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CardioRenal II > Biochemistry Lipoproteins > Flashcards

Biochemistry Lipoproteins Flashcards

1
Q

Apoprotein roles

A

1.) Structural role (ampipathic in nature) 2.) Recognition role important in lipoprotein metabolism ( enzymatic regulation of an enzyme, particle recognition for specific receptors)

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2
Q

Tangier disease

A

deficiency of ABCA1- cholesterol cannot be transferred from the plasma membrane to nascent HDL

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3
Q

Familial LCAT deficiency consequences

A

1.) Block in reverse cholesterol transport 2.) limited ability of HDL to acquire cholesterol from VLDL or chylomicrons 2.) Elevated blood cholesterol and triglycerides

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4
Q

Where is VLDL synthesized

A

Liver- assembled in the golgi

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5
Q

lipoprotein exterior

A

ampipathic molecules cholesterol and phospholid

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6
Q

Consequences of Familial Hypercholesterolemia

A

1.) Accelerated CHD (many homozygotes die of CHD by age 20) 2.) Xanthomas (visible subcutaneous lipid depositis that often occur over joints and tendons)

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7
Q

Type III dysbetalipoproteinemia treatment

A

dietary

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8
Q

Discuss what happens when chylomicron binds LPL

A

LPL removes 80-90% of the TAG causing the chylomicron to become smaller. Surface molecules are transferred to HDL (phospholipid, cholesterol, apoproteins A and C) The chylomicron remnant also gains from more apoE and cholesterol ester from HDL

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9
Q

Apoprotein CII

A

LPL cofactor

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10
Q

Apoprotein B-100 role

A

structural- binds LDL receptor

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11
Q

Phospholipid transfer protein (PLTP)

A

A PLASMA PROTIEN. Facilitates transfer of phospholipid from VLDL, IDL, LDL, ect to HDL

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12
Q

Apoprotien associated with LDL

A

ONLY B-100 (also not rich in apoprotein- may explain why its difficult to clear)

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13
Q

Persons with ApoE4 have an increased incidence of what

A

hypercholesterolemia, CHD, and late onset Alzheimer Disease

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14
Q

How is reverse cholesterol transport sill possible with CETP deficienct

A

through cholesteryl ester transport by SR-B1 receptors of liver and through endocytosis of HDL with multiple copies of apoE

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15
Q

Lecithin Cholesterol Acyltransferase (LCAT)

A

transferes fatty acid fron the 2 position of phosphotidylcholine (lecithin) to cholesterol. Synthesized in the liver and secreted into plasma where it becomes associated with HDL and is activiated by apoA-1 (on HDL)

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16
Q

LDL-receptor related protein (LRP)

A

similar to the LDL receptor but not as specific for lipoproteins. Recognizes apoE. NOT significantly affected by intracellular cholesterol

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17
Q

Apoprotien E4

A

associated with an increased risk of hypercholesterolemia and CHD due to increased down regulation of LDL receptoR. HIGHER AFFINITY FOR RECEPTORS

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18
Q

how does the aount of protein within a major lipoprotien correlate to its density

A

increased protien results in increased density

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19
Q

where is HDL synthesized

A

Liver and small intestine

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20
Q

which major lipoprotein is the smallest

A

HDL

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21
Q

80% of chylomicrons go where

A

to heart, adipose and muscle. Remaining 20% is liver uptake

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22
Q

Where are chylomicrons formed

A

formed in intestinal epithelial cells from the digestion of dietary lipids and are assembled in the golgi

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23
Q

which lipoprotein carries lipids synthesized by the liver

A

VLDL

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24
Q

What controls the proteolysis of internalized LDL receptor

A

proprotein convertase subilisin/kexin type 9 (PCSK9)

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25
Q

Symptoms of Type I hyperchylomicronemia

A

Eruptive xanthomas, abdominal pain after a fat containing meal recurrent pancreatitis

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26
Q

Causes of Type I hyperchylomicronemia

A

deficiency of LPL or apoC-II

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27
Q

Hepatic Lipase (HL)

A

non-convalently bound to heparan sulfate glycoproteins on the sinosoidal surface of liver cells. Hydrolyzed bith TAG and phospholipids

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28
Q

Cholesteryl ester tranfer protein (CEPT)

A

Facilitates transfer of cholesteryl ester from HDL to VLDL, IDL, and IDL. CEPT is synthesized in the liver and secreted into the plasma where it becomes associated with HDL

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29
Q

Purpose of HDL

A

resovoir for apoprotiens and cholesterol reverse transport

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30
Q

ATP-binding cassette transporters A1 (ABCA1) and G1 (ABCG1)

A

cellular plasma membrane protiens. ATP required- Moves cholesterol from the inner leaflet of the membrane to the outer leaflet (outer leaflet is “available” for the transfer to HDL- important in reverse cholesterol transport )

