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CPR Midterm > Lipids and Lipoproteins > Flashcards

Lipids and Lipoproteins Flashcards

1
Q

what are isoprenoids made from?

A

acetyl CoA

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2
Q

three acetyl CoAs are used to generate what?

A

1 IPP molecule

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3
Q

what serves as the building block for the synthesis of all isoprenoids?

A

IPP

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4
Q

what are some examples of what IPP can be converted into?

A

steroids (cholesterol), lipid-soluble vitamins, ubiquinone, and lipid anchors

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5
Q

what are some sources of acetyl CoA?

A

it is generated in the mitochondria from various pathways (oxidative decarboxylation of pyruvate, beta oxidation of fatty acids, and breakdown of amino acids)

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6
Q

how is acetyl CoA transported into the cytoplasm from the mitochondria?

A

via a citrate shuttle

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7
Q

what is the backbone of most steroids?

A

six units of IPP that form a tetracyclic sterane ring

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8
Q

what type of compound is cholesterol?

A

an allicyclic compound (there is a hydrophobic part and an amipatic part)

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9
Q

what is one important key identifier of a cholesterol molecule?

A

there is one hydroxyl group at the C3 position

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10
Q

cholesterol is a component of plasma membranes and a precursor of biologically active compounds such as what?

A

bile acids and bile salts, vitamin D, steroid hormones

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11
Q

what is biosynthesis of cholesterol like?

A

it is inversely proportional to dietary intake of cholesterol

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12
Q

what is the daily production of cholesterol and where does this take place?

A

.75-1.0 (mostly in the liver, small intestine, adrenal cortex, ovaries, testes, and skin)

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13
Q

the synthesis of cholesterol can divided into 2 phases- what are they?

A

Phase 1: generation of IPP from acetyl CoA; phase 2: generation of cholesterol from IPP

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14
Q

what is the rate limiting step of cholesterol synthesis?

A

the conversion of HMG CoA into mevalonate

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15
Q

what is the enzyme for the rate limiting step of cholesterol synthesis?

A

HMG CoA reductase

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16
Q

Which enzyme is impacted by statins?

A

HMG CoA reductase

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17
Q

anything that is going to impact IPP synthesis will in turn impact the synthesis of what?

A

prenylated proteins (e.g. Ras), Heme A, Dolichol, and ubiquinone

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18
Q

what is IPP converted into during cholesterol synthesis?

A

squalene

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19
Q

what is squalene converted into during cholesterol synthesis?

A

lanosterol

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20
Q

what is lanosterol converted into during cholesterol synthesis?

A

cholesterol

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21
Q

where is HMG-reductase found?

A

in the endoplasmic reticulum

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22
Q

what are the cholesterol lowering drugs?

A

statins

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23
Q

how do statins work?

A

they are strong competitive inhibitors of HMG CoA reductase

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24
Q

what is the Km for HMG CoA reductase? and what is the Ki for statins?

A

Km= 4 microM; Ki= 5-45 nM

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25
Q

what was a positive adverse effect of statin use?

A

transcription of LDL receptor and subsequent enhanced clearance of cholesterol via LDL-receptor mediated endocytosis

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26
Q

what was a negative adverse effect of statin use?

A

there are myotoxic side effects- statin mediated myopathy caused by depletion of muscle levels of ubiquinone (CoQ 10)- leads to impairment of mitochondria function

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27
Q

what are the 2 fates of cholesterol we focused on?

A

it is esterified to cholesterol esters by the enzyme ACAT or it is packaged into VLDL and released into the blood

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28
Q

what are the two types of regulation of cholesterol synthesis?

A

there is direct inhibition or there is covalent modification

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29
Q

what is direct inhibition of cholesterol synthesis?

A

by free fatty acids, bile acids, and oxysterols; and by statins

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30
Q

what is covalent modification of cholesterol synthesis?

A

the enzyme becomes inactive in its phosphorylated form and active in its dephosphorylated form

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31
Q

what phosphorylates HMG CoA reductase? and therefore inactivates it?

A

conditions of low energy, high AMP–> these activate AMPK; glucagon inactivates it

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32
Q

what dephosphorylates HMG CoA reductase? and therefore activates it

A

insulin

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33
Q

what are lipoproteins?

A

vehicles that transport TAGs and Cholesterol

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34
Q

why are TAGs, cholesterol, cholesterol esters, and fat soluble vitamins transported by lipoproteins?

