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Term 1 MD > Nutrition and Cardiovascular Disease, LDL, VLDL, Chylomicrons > Flashcards

Nutrition and Cardiovascular Disease, LDL, VLDL, Chylomicrons Flashcards

1
Q

Chylomicrons are released by the [ ] cells into the [ ] and contain dietary lipids including lipid-soluble vitamins.

A

Chylomicrons are released by the intestinal mucosal cells into the lymph and contain dietary lipids including lipid-soluble vitamins.

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2
Q

VLDLs are released by the [ ] into the blood and contain [ ] and [ ].

A

VLDLs are released by the liver into the blood and contain TAGs and cholesteryl esters.

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3
Q

What molecules are cleaved by lipoprotein lipase?

A

TAGS and VLDL remnants and are named IDL.

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4
Q

What is the function of LDLs?

A

To deliver cholesteryl esters to cells that need cholesterol. Most LDLs are taken up by the liver to prevent a high LDL blood level that can lead to CVD.

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5
Q

What is the function of HDLs?

A

They perform the reverse cholesterol transport to the liver and are filled in the blood with cholesteryl esters from cell turnover or from macrophages.

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6
Q

What is needed for the release of chylomicrons into the lymph?

A

apoB-48

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7
Q

Assembly of apoB-48 with lipids inside the cells needs what molecule?

A

MTP (microsomal TAG transfer Protein)

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8
Q

What is the difference between apoB100 and apoB48?

A

Cytidine deaminase forms the stop codon UAA leading to translation of only 48% of the mRNA (apoB-48) as opposed to apoB-100 where 100% of the mRNA is transcribed

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9
Q

How are nascent chylomicrons released into the lymph?

A

ApoB48 and MTP are needed for the assembly of and release of nascent chylomicrons into the lymph.

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10
Q

Where are lipoprotein lipases found?

A

Mainly anchored in capillaries of the heart, muscle, and adipose tissue.

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11
Q

Function of lipoprotein lipases:

A

Cleave TAGs in lipoproteins and generate free fatty acids, glycerol and lipoprotein that is a smaller size (a remnant)

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12
Q

What activates lipoprotein lipase in the blood?

A

ApoC-II (found in chylomicrons and VLDL)

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13
Q

What activates lipoprotein lipase in fat tissue?

A

Insulin is needed for activation of lipoprotein lipase which cleaves TAGs in blood and generates free fatty acids which can be stored as TAGs synthesis inside the fat cells.

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14
Q

Where are VLDLs formed?

A

Hepatocytes and VLDLs contain endogenous lipids
-This is to prevent TAG accumulation in hepatocytes and to provide substrates for lipoprotein lipase resulting in fatty acids for other cells.

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15
Q

What is the purpose of LDL?

A

To transport cholesteryl esters and deliver cholesterol to cells that need it for their plasma membranes or for steroid hormone synthesis

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16
Q

How do oxLDLs enter macrophages?

A

Via SR-A receptors which eventually lead to foam cells.

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17
Q

How do IDL form LDL?

A

TAGs in IDLs are cleaved by hepatic lipase which forms LDL

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18
Q

How are IDLs formed from VLDLs?

A

TAGs in VLDLs are cleaved by lipoprotein lipase which forms IDL.

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19
Q

Largest liporpotein

A

Chylomicrons

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20
Q

Ultra-centrifugation separates lipoproteins by:

A

Size and density: Chylomicrons > VLDL>IDL>LDL>HDL

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21
Q

Protein electrophoresis separates lipoproteins by

A

Overall charge and apoproteins

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22
Q

Which lipoproteins have the highest percentages of TAGS, cholesterol and proteins?

A

Chylomicrons

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23
Q

Which lipoprotein has the highest % of cholesterol?

A

LDL

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24
Q

Which lipoprotein has the highest % of protein?

A

HDL

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25
Q

Function of ApoB-48

A

Needed for synthesis and release of chylomicrons into the lymph

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26
Q

Function of ApoB100

A

Needed for synthesis and release of VLDLs into the blood and is needed for recognition by the LDL-receptor. ApoB-100 oxidation in LDL leads to oxLDL that enter macrophages which can lead to fatty streaks

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27
Q

ApoE function

A

Needed for recognition by the hepatic remnant receptors and for the uptake of chylomicron remnants and IDLs into the hepatocytes

28
Q

Function of ApoC-II

A

Activates lipoprotein lipase which cleaves TAGs in chylomicrons and VLDL

29
Q

Function of ApoA

A

Needed for the reverse cholesterol transport of HDL.

