Lipoprotein Biochemistry - Sahoo

Question 1

What’s the difference between a simple and mixed triglyceride? Which is more common in nature?

Answer 1

Simple TGs: Same fatty acid in all 3 positions. Mixed TGs: 2 or 3 different fatty acids. Most naturally-occurring TGs are Mixed.

Question 2

What can an elevated TG level predict independent of other risk factors?

Answer 2

-Risk of CV disease -Pancreatitis if several elevated (>1000mg/dL)

Question 3

Name 5 functions of cholesterol.

Answer 3

1) Essential cell membrane component 2) Important and enriched in lipid rafts 3) Reduces membrane fluidity* 4) Precursor for bile acids and steroid hormones 5) Covalent modification of embryonic signaling proteins *From what I can find, this helps make the cell membrane a little more structurally rigid (in a good way), and makes it less permeable to small water-soluble compounds that would otherwise diffuse into the cell.

Question 4

Name 5 classes of compounds derived from cholesterol and at least one specific compound in each class.

Answer 4

1) Androgens - Androsterone, Testosterone 2) Estrogens - Estradiol, Estriol, Estrone 3) Mineralocorticoids - Aldosterone, Corticosterone 4) Glucocorticoids - Cortisol 5) (Primary & Secondary) Bile Acids - Cholic acid (1°), Deoxycholic acid (2°)

Question 5

Name 5 ways in which excessive cholesterol is cytotoxic.

Answer 5

1) Cholesterol crystal formation 2) Triggering apoptotic pathways 3) Forming toxic oxysterols 4) Disruption of functional & signaling membrane domains 5) Promotes atherosclerosis

Question 6

Name the 4 major steps of cholesterol synthesis and the number of carbon atoms in each major compound

Answer 6

1) 3x Acetate (2C) –> Mevalonate (6C) 2) Mevalonate –> phosphorylated Isoprene (5C) 3) 6x Isoprene –> Squalene (30C) 4) Squalene –> Cholesterol (27C)

Question 7

Name 3 substeps in the formation of mevalonate from acetyl-CoA and the enzymes that catalyze them.

Answer 7

1) 2 Acetyl-CoA → Acetoacetyl-CoA
* via acetyl-CoA acyl transferase*
2) Acetoacetyl-CoA + Acetyl-CoA → HMG-CoA
* via HMG-CoA synthase*
3) HMG-CoA + 2 NADPH → Mevalonate
* via HMG-CoA reductase**

** **Rate-Limiting Step of Cholesterol Synthesis

Question 8

Name 3 substeps in the conversion of mevalonate to isoprene.

Answer 8

1) Stepwise transfer of 3 PO₄^3- from ATP to mevalonate.
2) Decarboxylation and hydrolysis forms the 5C isoprene
- Introduces a double bond
3) There are actually 2 isoprenes, which can isomerize back and forth
- Difference is location of double bond

Question 9

Name 3 substeps in the formation of squalene from isoprene units.

Answer 9

1) 2 isoprene → geranyl pyrophosphate
* -one of each isoprene isomer is needed*
2) geranyl pyrophosphate + isoprene → farnesyl pyrophosphate
3) 2 farnesyl pyrophosphate → squalene
* -squalene is phosphate-free*

Question 10

Name 3 substeps in the conversion of squalene to cholesterol and the enzymes that perform each step.

Answer 10

1) squalene + NADPH + O₂ → squalene 2,3-epoxide
* via squalene monooxygenase*
2) squalene 2,3-epoxide → lanosterol
* via cyclase*
3) lanosterol → cholesterol
* multistep - specifics not listed*

Question 11

Where does cholesterol synthesis diverge between animals and plants and fungi?

Answer 11

The fate of squalene 2,3-epoxide differs.

Animal: Lanosterol → Cholesterol

Plants, Fungi: Stigmasterol, Ergosterol

Question 12

1) Where is most cholesterol synthesized in the body?
2) In what forms?
3) What forms are later converted from cholesterol in other tissues?

Answer 12

1) Liver
2) Bile acids, Biliary Cholesterol, Cholesteryl Esters
3) Other tissues form steroid hormones, some others

Question 13

How do bile acids work?

Answer 13

They surround fat droplets and help to emulsify them. This increases the surface area available for attack by lipases.

Question 14

Which are more non-polar: cholesterol or cholesterol esters? What is a consequence of this?