A

they are all very hydrophobic substances, so if they were just released, they would adhere to the blood vessel wall

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35
Q

what is the general structure of a lipoprotein?

A

it has an outer shell and an inner core

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36
Q

what is the composition of the outer shell of a lipoprotein?

A

it has a monolayer of phospholipids, free cholesterol, and apolipoproteins

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37
Q

what is the composition of the inner core of a lipoprotein?

A

it is packed with TAGS, cholesterol, and cholesterol esters

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38
Q

how do lipoproteins contribute to lipid metabolism?

A

they serve as a means to transport and deliver TAGs to tissues for fuel or for storage

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39
Q

how do lipoproteins play a key role in cholesterol homeostasis?

A

lipoproteins transport the cholesterol from the site of synthesis, to sites of use, and finally to the liver for excretion

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40
Q

what do apolipoproteins serve as?

A

cell targeting signals/ ligands that bind to receptors to internalize lipoproteins

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41
Q

what do apolipoproteins activate?

A

various enzymes involved in lipoprotein metabolism and processing

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42
Q

what are the five different types of lipoproteins?

A

chylomicrons, very low density lipoproteins, intermediate density lipoproteins, low density lipoproteins (LDL), and high density lipoproteins (HDL)

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43
Q

how do the different types of lipoproteins vary?

A

based on size, density, and composition

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44
Q

which lipoprotein is the largest in size?

A

chylomicron

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45
Q

which is the smallest lipoprotein?

A

HDL

46
Q

which lipoprotein has the highest density?

A

HDL

47
Q

which lipoprotein has the smallest density?

A

chylomicron

48
Q

what are the chylomicrons richest in?

A

triglycerides

49
Q

what are the LDLs richest in?

A

cholesterol

50
Q

what are the HDLs richest in?

A

proteins

51
Q

what are chylomicrons formed from?

A

exogenous dietary fats

52
Q

what does the specific apoprotein ApoB-48 on the chylomicron do?

A

it facilitates transport

53
Q

what does the specific apoprotein ApoE on the chylomicron do?

A

it facilitates uptake into the liver

54
Q

what does the specific apoprotein ApoC-II on the chylomicron do?

A

it activates capillary lipoprotein lipase

55
Q

where are VLDLs made?

A

in the liver

56
Q

what are VLDLs packaged with?

A

TAGs and cholesterol

57
Q

what specific apoproteins are found on the surface of the VLDLs?

A

ApoB-100, ApoC-II, and ApoE

58
Q

what specific apoproteins are found on the surface of the IDL?

A

ApoB-100 and ApoE

59
Q

what apoprotein is found on the surface of the LDL lipoproteins?

A

ApoB-100

60
Q

why is the LDL considered to be the bad cholesterol?

A

the LDLs are very deficient in TAGs but have a high amount of cholesterol

61
Q

why are HDLs considered to be the good cholesterol?

A

because they have a high content of protein and phospholipids

62
Q

what specific Apoproteins are found on HDLs?

A

ApoC-II, ApoA-I, and ApoE

63
Q

what is the role of ApoC-II on the HDLs?

A

they activate capillary lipoprotein lipase

64
Q

what is the role of the ApoA-I on the HDLs?

A

they activate the enzyme that esterifies cholesterol

65
Q

what is the role of the ApoE on the HDLs?

A

they promote uptake into hepatocytes

66
Q

where are chylomicrons synthesized?

A

in the small intestine

67
Q

when they are initially synthesized, what are chylomicrons referred to as?

A

nascent chylomicrons

68
Q

what apoprotein is found on the nascent chylomicron?

A

ApoB-48

69
Q

how do you get a mature chylomicron?

A

you add ApoC-II and ApoE

70
Q

what is the role of the capillary lipoprotein lipase?

A

it hydrolyzes TAGs into glycerol and free fatty acids

71
Q

what happens once the capillary lipoprotein lipase hydrolyzes TAGs into glycerol and free fatty acids?

A

the mature chylomicron become a chylomicron remnant

72
Q

how do you get a chylomicron remnant?

A

the surface only has ApoB-48 and ApoE; you lost the ApoC-II

73
Q

what happens to the chylomicron remnants?

A

they will be taken up into the liver

74
Q

as the VLDLs are navigating in the bloodstream, what occurs?

A

the capillary lipoprotein lipase hydrolyzes the TAGs into glycerol and free fatty acids

75
Q

what happens to the VLDLs when the capillary lipoprotein lipase does its job?