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31
Q

Causes of Type IV hypertriglyceridemia

A

Primarily lifestyle: obesity, type 2 diabetes, alcoholism, progesterone rich contraceptives, excess dietary carbohydrates (especially sugars)

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32
Q

Apoproteins B-48

A

present only on chylomicrons - plays a structural role

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33
Q

Apoprotein(a)

A

structurally resembles plasminogen but with no plasminogen activity = interferes with fibrinolysis by competeing with authentic plasminogen

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34
Q

LDL receptor in the absense of PCSK9

A

LDL receptor is recycled to the pasma membrane

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35
Q

what regulates synthesis of LDL receptor

A

cholesterol within the cell

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36
Q

importance of apoC-III on chylomycrons

A

inhibit premature removal of chylomicrons from circulation by inhibiting binding to recptors (LDL receptor, LRP, etc)

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37
Q

Major lipoprotiens

A

Chylomicrons, VLDL, LDL, HDL

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38
Q

Homozygous Familial Hypercholesterolemia

A

rare (1/1,000,000) - no functional LDL receptors leading to plasma cholesterol levels of 600-1200 mg/dl

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39
Q

Type V hyperlipoproteinemias

A

RARE. Increased triglycerides, increased cholesterol.

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40
Q

One way to distinguish VLDL from chylomicron

A

Chylomicrons have B-48 and VLDL have B-100

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41
Q

Heterozygous Familial Hypercholesterolemia

A

50% reduction in LDL receptors may double LDL cholesterol

42
Q

Type V hyperlipoproteinemias treatment

A

dietary

43
Q

Where do nacent chylomicrons get secreted

A

lymphy

44
Q

HDL3 vs HDL2

A

HDL3 is smaller and relatively lipid poor - expresses high LCAT activity and removes cholesterol converting it to cholesteryl ester (CE) becomes HDL2 when it has acquired more TAG

45
Q

lipoprotein interior

A

hydrophobic molecules - triacylglycerols and cholesterol esters

46
Q

Apoproin(a) levels are an independent risk factor for

A

cardiovasuclar disease

47
Q

which major lipoprotein is the largest

A

chylomicrons

48
Q

Symptoms of Tangier Disease

A

Peripheral neuropathy, hepatosplenomegaly, lympadenopathy (only a mild tendenct for early artherosclerosis)

49
Q

fate of chylomicron remnants

A

binds to Lipoprotein receptors and are cleared from blood by the live. Once internalized the components are metabolized

50
Q

Type III dysbetalipoproteinemia causes

A

homozygotes for apoE2, low affinity for apoE2 receptor resulting in accumulation of chylomicron and VLDL remanants

51
Q

what promotes LPL synthesis and tranfer to the capillary endothelial cell surface

A

insulin

52
Q

what tissues express LDL (B-100/E) receptors? Where in these tissues are they expressed?

A

liver, adrenal glands, and gonads. Liver is most important. LDL receptor is found in claterin coated pits

53
Q

what tissues express apoE

A

liver, brain, and placenta

54
Q

importance of apoC-II on chylomicons

A

required for LPL activity

55
Q

Nacent HDL

A

disc shaped, phospholipid rich praticle with apoprotiens- from liver (A-I , A-II, E, and C) OR from the intestine (only A-I)

56
Q

which lipoprotien carries out reverse transport (what is reverse transport)

A

HDL- takes cholesterold from extrahepatic tissues back to the liver

57
Q

Lipoprotein Lipase (LPL) location

A

NOT EXPRESSED BY ADULT LIVER. Anchored to the surface of capillary endothelial cells of adipose, skeletal muscle and heart muscle through a non-covalent interaction with glycosylphoshatidylinositol-anchored high density lipoprotein bidning protein 1 (GPIHBP1)

58
Q

apoproteins present on nacent chylomircons

A

apoA proteins and apoB-48

59
Q

Abetalipoproteinemia consequences

A

severe fat malapsorption (cant form chylomircons from dietary intake) accumulation of triglycerides in intestine and liver, deficiencies of fat soluble vitamins (carried in chylomicrons)

60
Q

Consequences of Tangier Disease

A

Mature HDL cannot be formed, decreased LDL (no transfer of cholesteryl ester to VLDL from HDL), cholesteryl ester deposits in reticuloendothelial cells, bone marrow, schwann cells (cant get rid of cholesterol)

61
Q

What do Chylomicrons carry

A

lipids from the digestion of food stuffs

62
Q

What makes up a lipoproteins

A

HYDROPHILIC LAYER: Protien. Phospholipid HYDROPHOBIC LAYER: triacylglycerols, cholesterol and cholesterol esters

63
Q

Type III dysbetalipoproteinemia

A

RARE. Increaed triglycerides, increaed cholesterol. Symptoms include xanthomas and increased risk of CHD

64
Q

IDL

A

VLDL remnant - 50% cleared by the liver , 50% not cleared and remodeled to form LDL