Answer 14

Cholesterol esters. The added hydrophibicity makes then unable to enter membranes.

Question 15

Which LP class contains the most:

1) Protein
2) Phospholipids
3) Free Chol
4) Chol esters (CEs)
5) TGs

Answer 15

1) Protein: HDL
2) Phospholipids: HDL
3) Free Chol: VLDL/LDL
4) Chol esters (CEs): LDL
5) TGs: Chylomicrons

Question 16

What is the surface of a lipoprotein particle composed of?

What is the interior composed of?

Answer 16

Surface: apolipoproteins, phospholipid monolayer

Interior: cholesterol, cholesterol esters, TGs

Question 17

A lipoprotein’s density is [directly, inversely] related to its size.

Answer 17

Inversely

Question 18

Name the major subclasses of lipoproteins in order of increasing density.

Answer 18

1) Chylomicrons
2) VLDLs
3) VLDL remnants
4) IDLs
5) LDLs
6) Lp(A)
7) HDLs

Question 19

Name the identifying apolipoprotein (apoLP) and a major function/characteristic of:

1) Chylomicrons
2) VLDLs
3) IDLs
4) LDLs
5) Lp(A)
6) HDLs

Answer 19

1) Chylomicrons: apoB-48, C, E; delivers chol & TGs from gut to tissues & liver
2) VLDLs: apoB-100, C, E; made in liver and delivers TG to tissues as fatty acids
3) IDLs: apoB-100, some C, E; short-lived LP between VLDL and LDL
4) LDLs: apoB-100 ONLY; stays in circulation longest
5) Lp(A): apo(a), apoB-100; an odd LDL-like particle - apo(A) is structurally sim(ilar to plasminogen
6) HDLs: apoA-I & apoA-II, C, E; generally good

Question 20

Which LP class contains the least:

1) Protein
2) Phospholipids
3) Free Chol
4) Chol esters (CEs)
5) TGs

Answer 20

1) Protein: Chylomicrons
2) Phospholipids: Chylomicrons
3) Free Chol: Chylomicrons/HDL
4) Chol esters (CEs): Chylomicrons
5) TGs: HDL

Question 21

Name 4 functions of apolipoproteins.

Answer 21

1) Help solubilize the LP particle in the circulation
2) Change conformation to adjust to changing lipid contents, compositions, and metabolic states
3) Can activate or inhibit plasma enzymes
4) Serve as ligands for cell surface receptors

Question 22

Name the function(s) of:

1) ApoA-I
2) ApoA-II
3) ApoB-48
4) ApoB-100

Answer 22

1) ApoA-I: Activates LCAT, interacts with ABC transporter
2) ApoA-II: Inhibits LCAT, structural
3) ApoB-48: Chol & TG transport and clearance
4) ApoB-100: Binds LDL receptor to deliver endogenous chol

Question 23

Which ApoLPs are most strongly associated with

1) increased risk of atherosclerosis?
2) decreased risk of atherosclerosis?

Answer 23

Increased risk: apoB-100, apo(a)

Decreased risk: apoA-I

Question 24

How are triacylglycerols taken up by the gut? Where is this process mirrored?

Answer 24

In short, they are broken down, absorbed, then reformed.

In detail: bile salts emusify the fats, forming mixed micelles that are attacked by lipases. The lipases degrade TGs into fatty acids (FAs), which are taken up by the mucosa and converted back into TGs.

The process is mirrored in the capillaries: LP lipase converts TGs into FAs + glycerol, which are taken up by cells. Cells can resesterify these back into TGs (or utilize them as fuel).

Question 25

What lipoprotein are TGs taken up in the gut packaged into for transport?

Answer 25

Chylomicrons

Question 26

What protein mediates the absorption of cholesterol in the intestine? What drug inhibits this protein?

Answer 26

Protein: NPC1L1 (Neimann-Pick C1-Like 1 protein)

Drug: ezetimibe

Question 27

Which transporters prevent the assimilation of plant sterols into the body by channeling them back into the intestinal lumen?

What disease results from mutations in these proteins?

How is it inherited?

What symptoms to these patients show?

Answer 27

Transporters: ABCG5 and ABCG8

Disease: Sitosterolemia

Inheritance: Autosomal recessive

Sxs: Accumulation of plant sterols in blood & tissues, associated with tendon & subQ xanthomas and markedly increased risk of premature CHD.