A

the VLDLs will lose the ApoC-II and the VLDL becomes the IDL

76
Q

two things can happen to the IDL. What are they?

A
  1. It can be taken up by the liver through the IDL receptors in the hepatocytes
  2. It can be converted to LDL
77
Q

If the IDL is taken up by the liver, what happens to it?

A

the IDL will lose more TAGs via the action of hepatic lipoprotein lipase, and it loses ApoE and becomes LDL

78
Q

what is the main function of LDL?

A

it will transport cholesterol and delivery to the liver and peripheral tissues via ApoB-100

79
Q

each LDL particle contains a shell of phospholipids and free cholesterol and is packed with what else?

A

1500 cholesterol ester molecules in the core

80
Q

what happens to the LDL receptor once the LDL is endocytosed and broken down by lysosomes?

A

the receptor is recycled

81
Q

mutations that generate receptors that are unable to release the LDL cargo cause what?

A

familial hypercholesterolemia

82
Q

where are HDLs synthesized?

A

in the liver and small intestine

83
Q

what are HDLs initially known as when first released into the blood stream?

A

nascent HDL

84
Q

what does nascent HDL pick up from the peripheral tissue?

A

cholesterol

85
Q

what enzyme helps to esterify the cholesterol?

A

LCAT

86
Q

what happens to the cholesterol esters once the LCAT does its job?

A

the esters enter the HDL core- making it more spherical

87
Q

what happens to the HDL once the cholesterol esters enter the core?

A

it becomes mature

88
Q

what is one important function of the HDLs?

A

it interacts with all of the other lipoproteins to help them mature

89
Q

what does HDL donate and receive from chylomicrons?

A

ApoC-II and ApoE

90
Q

What effect does HDL have on LDLs?

A

HDL scavenges and removes LDL-cholesterol from the periphery and transports it to the liver where it can be recycled and processed

91
Q

What does loss of ABCA1 activity cause?

A

a very rare condition known as Tangier disease

92
Q

what is Tangier disease characterized by?

A

HDL deficency, accumulation of cholesterol in macrophages, and premature atherosclerosis

93
Q

What are HDL-C levels increased by?

A

weight loss, exercise, and smoking cessation

94
Q

What is another name for Type 1 hyperlipoproteinemia?

A

hyperchylomicronemia

95
Q

what occurs during type 1 hyperlipoproteinemia?

A

there is an inability to hydrolyze TAGs in chylomicrons and VLDL

96
Q

what causes type 1 hyperlipoproteinemia?

A

either a deficiency in capillary lipoprotein lipase or ApoC-II

97
Q

when does primary lipoprotein lipase deficiency manifest?

A

infancy

98
Q

when does ApoC-II manifest?

A

post-adolescence

99
Q

what is the marker for type I hyperlipoproteinemia?

A

Plasma TAG levels >1000 mg/dL

100
Q

what are the clinical symptoms of type 1 hyperlipoproteinemia?

A

abdominal pain, acute pancreatitis, cutaneous eruptive xanthomas

101
Q

what is the treatment for type I hyperlipoproteinemia?

A

low fat diet

102
Q

what does the blood sample look like in a patient with type I hyperlipoproteinemia?

A

it is creamy looking

103
Q

what is another name for type II hyperlipoproteinemia?

A

familial hypercholesterolemia

104
Q

what is the cause of type II hyperlipoproteinemia?

A

defects in the LDL receptor resulting in defects in the uptake of LDL via receptor mediated endocytosis

105
Q

what does defective uptake of LDL cause?

A

increased cholesterol in blood

106
Q

what does excessive LDL under the endothelial cells lining the blood vessels undergo?

A

oxidation to form oxidized LDL (oxLDL)

107
Q

what does oxLDL initiate?

A

an inflammatory response which leads to atherosclerosis

108
Q

in type II hyperlipoproteinemia, what is there an impaired ability to do?

A

recognize ApoB 100 on LDL

109
Q

what type of inheritance is type II hyperlipoproteinemia?

A

autosomal dominant

110
Q

what happens to untreated homozygotes of type II hyperlipoproteinemia?

A

they die of CAD before their teenage years

111
Q

what do heterozygotes of type II hyperlipoproteinemia respond to?

A

diet, statins, and bile acid binding resins

112
Q

what do homozygotes for type II hyperlipoproteinemia need for treatment?

A

they need LDL apheresis and liver transplantation

CPR Midterm (21 decks)

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