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Biochem Exam 2 > Lipid Metabolism > Flashcards

Lipid Metabolism Flashcards

1
Q

What is the structure of a saturated fatty acid?

A

No double bonds (palmitic or stearic acid) and

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2
Q

What does an omega carbon mean?

A

last carbon of the chain (furthest from the carboxyl group)

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3
Q

What is the structure of a unsaturated fatty acid, a monosaturated fatty acid and a polysaccharide fatty acid?

A

unsaturated has double bond
mono= one double bond
poly= 2+ double bond

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3
Q

What does the first number and the numbers in the super script after the delta in a fatty acid chain mean?

A

first: how many carbons
after delta: where double bonds are

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4
Q

What are the essential fatty acids?

A

linoleic acid
l-linolenic acid
arachidonic acid

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5
Q

insufficient amounts of the essential fatty acids can lead to

A

skin and kidney damage, cataracts, increased membrane permeability to water

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6
Q

virtually all the naturally occurring double bonds are

A

in cis configuration

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7
Q

w-6 20:4 is what fatty acid?

A

arachidonic

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8
Q

what is the major precursor to eicosanoids?

A

essential fatty acids, arachidonic acid
linoleic acid
l-linolenic acid

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9
Q

What is thromboxane’s needed for?

A

platelet aggregation

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10
Q

what is an eicosanoid?

A

prostaglandins, thromboxanes, and leukotrienes

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11
Q

What does eicosanoids regulate?

A

inflammatory response
– muscle contraction
– blood pressure
– bronchodilation
– bronchoconstriction
– water/sodium excretion

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12
Q

what does phosspholipase A2 do?

A

cleaves ester bond in second fatty acid

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13
Q

Where can trans fatty acids be found in the diet?

A

in processed foods

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14
Q

How are trans fatty acids formed?

A

induced to foods by hydrogenation (adding H to a double bond making it go from cis to trans, giving it a more liquid like structure)

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15
Q

Trans fatty acids increase ____

A

serum LDL cholesterol, triacylglycerol’s, platelet aggregation

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15
Q

What are cis double bonds role in the lipid bilayer?

A

make the membrane loosely packed which is important for proper fluidity and function of receptors and membrane proteins to function)

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16
Q

What does a trans double bond do to the lipid bilayer?

A

make the packing much tighter (decreases fluidity which can impair the function of membrane proteins and receptors)

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17
Q

What does trans fatty acids decease?

A

HDL cholesterol

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18
Q

What can trans fatty acids lead to? (due to the things they increase and decrease)

A

growth halt in new borns

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19
Q

What food is rich in omega 3 FA and what positve effect do these FA have?

A

fish oils and eggs
they decrease cardiovascular mortality

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20
Q

Where are acylglycerols stored?

A

adipose tissue

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21
Q

What are abundant lipids in mammalian cell membranes?

A

phosphoacylglycerols, sphingolipids, and cholesterol

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22
Q

What is the structure of a Phosphoacylglycerols?

A

● Glycerol backbone
● Fatty acids are linked to
C1 and C2 of the glycerol
backbone.
● The fatty acyl chains have
varying numbers of carbons
and double bonds.
● All of them have a
phosphate moiety (P) linking
to C3 of the glycerol
backbone and then a head group can bond to that

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23
Q

If only a phosphate group is attached to C3 of the glycerol
backbone, the lipid is called ______.

A

phosphatidic acid (PA)

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24
Q

If a choline group is attached to the phosphate, the compound is
called ________

A

phosphatidylcholine (PC)

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25
Q

What is the importance of the charge of the amine group of phosphatidylcholine and the phosphate group?

A

gives a local negative charge (these are important at the surface of membranes)

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26
Q

Phosphatidylcholine is also called _______

A

lecithin

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27
Q

Phosphatidylethanolamine (PE) has what head group?

A

2C and1 N

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27
Q

What is lysolecithin?

A

FA with one FA chain associated

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28
Q

Phosphatidylinositol 4,5-
bisphosphate (PIP2) is important for what?

A

signal transduction (some can have neg charge, some no charge)

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29
Q

What role does phosphoacylglycerol play in the lungs?

A

surfactant

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29
Q

What are some key functions of Phosphoacylglycerols?

A

– key components of cell membranes
– playing a pivotal role in signal transduction and
metabolic pathways
– a major determinant of cell membrane fluidity and
membrane lateral organization, thus regulating cell
membrane functions

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30
Q

What is the structure of sphingolipids?