Question 28

When can chylomicrons be detected in plasma?

Answer 28

Elevated for 3-6 hours after eating a fat-containing meal. No chylomicrons remain after a fast of 10-12 hours, except in patients with disorders in chylomicron metabolism.

Question 29

What is the % fat content of a chylomicron?

What % of this is dietary TGs?

Answer 29

98-99% fat

85% TGs

Question 30

What gives apoB-48 its name?

Answer 30

48% of the MW of apoB-100

Question 31

What apoLP activates lipoprotein lipase (LPL), allowing lipoproteins to release free fatty acids for fuel to adipose tissue, heart, and skeletal muscle?

Answer 31

ApoC-II

Question 32

Where is lipoprotein lipase (LPL) located?

Answer 32

LPL is bound to capillary endothelium in various tissues. Lipolysis therefore takes place at the vascular endothelial surface.

(Heart, skeletal muscle, adipose tissue, mammary glands, others.)

Question 33

What is the conseqence of LPL deficiency?

Answer 33

Lethal in mice: die of severe hypertriglyceridemia

Question 34

1. How is LPL regulated?
2. What are LPLs cofactors?
3. Which of these cofactors allows for measurement of LPL?

Answer 34

1. Increased plasma glucose and insulin release upregulate LPL transcription to facilitate FA storage in adipocytes.

Conversely, LPL activity of adipose tissue falls during prolonged fasting or in diabetic ketoacidosis, preventing FA storage.

2. ApoC-II and heparin
3. Heparin, given IV, will displace LPL activity into the plasma, allowing its measurement

Question 35

What happens to chylomicrons after they are depleted of dietary TG via LPL activity in the body tissues? What ligand:receptor interaction is necessary for this?

Answer 35

Chylomicron remnants go to the liver. There:

• apoE **acts as a ligand for LDL receptor or the related LRP to stimulates endocytosis
• ApoB-48 is degraded
• dietary cholesterol is released into the liver

Question 36

What is LRP? What is it for?

Answer 36

LDL receptor-related protein.

It is the backup receptor (behind LDLR) responsible for uptake and clearance of chylomicron remnants and VLDL.

Question 37

ApoE deficiency causes what disease? What is a consequence of this?

Answer 37

Type III hyperlipoproteinemia

Increased TGs and cholesterol in the plasma due to impeded clearance of remnants

Question 38

What LP particle is produced by the liver for transporting endogenous lipids? What stimulates the liver to synthesize this particle?

Answer 38

Particle: VLDLs

Stimulation: Increased flux of free FAs or increased de novo FA synthesis in liver

Question 39

What apoLPs do VLDLs contain? Where are these proteins synthesized?

Answer 39

ApoB-100, apoC-I, apoC-II, apoC-III, apoE.

All constituitively synthesized in the liver.

Question 40

Other than fat, excess of what food type can also be converted into TGs by the liver?

Answer 40

Carbohydrates

Question 41

1) What enzyme transports newly synthesized TGs from the ER to sites of VLDL and chylomicron formation?
2) What is at these sites?

Answer 41

1) Microsomal tryglyceride transfer protein (MTP)
2) apoB-100 (VLDLs) or apoB-48 (chylomicrons)

Question 42

1) A defect in microsomal tryglyceride transfer protein (MTP) causes what disease?
2) What is the pathophysiology of this disease?
3) What symptoms do patients with this disease exhibit?

Answer 42

1) abetalipoproteinemia
2) failure to produce any apoB-containing LP particles (chylomicrons, VLDLs, LDLs) - unable to concentrate TGs within these particles to form them
3) vitamin deficiency, steatorrhea, developmental delays

Question 43

Which enzyme esterifies free cholesterol into cholesterol esters (CEs)?

Why bother making the CEs at all?

Answer 43

Acyl-CoA:cholesterol Acyltransferase (ACAT)

Better storage

Question 44

Which isoform of ACAT is located in the intestine and the liver?

What does it do in the intestine?

Why might it be medically important?

Answer 44

ACAT-2

Regulates the absorption of dietary cholesterol

Due to its function, is a potential pharmacological target for reducing blood cholesterol

Question 45

In what tissues is the ACAT-1 isoform located?

Answer 45

1) Macrophages (including foam cells)
2) Adrenocortical cells
3) Skin sebaceous glands

Question 46

In what ways are VLDLs and chylomicrons similar?