30
Q

ApoB48 deficiency leads to:

A

Low levels of chylomicrons as the assembly and release needs apoB48

31
Q

ApoB100 deficiency leads to:

A

Low levels of VLDLs, IDL,s and LDLs as the assembly and release of VLDLs needs apoB100

32
Q

ApoE deficiency leads to :

A

high levels of chylomicron remnants and IDLs as the hepatic remnant receptors needs apoE for endocytosis

33
Q

ApoC-II deficiency leads to:

A

High levels of chylomicrons and VLDLs as apoC-II is needed for activation of lipoprotein lipase

34
Q

Apo A deficiency leads to:

A

Early degradation and very low HDL

35
Q

What molecule releases free cholesterol into the blood from membranes undergoing turnover and from dying cells?

A

Cholesterol ABC transporters

36
Q

How are cholesteryl esters formed from HDL?

A

Using Lecithin-cholesterol-acyl-transferase (LCAT), an enzyme synthesized in the liver and released into the blood.

37
Q

LCAT needs activation by:
and uses a [ ] from phosphatidylcholine (PC) of the HDL membrane to form cholesteryl esters (CE) in the blood.

A

apoA-1, and uses a fatty acid from phosphatidylcholine of the HDL membrane to form cholesteryl esters in the blood.

38
Q

Action of cholesteryl ester transfer protein (CETP)

A

CETP is a protein that forms a hydrophobic channel and connects HDL and VLDL for exchange of nonpolar lipids

39
Q

Treatment for hypercholesterolemia

A

1) Stimulated LDL-R synthesis at low hepatic free cholesterol. Use of statin drugs that competitively inhibit HMG CoA reductase.
2) Treatment with PCSK9-inhibitor drugs when statins do not work.

40
Q

What is the normal function of PCSK9?

A

It prevents the recycling of the LDL-receptor and leads to its degradation in lysosomes

41
Q

What is lipoprotein(a)?

A

Very similar to LDL but it has apo(a) linked to apoB-100 by a disulfide bond. It is also a structural analog to plasminogen and may compete for the binding to fibrin. It may reduce the removal of blood clots, which could trigger MI or stroke.

42
Q

Does Lp(a) reduce or increase blood clot removal?

A

Reduce

43
Q

HDL is a [ ]-lipoprotein

A

alpha-lipoprotein

44
Q

LDL is a [ ]-lipoprotein

A

beta-lipoprotein

45
Q

VLDL is a [ ]-lipoprotein

A

pre-beta-lipoprotein

46
Q

Cox-1 is a [ ] enzyme

A

Cox-1 is a constitutive enzyme

47
Q

Cox-2 is a [ ] enzyme

A

Cox-2 in an inducible enzyme (inflammation)

48
Q

Leukotriene A4 is produced in:

A

Leukocytes, platelets, mast cells, and heart and lung vascular tissues

49
Q

Function of Prostacyclin

A

PGI2: Produced by COX-2 primarily in endothelium of vessels for vasodilation and inhibition of platelet aggregation

50
Q

Celecoxib acts to:

A

Selectively inhibits COX-2

51
Q

Function of prostaglandin F2alpha

A

PGF2alpha: produced by most tissues, vasoconstriction and bronchoconstriction, contraction of smooth muscle, stimulates uterine contractions

52
Q

Function of thromboxane A2

A

Produced by COX-1 primarily in platelets.
-Promotes platelet aggregation
-Vasoconstriction and bronchoconstriction
-Mobilizes intracellular calcium
-Contraction of smooth muscle

53
Q

PGE2

A

Mediator of inflammation; Released from activated macrophages. Cause local vasodilation (redness); pain; fever (signs of inflammatory response)
-Protects gastric mucosa

54
Q

Which two molecules induces labor in pregnant uterus?

A

PGE2 and PGF2-alpha

55
Q

Cortisol inhibits which molecule?

A

Phospholipase A2: release of arachidonic acid from membrane phospholipids
and also
COX-2: anti-inflammatory agent

56
Q

The cysteinyl leuotrienes

A

LTC4, LTD4, LTE4

57
Q

Major site of synthesis for PGE2

A

Activated macrophages

58
Q

Major site of synthesis for PGF2-alpha

A

Uterine tissues

59
Q

Major site of synthesis for Prostacyclin

A

Endothelium of blood vessels

60
Q

Major site of synthesis for platelets:

A

Thromboxane A2

61
Q

Major site of synthesis for mast cells:

A

Cysteinyl leukotrienes: LTC4: LTD4: LTE4

62
Q

Major mediator of inflammation; Vasodilation (redness); Pain; Swelling

A

PGE2

63
Q

Stimulates uterine contractions

A

PGF2-alpha

64
Q

Inhibits platelet aggregation; Increases formation of cAMP in platelets; Vasodilation

A

Prostacyclin

65
Q

Promotes platelet aggregation; Vasoconstriction; decreases formation of cAMP in platelets; mobilizes intracellular Calcium

A

Thromboxane A2

66
Q

Bronchoconstriction; Increases vascular permeability; Component of slow-reacting substance of anaphylaxis (SRS-A)

A

Cysteinyl leukotrienes

Term 1 MD (54 decks)

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