A

–Sphingosine backbone (18 carbons) of sphingolipids.
–Sphingosine is part of ceramide.
–The first C on sphingosine is linked to a phosphate (for sphingomyelin) or a sugar (for sphingoglycolipid) moiety.
–The second C (C2) is linked to an amino group.
–C3 is linked to a hydrocarbon chain

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31
Q

What are the two groups of sphingolipids?

A

sphingomyelin and sphingoglycolipid

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32
Q

What is the difference between a sphingomyelin and sphingoglycolipid?

A

Sphingomyelin: first C on phosphate
Sphingoglycolipid: first C on sugar

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33
Q

All sphingolipids are derivatives of _______

A

ceramide

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34
Q

When galactose is linked to –OH
on C1 oh a ceramide, it is

A

galactocerebroside

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35
Q

When phosphorylcholine is linked to –OH on C1 of ceramide, the compound is called
______

A

sphingomyelin

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36
Q

When an oligosaccharide is
linked to –OH on C1 on a ceramide, it is called

A

ganglioside

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37
Q

NANA = ______________;
GalNAc = _______________

A

N-acetylneuraminic acid
N-acetylgalactosamine

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38
Q

What is sphingolipids role biologically?

A

– key components of cell membranes (particularly abundant in nerve cell membranes)
– regulators in cell death/survival, toxin binding, and cell-cell recognition

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38
Q

Cholesterol structure:
* Cholesterol is very _________and contains a tatracyclic ring
* Humans do not have
____ to degrade this ring
structure.

A

non-polar (not soluble in water)
enzymes

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39
Q

Cholesterol is a major component in cell membranes, but________ are not
embedded in the membranes. They are located inside the cell as part of oily droplets or they are located in blood lipoprotein particles

A

cholesterol esters

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39
Q

What is Sphingosine 1-phosphate (S1P)?

A

Sphingosine 1-phosphate (S1P): an intracellular second
messenger and an extracellular mediator. It plays an
important role in signaling pathways. It stimulates cell
proliferation and survival, and regulates cell motility and
cytoskeletal reorganization

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39
Q

Ceraminde is also a regulator of:

A

cell death

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40
Q

Free cholesterol can be converted to

A

cholesterol esters

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41
Q

does cholesterol make lipid bilayers?

A

no but it can insert itself into bilayers formed by sphingolipids and phosphoacylglycerols

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42
Q

What is the key takeaway of sphingolipid metabolites?

A

degradations products are important in signaling and cell functions

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42
Q

in the cell membrane carbohydrate moieties residing in the ________ side

A

extracellular

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43
Q

Dietary TGs can be digested by
______ produced by glands
in the tongue and soft palate

A

lingual lipase

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44
Q

Dietary TGs can also be digested
by _____ produced in the
stomach

A

gastric lipase

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45
Q

The function of the co-lipase is to:

A

attract and anchor
the pancreatic lipase to
the surface of the emulsion particles

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45
Q

90% of dietary lipids are ____

A

Triacylglycerols

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46
Q

What is the difference between bile acids and bile salts?

A

bile acids are protonated
the deprotonated form is what has detergent properties and is needed for lipid emulsion

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46
Q

What is the structure of a emulsion particle and mixed micelle?

A

non polar core lipids (TGs)
polar surface lipids

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46
Q

Digestion of dietaryTGs in the small intestine requires:

A

Pancreatic lipase
Bile salts
Co-lipase
Bicarbonate

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47
Q

Bile ____ is more common at physiological pH

A

salt (anionic form)

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48
Q

Bile Salts are used to make ____

A

emulsion particles

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48
Q

What is bicarbonates role in lipid absorption in the small intestine

A

raise pH to increase number of anionic species which drives lipid digestion and absorption

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49
Q

How are the 2MG and FA taken up by intestinal epithelial cells?

A

they are hydrophobic so they need to be take up by a micelle (once taken up its a mixed micelle) to be transported out of the lumen of SI

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50
Q

In the small intestine, dietary TGs are hydrolyzed to what products?

A

2-monoacylglycerol
(2-MG) and fatty acids (FA)

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50
Q

Bicarbonates effect in enzymes is…

A

changes the pH making the enzymes as active as possible

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51
Q

What happens once the mixed micelle crosses the epithelium of the SI?

