bonds were.
  6. isomerase acts again to move the double bond back to where it needs to be to do the last three steps of beta oxidation.
103
Q

How do you get rid of the first double bond of a polyunsaturated fat

A

isomerase comes in and turns it into a trans double bond, then does the last three steps of beta oxidation and cleaves off the two end carbons

104
Q

What happens after you have gotten rid of the first cis double bond of a polyunsaturated fat, and have removed the end 2 carbons

A

you will do the first step of beta oxidation and create a trans double bond between the alpha and beta carbons

105
Q

what happens when you have a trans double bond between the alpha and beta carbons, and a cis double bond that begins one carbon away

A

reductase will come in and reduce the two double bonds into one trans double bond in between where the two double bonds were. then isomerase will come in and move the double bond back between the alpha and beta carbons

106
Q

what happens after you have used reductase to turn the two double bonds (of a polyunsaturated fat) into one double bond, then moved i to between the alpha and beta carbon.

A

you will finish out the last three steps of beta oxidation and continue on.

107
Q

What happens when you try beta oxidation of a fatty acid with an uneven number of carbons

A

you will do beta oxidation until you have just the three carbons left

108
Q

what is the molecule called that is made up of the last three carbons of an uneven numbered fatty acid that has gone through beta oxidation

A

propionyl-CoA

109
Q

What happens to the propionyl-CoA that results from the beta-oxidation of an uneven numbered fatty acid

A
  1. bicarbonate, ATP and Biotin are used to add a carboxy group to the middle carbon of propionyl-CoA
  2. (Isomeration) the carboxy group is then moved to the third carbon of propionyl-CoA
  3. This molecule is succinyl-CoA, it enters the krebs cycle
110
Q

What is required for the carboxylation of propionyl-CoA

A
  1. bicarbonate
  2. ATP
  3. biotin
111
Q

What does biotin usually do

A

add a carbon

112
Q

What is required for isomerization of propionyl-CoA (after carboxylation)

A

Coenzyme B

113
Q

What causes ketone bodies to be made

A

depletion of oxaloacetate

114
Q

How does the formation of ketone bodies allow beta oxidation to continue

A

it releases CoA so it can be used more in beta oxidation

115
Q

What is required for acetyl-CoA to enter krebs cycle

A

oxaloacetate

116
Q

what happens to acetyl-CoA when oxaloacetate is depleted

A

it is turned into ketone bodies

117
Q

What enzyme does the first step of ketone body formation from acetyl-CoA

A

thiolase (last step of beta oxidation)

118
Q

What is the process of formation of ketone bodies from acetyl-CoA

A
  1. twp Acetyl-CoAs are joined by thiolase)

2. Then one or two reactions occur producing the two ketone bodies

119
Q

where does the formation of ketone bodies take place

A

in the liver

120
Q

What are the two ketone bodies formed in the liver

A
  1. Acetoacetate

2. beta-hydroxybutarate

121
Q

what happens to the ketone bodies acetoacetate and beta-hydroxybutarate after they are formed in the liver

A

they are exported to the heart, muscle, kidney, and brain to be used as energy

122
Q

What are the building blocks of fatty acid synthesis, What molecules is added one at a time to a growing fatty acid chain

A

Acetate (though it is malonyl-CoA is where the acetate comes from)

123
Q

What is the function of ACC (Acetyl-CoA carboxylase) in fatty acid synthesis

A

It is responsible for synthesizing malanyl-CoA from bicarbonate and acetyl-CoA

124
Q

What are the two parts of the ACC

A
  1. biotin Carboxylase

2. transcarboxylase

125
Q

what happens at the biotin carboxylase portion of the ACC

A
  1. Biotin binds

2. then the ACC Adds bicarbonate to the biotin molecule create a carbonyl group

126
Q

What happens after the ACC has added a carbonyl group to biotin in the biotin carboxylase portion of ACC

A

The biotin/carbonyl group flips over to the transcarboxylase site

127
Q

what happens in the transcarboxylase site of the ACC

A

Acetyl-CoA comes and pulls the carbonyl group off of biotin, creating Malonyl-CoA

128
Q

What does malonyl-CoA do in fatty acid synthesis

A

it is the molecule that adds 2Cs to the fatty acid with each pass through the process

129
Q

what is the fatty acid synthase (FAS)

A

the enzyme to which malonyl-CoA will bind to, then a fatty acid will elongate from there

130
Q

What is the first molecule to add to FAS

A

Acetyl-CoA

131
Q

where will the Acetyl-CoA that first attaches to the FAS end up in the fatty acid

A

it will be the very end, the tail of the fatty acid

132
Q

What are the steps of fatty acid synthesis

A
  1. Acetyl-CoA binds to the FAS
  2. Malonyl-CoA binds to the FAS at a different site
  3. The acetate portion of Malonyl-CoA is added to the front of the existing Acetyl-CoA, CO2 is given off (CO2 is the other half of malonyl-CoA)
    - Now we have a 4 carbon chain with 2 carbonyl groups
  4. The back carbonyl is reduced to an alcohol
  5. Then the alcohol is dehydrogenated and creates a C-C double bond
  6. NADPH is used to reduce the C-C double bond to a C-C single bond.
  7. Another Malonyl-CoA binds and goes through the process again
133
Q

What is the overall goal of each round of fatty acid synthesis

A

to attach a two-C acetate from malonyl-CoA to a growing chain and reduce it

134
Q

Fatty acid synthesis has four enzyme catalyzed steps, what kinds of reactions are they