Answer 46

1) Both used to transport TGs to adipose tissue and muscle
2) In both, apoC-II activates LPL to release FFAs

(Think of chylomicrons as mainly for the exogenous pathway and VLDLs mainly for the endogenous pathway)

Question 47

How is IDL formed?

Answer 47

IDL is essentially the TG-depleted remnants of VLDL

Question 48

What is the half-life of VLDL remnants / IDL? What are the two fates possible for this lipoprotein?

Answer 48

t_1/2 < 30min

Fate 1: 40-60% are cleared from plasma by liver via LDLR and LRP

Fate 2: LPL and hepatic lipase (HL) convert the remainder of remnants/ID to LDL by further TG removal. Virtually all LDL is derived from VLDL remnants.

Question 49

What determines the rate of LDL production?

What is enriched in LDLs?

What’s the major apoLP in LDL?

Answer 49

The rate of VLDL remnant clearance - the remainder of remnants that escape uptake become LDLs

Cholesterol is considered to be enriched in LDLs because TG has been removed.

ApoB-100 is the major apoLP

Question 50

In the formation of LDL, which apoLP facilitates the removal of residual TG by hepatic lipase?

Answer 50

ApoE

Question 51

What receptor mediates the clearance of LDL particles?

What apoLP is the ligand for this receptor?

Why is this interaction clinically significant?

Answer 51

Receptor: LDL receptors

Ligand: ApoB-100

Significance: manipulation of hepatic LDL receptor gene expression is the most effective way of modulating plasma LDL levels

Question 52

Name two conditions in which LDL become atherogenic.

Answer 52

1) Modification by oxidation
2) Uptake by macrophage scavenger receptors

Question 53

True or False:

LDLs can carry cholesterol from the liver to muscle and adipose tissue like chylomicrons and VLDLs can.

Answer 53

True

Question 54

How does the half-life of an LP correlate with its density?

Answer 54

The trend appears to be: as density increases, t_1/2 increases.

Chylomicrons: 5-20min

VLDL: 30min-1hr

LDL: 2.5days

Question 55

After endocytosis of LDL particles, what are the fates of the endosomal components?

Answer 55

1) After lysosomal fusion, apoB-100 and CEs are degrades to release amino acids, FAs, and cholesterol.
2) The LDL receptor, however, is segregated into vesicles and recycled to the cell surface.

Question 56

Mutations in what protein are the most common cause of autosomal dominant hypercholesterolemia?

Answer 56

LDL Receptor (LDLR) - Over 900 known mutations

Question 57

Name two endogenous hormones that can lower LDL levels. How do they accomplish this?

Answer 57

1) Thyroxine & estrogen
2) Enhancement of LDLR gene expression - increases LDL uptake

Question 58

What is single most effective:

1) dietary alteration
2) pharmacological treatment

for hypercholesterolemia?

3) How do they both work?

Answer 58

1) Eat fewer saturated fats and cholesterol
2) Statins
3) Enhancing hepatic LDLR expression

[one would assume less cholesterol/fat itself would also help…]

Question 59

What transcription factors mediate the regulation of LDLR expression?

Answer 59

Sterol Regulatory Element Binding Proteins (SREBPs)

and

SREBP cleavage activating protein (Scap)

[Nested acronyms should be illegal]

Question 60

1) What serine protease descreases the expression of LDLR on hepatocytes?
2) How does the LDLR get downregulated, specifically?
3) Given the above, what would a gain-of-function mutation in this protease dispose a patient to?
4) How about a loss-of-function mutation?

Answer 60

1) Protease: Proprotein convertase subtilisin/kexin type 9 (PCSK9)
2) How: PCSK9 binds LDLR, and the complex of the two is internalized and targeted to the lysosome for degradation.
3) Gain: Less LDLR means more LDL. More LDL and cholesterol in plasma → increased risk of CHD
4) Loss: More LDLR means lower LDL cholesterol levels and protection from CHD.

Question 61

Name a protein that, when mutated, causes autosomal dominant hypercholesteremia that isn’t LDLR.

Answer 61

PCSK9 (Gain-of-function mutation)

Question 62

Lp(a):

1) What the hell is it?
2) What is its identifying apoLP?
3) Good or Bad?
4) Why?
5) Half-life?