A

the 2MG and FA are release from the micelle and can reform the TG

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51
Q

What can happen once the TGs are reformed in the epithelium?

A

combine with other
lipid-soluble materials and apo-proteins to form chylomicrons and can be taken to lymph then blood (fat soluble vitamins and essential fatty acids can be taken up same way)

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52
Q

What is lipid malabsorption?

A

Inability to digest triacylglycerols (TGs) due to pancreatic lipase or bile acid deficiencies

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53
Q

Lipid malabsorption causes

A

steatorrhea

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54
Q

What can steatorrhea lead to?

A

leading to a loss of important energy fuels, severe weight loss, and vitamin (fat-soluble vitamins, A, D, E, and K) as well as essential fatty acid and caloric deficiencies

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55
Q

If you have a problem secreting bile salts what health issue could occur?

A

deficiency of essential fatty acids, fat soluble vitamins and TGs

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56
Q

Acyl Co A has ____ carbons in the fatty acyl chain

A

2

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57
Q

What is the starting material for fatty acid synthesis?

A

acetyl coA

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57
Q

What is the most abundant FA in the body?

A

palmitate

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58
Q

Why do you have to go through the mitochondria to make acetyl co A

A

because you need pyruvate dehydrogenase which is in the mitochondria

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59
Q

the rxn catalyzed by pyruvate dehydrogenase has what properties?

A

large negitive delta G
makes it irreversible

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60
Q

Can you make acetyl co A from pyruvate?

A

no

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61
Q

Describe the structure of acetyl coA, what effect does its structure have?

A

big and very negative (4 negative charges), it cant pass through the mitochondria, must be converted to citrate, then it can pass

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62
Q

The malic enzyme pathway generates ______

A

NADPH

62
Q

How is citrate transformed to acetyl co A?

A

citrate lyase

63
Q

How does citrate get from the mitochondria to the cytosol?

A

A membrane-bound
tricarboxylate translocase
transports citrate from
mitochondria to cytosol

64
Q

Both _____ and _____
are needed in order to synthesize long-chain fatty acids

A

NADPH and acetyl CoA

65
Q

What triggers NADPH production?

A

citrate moving into the cytosol

66
Q

what is G6P dehydrogenase equivalent to?

A

pyruvate dehydrogenase
this is incorrect. ignore.

66
Q

what is glucose 6 phosphate dehydrogenase?

A

rate limiting step of pentose pathway

66
Q

What is the other way to generate NADPH?

A

pentose P pathway

67
Q

what does g6p DHase do?

A

produces NADPH (which is also an inhibitor for that enzyme)

68
Q

pentose phosphate pathway is active when ____ is active

A

fatty acid synthesis

69
Q

what are some functional differences between NADPH and NADH?

A

NADPH mainly for reductive biosynthesis ( like fatty acid and cholesterol synthesis)

NADH mainly for ATP generation

70
Q

what is the most important enzyme in fatty acid synthesis?

A

acetyl CoA carboxylase

71
Q

what does malonyl co A do?

A

inhibits the CBD 1 receptor involved in carnitine transport of long chain fatty acids degradation fatty acid synthesis, thus driving FA synthesis

71
Q

What is biotins role in malonyl CoA formation?

A

carrier of activated CO2

72
Q

Carboxylation of Acetyl CoA to Forms what? needs which enzyme?

A

Malonyl CoA
Acetyl CoA Carboxylase

73
Q

what is the rate limiting step of fatty acid synthesis from carbohydrates

A

carboxylation of acetyl CoA to Malonyl CoA by Acetyl CoA Carboxylase

74
Q

What does NADPH do during syn of palmitate on fatty acid synthase complex?

A

reducing agent ( reduce carboxyl to hydroxyl and reduces double bond to single

75
Q

WHat does malyonyl co A do during the syn of palmitate?

A

donates 2 carbons

76
Q

Can the body synthesize FA less than 16 carbons?

A

yes by using thioesterase you can cleave where needed to make lower carbon lengths

76
Q

How many cycles are needed to make palmitate, a 16 carbon ayl chain fatty acid?

A

7 cycles

77
Q

How to release the palmitoyl chain from the fatty acid
synthase complex?

A

use the thioesterase (cleave thioester bond)

78
Q

Can the body synthesize FA with more than 16 carbons?