A
  1. Condensation (adding acetate to the chain)
  2. Reduction (carbonyl to alcohol)
  3. Dehydration (alcohol to trans alkene)
  4. Reduction (alkene to alkane)
135
Q

What happens in the condensation reaction of fatty acid synthesis

A

the acetate portion of a malonyl-CoA is added to the front of the growing fatty acid. now we have two carbonyl groups (this one is in front) CO2 is released (the Chain becomes 2 C longer)

136
Q

what happens in the first reduction reaction of fatty acid synthesis

A

the back carbonyl group is reduced to an alcohol by NADPH

137
Q

What happens in the dehydration reaction of fatty acid synthesis

A

the OH alcohol leaves as water, and a C=C trans double bond is formed

138
Q

What happens in the second reduction reaction of fatty acid synthesis

A

the double bond is reduced to a single bond by NADPH (it is also after this step that the growing chain moves back to the original binding site, opening up the other for another malonyl-CoA)

139
Q

What happens after the second reduction reaction of fatty acid synthesis

A

the growing chain moves back to the original binding site, opening up the other for another malonyl-CoA, once that binds the process is repeated over and over again

140
Q

to form palmitate, how many ATP, and Acetyl CoA are used to make the necessary Malonyl-CoA

A

7 ATP and 7 Acetyle-CoA are used to make the 7 Malonyl-CoA we will need to synthesize palmitate

141
Q

What is needed with the 7 Malonyl-CoA (formed from ATP And Acetyl-CoA) to form palmitate

A
  1. Another Acetyl-CoA
  2. 14 NADH (two used per cycle in the reduction reactions)
  3. 14 H+ (two used per cycle in the reduction reactions)
  4. (we also use the 7 Malonyl-CoA)
142
Q

What are all of the things needed to make palmitate

A
  1. 8 Acetyl-Coa
  2. 7 ATP
  3. 7 Malonyl-CoA (from 7 of the Acetyl-CoA and the ATP)
  4. 14 NADH
  5. 14 H+
143
Q

What are all of the products formed when making palmitate

A
  1. 7ADP
  2. 7 Pi
  3. 7 CO2
  4. 8 CoA
  5. 14 NADP+
  6. 7 H2O
144
Q

In eukaryotes how does the amount of ATP used in fatty acid synthesis change

A

you use 3 ATP per cycle instead of just one

145
Q

Why do eukaryotes use 3 ATP per cycle instead of just 1

A

because in eukaryotes Fatty acid synthesis occurs in the cytosol, so Acetyl-CoA is transported out of the mitochondria into the cytosol at the cost of 2 ATP

146
Q

What is required for fatty acid synthesis

147
Q

will fatty acid synthesis occur when NADPH levels are low

148
Q

What are the two ways that we get NADPH

A
  1. pentose phosphate pathway

2. Malic enzyme

149
Q

Where do we have the pentose phosphate pathway happening

A

adipocytes, hepatocytes, mammary gland

150
Q

Where do we have the malic enzyme making NADPH

A

in adipocytes

151
Q

What is the process of making NADPH with the malic enzyme

A

Malate is oxidized by the malic enzyme and NADP to make Pyruvate, CO2 and NADPH

152
Q

what are the substrates in the malic enzyme creation of NADPH

A
  1. Malate

2. NADP+

153
Q

What are the products of the malic enzyme creation of NADPH

A
  1. NADPH
  2. Pyruvate
  3. COs
  4. H+
154
Q

How many NADPH are made by each pass through the malic enzyme

155
Q

How many NADPH are made by each pass through the pentose phosphate pathway

156
Q

What are the substrates in the pentose phosphate pathwya

A
  1. Glucose-6-phosphate

2. two NADP+

157
Q

what are the products of the pentose phosphate pathway

A
  1. two NADPH

2. Ribose-5-Phosphate

158
Q

What is the process of getting Acetyl-CoA out of the mitochondria and into the cytosol for fatty acid synthesis

A
  1. Acetyl-CoA and oxaloacetate are syntesized into citrate
  2. citrate leaves through the citrate transporter
  3. Acetyl-CoA breaks off for fatty acid synthesis
  4. Oxaloacetate left is made into malate
  5. malate enters the mitochondria through a malate transporter
  6. malate is converted back into oxaloacetate ready to do another shuttle
159
Q

What is the simple version of the moving of Acetyl-CoA from the mitocohdria to the cytosol

A
  1. Acetyl-CoA + oxaloacetate –> citrate
  2. citrate leaves to cytosol
  3. citrate - Acetyl-Coa –> oxaloacetate
  4. Oxaloacetate –> malate
  5. Malate enters mitochondria
  6. Malate –> oxaloacetate
160
Q

What enzyme regulates fatty acid synthesis

161
Q

what inhibits the ACC

A

palmitoyl-CoA

162
Q

What activates the ACC

163
Q

What causes high levels of citrate that lead to fatty acid synthesis

A

high levels of Acetyl-CoA in the mitochondria

164
Q

When is fatty acid synthesis inhibited

A

when energy is needed

165
Q

what hormones lead to phosphorylation and inactivation of the ACC

A

glucagon and epinepherine

166
Q

What does fatty acyl-CoA desaturase do

A

desaturates fatty acids at the Delta 9 location (makes a double bond there)

DMD 5242 (10 decks)

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