Answer 62

Lp(a)

1) What: An LDL-like particle
2) ApoLP: apo(a), which is covalently bound to apoB-100.
3) Bad.
4) Not discussed - may have anti-fibrinolytic qualities
5) t_1/2: 3-4 days

Question 63

What protein is apo(a) highly homologous to?

What structural domain causes apo(a) to vary in size?

Answer 63

Plasminogen.

A variable number of kringle IV repeats.

Question 64

Name 7 ways in which HDL is atheroprotective.

Answer 64

1) Anti-oxidant
2) Anti-thrombotic
3) Anti-inflammatory
4) Reduces endothelial expression of adhesion molecules
5) Stimulates endothelial repair
6) Promotes endothelial function
7) Stabilizes atherosclerotic plaques

Question 65

In general, LDL (deposits / removes) cholesterol (in / from) the periphery. In contrast, HDL generally (deposits / removes) cholesterol (in / from) the periphery.

Answer 65

In general, LDL (deposits / removes) cholesterol (in / from) the periphery. In contrast, HDL generally (deposits / removes) cholesterol (in / from) the periphery.

Question 66

What are the most abundant apoLPs in HDLs?

Answer 66

1) ApoA-I (70% of protein)
2) ApoA-II (20% of protein)
3) ApoC
4) Lecithin-cholesterol acyl transferases (LCAT)

Question 67

A loss-of-function mutation in what gene might cause HDL deficiency?

What risk would this present?

Answer 67

apoA-I gene.

Risk of accelerated atherogenesis.

(Conversely, a gain-of-function mutation likely protects against atherogenesis.)

Question 68

1) What transporter promotes the release of cellular phospholipids and cholesterol to join apoA-I and form HDL?
2) What form of HDL is produced this way?

Answer 68

1) ATP binding cassette transporter (ABCA1)
2) Discoidal HDL, not spherical HDL

Question 69

1) Mutations in ABCA1 cause what rare disease?
2) What is the pathophysiology?
3) What clinical symptoms are seen?
4) Are plasma cholesterol levels low or high?

Answer 69

1) Tangier disease
2) Defective ABCA1 results in severely reduced cholesterol efflux to apoA-I. Pooly-lipidated nascent HDL is rapidly metabolized, resulting to markedly reduced HDL levels and cholersterol deposition in various tissues (liver, speen, tonsils, peripheral neurons)
3) Enlarged spleens & tonsils. Tonsils are orange from carotenoid accumulation.
4) Notably, plasma cholesterol levels are very low.

Question 70

1) What is another name for discoidal HDL?
2) Where is the majority of discoidal HDL formed?
3) What’s godd about discoidal HDL?

Answer 70

1) preß-HDL
2) Liver and intestine
3) It’s a cholesterol sponge that can acquire free, unesterified cholesterol from tissue cell membranes, including arterial wall macrophages.

Question 71

1) What protein is important in the generation of spherical HDL from discoidal HDL?
2) How does it accomplish this?
3) What apoLP on HDL activates this protein again?

Answer 71

1) Lecithin-Cholesterol Acyl Transferase (LCAT)
2) LCAT associates with HDL and esterifies free cholesterol that is acquired by discoidal HDL. The hydrophobic CEs move to the core of the HDL particle, increasing its size and eventually making it spherical.
3) apoA-I

Question 72

1) What protein promotes the release of cholesterol to already-spherical HDL?
2) In what tisses is it found?
3) What remodeling processes does this assist in?

Answer 72

1) ABCG1
2) Spleen, thymus, lung, brain, liver, and macrophages
3) HDL remodeling and alteration of cholesterol distribution on “donor” cell membranes.

Question 73

Why is HDL remodeling important?

Answer 73

It influences the metabolism, function, and plasma concentrations of HDL.

Question 74

1) What does cholesterol ester transfer protein (CETP) do?
2) Is CETP activity beneficial or harmful? Why?

Answer 74

1) Promotes the transfer of CEs from HDL to VLDL, IDL, and LDL in exchange for TGs.
2) Harmful. Inceased CETP means more CEs moved into LDL-like particles, which can deposit those CEs into tissues and cause atherogenesis. A known Japanese population of CETP deficient people have reduced CAD risk.

Question 75

Name 4 functions Phospholipid Transfer Protein (PLTP).