A

yes still use malonyl and NADPH then other enzymes

79
Q

can the body synthesize fatty acids with double bonds?

A

yes, there are proteins on the ER membrane that can add double bonds

80
Q

Humans lack the fatty acid needed to induce a double bond between _________

A

C10 and omega carbon (plants can do this)

81
Q

Why is it important to understand why we cant add double bonds onto the C10 and omega carbon?

A

because in order to synthesize linoleic acid, l-linolenic acid and arachidonic acid

82
Q

What reacts to form TGs?

A

Fatty acyl CoAs react
with glycerol-3-
phosphate to form TGs.

83
Q

How are VLDLs made?

A

TGs combine with other lipids and certain proteins to form VLDL. The fate of fatty acids synthesized in the liver

83
Q

What does triclosan do?

A

inhibits enol-acyl carrier protein reductase which is necessary for fatty acid synthesis in germs

84
Q

when is acetyl CoA carboxylase active?

A

when insulin is high it triggers phosphatase which activates acetyl CoA carboxylase

85
Q

acetyl CoA carboxylase is activated in the dephosphorylated state, this state is also known as

A

the fed state

86
Q

When is acetyl CoA carboxylase inactivated

A

palmitoyl CoA, low energy levels (causes phosphorylation)

87
Q

Fatty acid synthesis ceases when the blood glucose level is

A

low.

87
Q

he synthesis of fatty acids is maximal when

A

carbohydrate is abundant and the level of fatty acids is
low

87
Q

Fatty acids can be synthesized from _______ and proteins in many different tissues with the liver as the major site

A

dietary carbohydrates

88
Q

Insulin activates _______ by stimulating the phosphatase that dephosphorylates the enzyme to an active form.

A

pyruvate dehydrogenase

88
Q

____________________, the rate limiting enzyme in fatty acid synthesis, converts acetyl CoA to malonyl CoA. This enzyme requires ________, which serves as the carrier of activated carbon dioxide

A

Acetyl CoA carboxylase
biotin

88
Q

The synthesis of malic enzyme, glucose-6- phosphate dehydrogenase, fatty acid synthase and citrate lyase is induced ____________________.

A

by the high insulin/glucagon ratio

88
Q

_____________ provides two carbon units for fatty acid chain elongation.

A

Malonyl CoA

89
Q

Fatty acyl chain elongation occurs on fatty acid synthase. ______is the starting material.

A

Acetyl CoA

90
Q

_________________ is the typical product but fatty acids with chain length shorter or longer than 16 carbons can also be synthesized

A

Palmitate (a 16-carbon fatty acid)

90
Q

______ is used as a reducing agent.

A

NADPH

91
Q
A
91
Q

how are double bonds added to the fatty acyl chain?

A

Double bonds (C=C) can be introduced to the fatty acyl chain by a desaturation enzyme system embedded in the ER membrane. However, there is a limitation. Humans do not have enzymes to generate double bonds
between C-10 and the terminal carbon (-carbon)

92
Q

Where does cholesterol synthesis happen?

A

occurs in the cytosol,
particularly on the cytoplasmic face of the endoplasmic reticulum (ER), of liver and intestinal cells.

93
Q

what occurs during stage one of cholesterol synthesis?

A

synthesis of mevalonate from acetyl CoA

94
Q

What is the starting material for cholesterol synthesis?

A

acetyl CoA (remember also makes long chain fatty acids too)

94
Q

What is the rate limiting step for cholesterol synthesis?

A

The conversion of HMG-CoA to mevalonate is the rate limiting step (this enzyme is in the ER membrane)

94
Q

What is the rate limiting enzyme for cholesterol synthesis?

A

HMG-CoA reductase is the rate limiting enzyme.

94
Q

What is stage two of cholesterol synthesis?

A

Formation
of activated isoprene
units and condensation of six
5-carbon isoprenes to from the 30-carbon squalene

95
Q

What else is required for cholesterol synthesis step one?

A

NADPH to reduce

95
Q

What is the third step of cholesterol synthesis?

A

Stage III: Conversion of squalene to cholesterol

95
Q

What is Transcriptional control of chol syn?

A

synthesis of HMG-CoA reductase mRNA is enhanced by
SREBP-NH3+. When [chol] is high, expression of HMG-CoA reductase is reduced.

95
Q

when cholesterol levels are high what happens?