65
Q

apoproteins

A

proteins associated with lipoproteins

66
Q

Familial hypercholesterolemia

A

AUTOSOMAL DOMINANT - deficienct in LDL receptor

67
Q

Is cholesterol esterase ampipathic

A

no- only lipid soluble

68
Q

apoproteins present on newly synthesized VLDL

A

apoB 100 and small amounts of apoE ad apoC f

69
Q

Apoprotien E2

A

associated with familial dysbetalipoproteinemia due to less efficienct clearance of VLDL and chylomicrons. LOWER AFFINITY FOR RECEPTORS

70
Q

LPL tissue Km - what is the significance of this

A

large Km in adipose and small Km in the heart - Significance: heart gets first crack at it- only when you have excess (high amounts) does it go to adipose tissue (store excess as fat)

71
Q

where do you find the highest concentration of Lipoprotein lipase (LPL)

A

in the heart

72
Q

Familial LCAt deficiency symptoms

A

Free cholesterol accumulates in most tissues, kidney disease, corneal clouding , mild tendency for early atherosclerosis

73
Q

Untreated Abetalipoproteinemia leads to

A

Ataxia, retinitis pigmentosa, myopathy

74
Q

** LDL (B-100/E) receptor **

A

plasma membrane receptor found in clathrin coated pits. LDL binds receptor and results in internalization of LDL and further metabolism of its contents

75
Q

CETP deficiency

A

BENIGN- common in Japan. Cholesteryl esters cannot be transferred from HDL to other lipoproteins. Homozygotes may have 4x elevation of HDL cholesterol, LDL cholesterol is normal and low

76
Q

which major lipoprotein is the most dense

A

HDL

77
Q

Type IV hypertriglyceridemia

A

COMMON. Increased triglycerides and usually some hypercholesterolemia due to cholesterol content of VLDL

78
Q

Lipoprotein lipase (LPL) function

A

1.) catalyzes step wise hydrolysis of triacylglycerol to glycerol and 3 NEFA.

79
Q

Fate of VLDL remanants

A

1.) Some go to liver 2.) Some get attached to liver hepatic lipase 3.) some are lost 4.) some associate with B100 to form LDL

80
Q

clearance of LDL

A

70% by liver (LDL receptor, LRP receptor) 30% by extrahepatic tissues (ex: adrenals use cholesterol to form steroid hormones)

81
Q

HDL purpose

A

1.) serves as a resovoir for apoproteins needed by nascent chylomicrons and nacent VLDL 2.) reverse cholesterol transport

82
Q

Abetalipoproteinemia

A

deficiency of triglyceride transfer protein in the endoplasmic reticulum. Liver and intestine are unable to assemble or secrete apoB-containing lipoproteins - chylomicrons, VLDL and LDL essesntially absent

83
Q

Chylomicrons are composed of mostly what

A

triacylglycerides

84
Q

which lipoprotien carries lipids from digestion

A

chylomicrons

85
Q

Lp (a)

A

modified LDL- B-100 with apoprotein(a) covalently bound via disulfide bond

86
Q

Causes of Type V hyperlipoproteinemias

A

increased chylomurons and VLDL. Associated with uncontrolled diabetes and kidney disease.

87
Q

Which apoproteins do chylomicrons accumulate in the blood? What is the source of these apoprotiens?

A

apoC (I and II) and apoE from circulating HDL

88
Q

how are apoprotein(a) levels determined

A

genetically - derived from its own gene (LPA) which is thought to have evolved from the plasminogen gene (PLG)

89
Q

Apoprotein E function

A

binds to LDL receptor

90
Q

which major lipoprotein is the least dense

A

chylomicrons

91
Q

Type II hypercholesterolemia

A

COMMON. Elevated LDL cholesterol caused by familial hypercholesterolemia. Seconday causes are more common and include obesity and diabetes. Major risk pattern for atherosclerosis

92
Q

LDL metabolism

A

long plasma halflife (up to several days)

93
Q

Apoprotein A1 function

A

activates LCAT

94
Q

Type I hyperchylomicronemia

A

increased triglycerides (up to 1000 mg/dl), slightly elevated cholesterol, NOT associated with increased atherosclerosis

95
Q

when is the only time chylomicrons are present in the body?

A

after a meal - half life is less than 1 hour

96
Q

Treatment of Abetalipoproteinemia

A

clinical signs respond to treatment with vitamin E

97
Q

Scavenger receptor B1 (SR-B1)

A

binds HDL via apoA-1 - transderes cholesteryl esters from HDL from liver. Mostly expressed in the liver

98
Q

What do VLFL carry

A

lipids synthesized by the liver

99
Q

LDL receptor fate in the presence of PCSk9

A

More destruction/downregulation of the LDL receptor - less LDL is brought into the liver = Hyperlipidemia

100
Q

Treatment of type I hyperchylomicronemia

A

low fat diet

CardioRenal II (12 decks)

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