Answer 75

1) Transfer of excess free cholesterol and phospholipids from cylomicrons and VLDLs to HDL
2) Needed for maximal activity of LCAT
3) Major role in generating preß-HDL (discoidal HDL)
4) Promotes phospholipid efflux to preformed HDL

Question 76

1) What is the function of Hepatic Lipase (HL)?
2) When does HL act?
3) How do androgens and estrogens affect HL gene expression?

Answer 76

1) Function: Hydrolyzes TGs and phospholipids to generate smaller spherical HDL particles. These smaller particles can recirculate and soak up additional free cholesterol.
2) When: After CETP and PLTP action, the TG-enriched HDL is a better substrate for HL.
3) Androgens: increase HL activity; thus, men often have lower HDL-cholesterol levels than women

Estogens: reduce HL activity, but the increase is minor compared to the increase in men from androgens.

Question 77

1) What protein hydrolyzes HDL phospholipids?
2) What is the result of this hydrolysis?
3) Is this protein therefore atherogenic or atheroprotective?
4) What apoLP may inhibit this protein’s activity?

Answer 77

1) Endothelial Lipase (EL)
2) Generates smaller HDL particles that are catabolized faster
3) Atherogenic. EL overexpression has been seen to reduce apoA-I and HDL-C levels to almost zero
4) ApoA-II may inhibit EL activity (HDL with ApoA-II are catabolized more slowly)

Question 78

1) What is the function of Scavenger Receptor BI (SR-BI)?
2) Is SR-BI atherogenic or atheroprotective?

Answer 78

1) A major HDL receptor. It plays a critical role in maintaining plasma cholesterol levels and acts to deliver cholesterol to the adrenal cortex and gonads to support steroidogenesis.
2) Atheroprotective.

Question 79

How does the transfer process of HDL components via SR-BI occur? What happens to the HDL after transfer?

Answer 79

• ONLY lipid is trasnferred to cells
• The entire HDL particle is NOT internalized

After transfer, HDL can recirculate to pick up more cholesterol

Question 80

During HDL catabolism, how are apoA-I and apoA-II degraded? Where?

Answer 80

They are degraded synchronously, in the liver and kidney.

Question 81

What enzyme initiates the conversion of cholesterol to bile acids?

Answer 81

cholesterol 7ɑ-hydroxylase

Question 82

1) What is the fate of most bile acids?
2) What happens to the remainder of bile acids?
3) How is this important pharmacologically?

Answer 82

1) Most bile acids are reabsorbed, returned to the liver via the portal vein, and resecreted.
2) A small amount is lost in the stool, which provides a means of cholesterol elimination
3) Agents that bind bile salts and prevent their reabsorption are used to treat high blood cholesterol.

Question 83

Name 4 regulatory mechanisms for the synthesis and transport of cholesterol.

Answer 83

1) Covalent modification of HMG-CoA reductase
2) Transcriptional regulation of HMG-CoA reductase gene
3) Activation of ACAT (increases esterification for storage)
4) Transcriptional regulation of the LDL Receptor

Question 84

How do the following proteins affect the activity of HMG-CoA Reductase?

1) AMP-dependent protein kinase (AMPK)
2) Glucagon
3) Epinephrine
4) Insulin

Do they provide short or long-term regulation?

Answer 84

1) AMPK: phosphorylation, decreased activity
2) Glucagon: Cascades lead to phosphorylation, decreased activity
3) Epinephrine: Cascades lead to phosphorylation, decreased activity
4) Insulin: Cascades lead to dephosphorylation, increased activity

Covalent modification (phosphorylation) provides short-term regulation

Question 85

1) What transcription factors control long-term regulation of HMG-CoA Reductase?
2) How are these transcription factors activated?
3) What other genes do these transcription factors upregulate?

Answer 85

1) Sterol regulatory element-binding proteins (SREBPs) and SREBP cleavage activating protein (Scap, which inhibits SREBP)
2) High cellular sterol levels: Sterol-bound Scap binds SREBP in ER and holds it there

Low cellular sterol levels: Scap/SREBPcomplex cleaved, SREBP moves to nucleus and activates transcription

3) LDL Receptor, others

Question 86

What sorts of feedback regulation of cholesterol synthesis and metabolism might you expect in a cell after it binds and internalizes an LDL particle?

Answer 86

• Decreased HMG-CoA activity
• Decreased LDL receptor expression
• Increased expression of storage enzymes