Final FA synthesis Flashcards

1
Q

Where does fatty acid synthesis occur?

A

Liver and Adipose
(occurs w/ excess CHO)
(107)

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2
Q

What is the main precursor for fatty acid synthesis?

A

Acetyl-CoA

107

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3
Q

What is the term for a substance that can be taken to acetyl-CoA and can be stored as fatty acids to be used as fuel?

A

Lipogenic

107

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4
Q

What 3 molecules are required in the cytoplasmic system of fatty acid synthesis?

A

Acetyl-CoA
malonyl-CoA
2 NADPH (from pentose shunt)
(107-110)

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5
Q

How do you form Malonyl-CoA?

What activates the enzyme acetly-CoA carboxylase to do this?

A

Acetyl-CoA + HCO3 = Malonyl-CoA
*Citrate activates acetyl-CoA carboxylase
(108)

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6
Q

What are the 2 major functions of citrate?

What happens to citrate with increased ATP/ADP?

A

1) Activate acetly-CoA carboxylase
2) Transfer acetyl-CoA to cytoplasm
W/ increased ATP/ADP ratio, KC slows = citrate accumulates = leaves mito into cytoplasm
(108)

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7
Q

What is the coenzyme for malonyl-CoA?

A

Biotin

109

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8
Q

What is required for the synthesis of Palmitic Acid?

A

NADPH
Malonyl-CoA (predominant way to add C’s)
(111)

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9
Q

Where does the microsomal system of fatty acid synthesis take place?

A
Endoplasmic Reticulum
(113)
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10
Q

True or False: Linoleic acid and alpha-Linolenic acid are essential fatty acids, whereas gamma-Linolenic acid is non-essential?

A

True
Gamma-Linolenic acid can be made in the body if Linoleic (essential FA) is present
**Arachidonic acid (derivative of gamma-Linolenic acid) is therefore NON-essential
(113)

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11
Q

True or False: We can make C=C in the back half of a fatty acid?

A

False

113

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12
Q

In the endoplasmic reticulum, what happens to fatty acids such as palmitic acid? (16 carbons)

A

Elongated to 18 carbons
I.E. Stearic acid, Oleic acid, Linoleic acid, Palmitoleic acid, etc
(113)

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13
Q

What does Acetyl-CoA carboxylase do?

What 3 things activate Acetyl-CoA carboxylase?

A

Converts acetyl-CoA to malonyl-CoA
Activated by citrate, insulin, increased CHO (or decreased fat)
(114)

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14
Q

When citrate activates Acetyl-CoA carboxylase, this means there are large amounts of both OA and acetyl-CoA. What happens if OA is decreased?

A

Decreased OA favors ketone production

114

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15
Q

What happens to FA after the mitochondrial system (elongation)?

A

Triglyceride and Phosphoglyceride synthesis

115

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16
Q

Where does cholesterol metabolism primarily occur?

A

Liver

119

17
Q

What are the 4 requirements to make cholesterol?

A

Acetyl-CoA, NADPH, ATP, Isoprene units

120

18
Q

What is the regulatory enzyme (committed step) for cholesterol synthesis?

A

HMG-CoA reductase (in the cytoplasm)

120

19
Q

What are competitive inhibitors of HMG-CoA reductase?

A

Statins

121

20
Q

What is the fate of cholesterol? (3 things)

A

Can be 1) packaged w/ VLDL’s 2) excreted 3) Converted to bile acids (122)

21
Q

What is another name for bile acids?

Are bile acids amphipathic?

A

Emulsifying agents
*Are amphipathic b/c -OH groups
(119)

22
Q

Name the catabolic pathway to get rid of excess cholesterol

A

There is no catabolic pathway to get rid of excess cholesterol
(122)

23
Q

Does a VLDL, LDL, HDL, or chylomicron has the highest % of triglyceride?

A

Chylomicron is 90% TG

124

24
Q

Does a VLDL, LDL, HDL, or chylomicron have the highest % of protein?

A

HDL

124

25
Q

Does a VLDL, LDL, HDL, or chylomicron have the highest % of cholesterol esters?

A

LDL = 50% made up of cholesterol ester

124

26
Q

Does a VLDL or a LDL have a higher % make up of TG? Which one has higher cholesterol ester %?

A

VLDL = 65% TG (LDL=3%)
VLDL = 10% CE (LDL=50%)
(124)

27
Q

What does apoprotein B do?

What does apoprotein LCAT do?

A

Apoprotein B binds at LDL receptor
Apoprotein LCAT makes cholesterol esters (add FA to cholesterol)
(124)

28
Q

What does an increase in dietary CHO do to VLDL synthesis?

A

Increases

125

29
Q

What does the deposit of TG in tissues require?

A
Lipoprotein Lipase (LPLase) 
*breaks down TG to FA and glycerol
(125)
30
Q

When LDLs become oxidized, what happens to their half life? What are they taken up by?

A

Half life increases
Taken up by macrophages
(125)

31
Q

What do HDLs do to excess cholesterol?

What is required to do this?

A

Transferred back to LDLs or delivered back to liver *=reverse cholesterol transport
Requires LCAT - lecethin cholesterol acyl transferase (adds FA to cholesterol = cholesterol ester which goes into center of HDL)
(126)

32
Q

What is increased HDLc a protective factor against?

A

Atherosclerosis

126

33
Q

What do chylomicrons do?

A

Carry dietary fats

126

34
Q

What effect does increase cholesterol have on HMG-CoA reductase? What does this do to LDL receptors?

A

Increase serum cholesterol = (-) HMG-CoA reductase = decreased LDL receptors == further increase of serum cholesterol
(vicious cycle)
(128)

35
Q

What disease is associated w/ decreased LDL receptors?

A

Familial hypercholesterolemia
(the heterozygous form has about 1/2 LDL receptors)
(128)

36
Q

What is the shape of an HDL as it leaves the liver BEFORE it picks up cholesterol?

A

Discoid

129

37
Q

What effect does increase ethanol intake on gluconeogenesis and TG synthesis?

A

Excess ethanol intake = decrease gluconeogenesis = hypoglycemia & NADH/NAD increases = inhibit gluconeogenesis
Ethanol gets converted to acetate, then acetyl-CoA. Excess goes to TG which can = fatty liver
(133)

38
Q

What effects do diabetes, starvation, and excess ethanol have on your liver?

A

Increase TG synthesis (in liver) and have decrease VLDL production from decrease dietary protein = TG accumulation in liver a.k.a Fatty Liver
(133)