Final FA synthesis

Question 1

Where does fatty acid synthesis occur?

Answer 1

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

Question 2

What is the main precursor for fatty acid synthesis?

Answer 2

Acetyl-CoA

107

Question 3

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?

Answer 3

Lipogenic

107

Question 4

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

Answer 4

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

Question 5

How do you form Malonyl-CoA?

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

Answer 5

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

Question 6

What are the 2 major functions of citrate?

What happens to citrate with increased ATP/ADP?

Answer 6

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)

Question 7

What is the coenzyme for malonyl-CoA?

Answer 7

Biotin

109

Question 8

What is required for the synthesis of Palmitic Acid?

Answer 8

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

Question 9

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

Answer 9

Endoplasmic Reticulum
(113)

Question 10

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

Answer 10

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)

Question 11

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

Answer 11

False

113

Question 12

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

Answer 12

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

Question 13

What does Acetyl-CoA carboxylase do?

What 3 things activate Acetyl-CoA carboxylase?

Answer 13

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

Question 14

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

Answer 14

Decreased OA favors ketone production

114

Question 15

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

Answer 15

Triglyceride and Phosphoglyceride synthesis

115

Question 16

Where does cholesterol metabolism primarily occur?

Answer 16

Liver

119

Question 17

What are the 4 requirements to make cholesterol?

Answer 17

Acetyl-CoA, NADPH, ATP, Isoprene units

120

Question 18

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

Answer 18

HMG-CoA reductase (in the cytoplasm)

120

Question 19

What are competitive inhibitors of HMG-CoA reductase?

Answer 19

Statins

121

Question 20

What is the fate of cholesterol? (3 things)

Answer 20

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

Question 21

What is another name for bile acids?

Are bile acids amphipathic?

Answer 21

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

Question 22

Name the catabolic pathway to get rid of excess cholesterol

Answer 22

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

Question 23

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

Answer 23

Chylomicron is 90% TG

124

Question 24

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

Answer 24

HDL

124

Question 25

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

Answer 25

LDL = 50% made up of cholesterol ester | 124

Question 26

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

Answer 26

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

Question 27

What does apoprotein B do? | What does apoprotein LCAT do?

Answer 27

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

Question 28

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

Answer 28

Increases | 125

Question 29

What does the deposit of TG in tissues require?

Answer 29

``` Lipoprotein Lipase (LPLase) *breaks down TG to FA and glycerol (125) ```

Question 30

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

Answer 30

Half life increases Taken up by macrophages (125)

Question 31

What do HDLs do to excess cholesterol? | What is required to do this?

Answer 31

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)

Question 32

What is increased HDLc a protective factor against?

Answer 32

Atherosclerosis | 126

Question 33

What do chylomicrons do?

Answer 33

Carry dietary fats | 126

Question 34

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

Answer 34

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

Question 35

What disease is associated w/ decreased LDL receptors?

Answer 35

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

Question 36

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

Answer 36

Discoid | 129

Question 37

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

Answer 37

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)

Question 38

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

Answer 38

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