A

the reductase conformation is changed making them more susceptible to photolyase to slow down synthesis

95
Q

How is cholesterol controlled by insulin/glucagon levels?

A

insulin activates the reductase, glucagon does the opposite

95
Q

Cholesterol synthesized in the ____ is transported to other tissues via ____

A

liver, VLDL

95
Q

where does bile salt synthesiss occur?

A

liver

95
Q

What is the rate limiting enzyme for bile salt synthesis from cholesterol in the liver?

A

7-a-hydrolase

96
Q

what is a primary bile acid?

A

bile acid made in liver from cholesterol

96
Q

What does the bacteria in the intestine do to bile acid?

A

deconjugate and dehydroxylate them forming SECONDARY BILE SALT

96
Q

Where are bile acids stored?

A

gallbladder, upon stimulation they are secreted into the intestine to aid digestion

96
Q

What are conjugated bile salts?

A

lowers the pKA which makes them better emulsifying agents

96
Q

What can happen if you cant degrade sphinholipids?

A

Niemann-Pick (NP) disease caused by acid sphingomyelinase
deficiencies (causes a build up in fat cells and causes cell disfunction over time that can cause loss of nerves and brain tissue overtime)

97
Q

what are some examples of sphingolipidoses?

A

tay-sachs and Gaucher’s

97
Q

Why are secondary bile salts good for us?

A

they are not absorbed great so they become excreted, this is key for controlling the amount of cholesterol in the body

98
Q

What kind of lipids can be found in blood plasma?

A

components of lipoproteins and fatty acids

99
Q

Triglycerides, cholesterol, cholesterol esters and
phospholipids form non-covalent aggregates with
proteins forming a complex known as a

A

lipoprotein

99
Q

LDL has a lot of _______

A

cholesterol esters and cholesterol

99
Q

Where are VLDL produced?

A

liver from dietary carbohydrate

99
Q

Hydrophobic lipids
(triglycerides, cholesterol
esters) form the _____ of
the lipoprotein

A

core

99
Q

Amphipathic lipids (e.g.,
phospholipids) are at the
________ ___________ _________ _________.The apoproteins of the
particle are amphipathic
as well

A

interface between the
aqueous medium and the
hydrophobic core (proteins there also)

99
Q

What is important about chylomicrons and VLDL?

A

they act as carriers for TGs in blood

100
Q

VLDL and chylomicrons contain a lot of _____

A

TGs (in chylomicrons come from diet, VLDL are syn in liver, these molecules are carriers of TGs for storage or use)

100
Q

HDL has the highest ______ content

A

proteins (this is why that are higher density, proteins more dense than fats)

100
Q

What is the fate of the chylomicron once in the blood?

A

ender blood, encounter HDL particles, HDL donates apoprotein E and C2 making chylomicrons mature particles, become larger and more spherical

100
Q

Where are chylomicrons produced?

A

intestinal epithelial cells

100
Q

What are the two tissues associated with LPL and what do they do?

A

muscles and adipose secrete lipoprotein lipase into the surface of capillaries

100
Q

C2 is

A

activator or lipoprotein lipase (most imp enzyme in lipoprotein metabolism)

101
Q

Where are IDL and LDL produced?

A

blood

101
Q

Where are HDL produced?

A

liver and intestine

101
Q

What does E apoprotein do?

A

ligand for LDL receptor and chylomicron remnant receptor

101
Q

a1 is an

A

activator of LCAT enzyme

101
Q

b100 apoprotein is

A

ligant for LDL receptor

101
Q

What does hepatic lipase do??

A

also called hepatic triglyceride lipase (HTGL) converts IDL to LDL

101
Q

A and B apoprtoeins are

A

structure units

101
Q

What is the difference between VLDL and HDL functions?

A

VLDL brings cholesterol to tissues, HDL takes cholesterol from tissues and brings back to liver

101
Q

LCAT and ACAT both do what? what is the difference between them?

A

they both take free cholesterol and esterize them
they are found in different places

101
Q

What is the most important enzyme in lipoprotein metabolism and what does it do?

A

Lipoprotein Lipase (LPL) – involved in processing of
chylomicrons and VLDL

101
Q

What does Lecithin-Cholesterol Acyltransferase(LCAT) do?

A

catalyzes transfer of long chain fatty acids to cholesterol, forming
cholesterol esters

101
Q

AcylCoA: Cholesterol Acyltransferase (ACAT) do?

A

intracellular enzyme that esterifies cholesterol

101
Q

Where are TGs regenerated and how?

A

after the mixed micelle enters the cell, the FA and 2MG recombine
IN THE SER (then at surface of RER there is syn of apoprotein B48, then protein and TGs put together, sent to golgi, make lipid vesicles and be exocytosis)

101
Q

When are chylomicrons called nascent?

A

when that contain protein and TGs

102
Q

WHat does lipoprotein lipase do to the chylomicron?

A

hydrolyzes it down to FA and glytherol

103
Q

What is CII’s role in lipoprotein lipase?

A

it is needed to activate the LPL to hydrolyze the chylomicron

104
Q

What is the fate of VLDL?

A

released to blood from liver to blood, receives C2 and E and cholesterol esters (from HDL) making the VLDL a mature particle, LPL will degrade VLDL to FA and glytherol

105
Q

What happens to the chylomicron remnants after breakdown by LPL?

A

they are sent to the liver where they are degraded by lysosomes

105
Q

what is left after LPL degrades VLVL?

A

IDL is produced, (you could say (VLDL is the precursor of IDL)

106
Q

What are the two differences between LPL and HTGL?

A

1- LPL made in muscle/adipose
HGTL made in liver
2: LPL likes bigger molecules, HTGL likes smaller

106
Q

What does HTGL make?

A

FA and Glycerol and LDL

107
Q

In summary what happens to VLDL once it enters the blood?

A

after LPL it becomes IDL, after HTGL it becomes LDL where it can be taken up by peripheral cells or liver

108
Q

What damage can be done by LDL?

A

they can become oxidized which causes damage to blood vessel endothelium

109
Q

What can happen with the damage to endothelium in blood vessels?

A

this recruits macrophages that will take up the oxidized LDL, once filled with lipids they become foam cells, which causes atherosclerosis long term

110
Q

What causes familial dyslipidemias type 1? How do you treat it?

A

caused by familial lipoprotein lipase (LPL) or apoprotein CII deficiency, resulting in increased
chylomicrons, VLDL, TGs, and cholesterol in the blood

restrict dietary fat intake

111
Q

Lipoprotein lipase (LPL) from adipose cells is stimulated by____ and _____

A

CII and insulin (Deficiency of LPL or apo C-II increases chylomicrons and VLDL in plasma)

112
Q

LDL recepotors bind what?

A

LDL-receptor binds LDL, VLDL, IDL, and chylomicron remnants
NOT ONLY LDL

113
Q

Where are LDL receptors found?

A

not only in liver, other tissues too

114
Q

LDL receptor mutations could lead to

A

– decreased transcription of receptor
– a decrease in LDL intracellular trafficking
– decreased incorporation into cell membrane
– a decrease in LDL binding
– abnormal endocytosis

115
Q

LDL receptor mutations could lead to a disorder known as familial hypercholesterolemia which causes

A

– increased plasma cholesterol
– premature atherosclerosis

116
Q

HDL is produced by ____ in a ____ shape. After it ______ it changes shape to _____ where it can then _____

A

liver cells, disk, donates C2 and E it becomes mature and can then pick up cholesterol to bring back to the liver

117
Q

Where is LCAT found and what does it do?

A

on HDL, it converts the cholesterol to cholesterol esters, then they migrate to VLDL and the VLDL gives HDL TG

118
Q

Where is the only place we can get rid of cholesterol and why?

A

lover because its the only place that can convert cholesterol to bile and bile salts, 5% bile salt excreted a day getting rid of cholesterol

119
Q

Where is LCAT vs ACAT?

A

LCAT in the blood, ACAT in the ER cell

120
Q

There is a positive correlation between _____ levels in blood and death

A

cholesterol

121
Q

Formation of _____ is the first step in atherosclerosis.

A

foam cells (causes endothelial damage)

122
Q

What drugs can be used to reduce cholesterol biosynthesis?

A

statin

123
Q

How does the drug statin work at the cellular level?

A

inhibits cholesterol synthesis then makes more LDL receptors on the cells so the cells can take up more LDL which then lowers the amount of LDL in blood

124
Q

How does the cholestyramine drugs work?

A

binds some bile salts causing down regulation of intracellular cholesterol, up regulates LDL receptors, down regulates serum cholesterol causing excretion of bile salts through feces

Biochem Exam 2 (6 decks)

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