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Clinical Chemistry II - 4378 > Lipo mechinisms > Flashcards

Lipo mechinisms Flashcards

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1
Q

LCAT involves the transfer of what to what

A

Fatty acid from phospholipid to cholesterol

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2
Q

LCAT is associated with

A

HDL

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3
Q

HDL take LCAT to

A

Cholesterol

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4
Q

HDL goes to

A

Peripheral tissue where cholesterol is being acclumulating

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5
Q

HDL + LCAT to tissue then

A

LCAT makes cholesterol ester and it then gets in center of HDL and then HDL moves cholesterol to liver.

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6
Q

Is there a pathological disease caused by LCAT

A

Yes, Lcat deficiency will cause an accumulation of cholesterol.

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7
Q

Acyl coA is a source of

A

FA’s for esterification

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8
Q

Hyper lipid conditions are associated with

A

more LCAT

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9
Q

TG’s store

A

Fatty acids

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10
Q

Plasma TG’s are from

A

Intestines and liver

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11
Q

Unsaturated Fatty acids

A

Have double bonds

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12
Q

Saturated fatty acids have

A

no double bonds

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13
Q

Vegatables contains more

A

Unsaturated fatty acids which are healthier and are liquid at room temperature

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14
Q

meat contains more

A

saturated fatty acids which are solids at room temp and are unhealthier

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15
Q

Lipids + sugar

A

glycolipids

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16
Q

Prostaglandins

A

Do cell to cell communication and are synthesised as needed. They have a short half life

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17
Q

PGA with subscript 2

A

Prostaglandin A with 2 double bonds

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18
Q

Phospholipids are

A

water soluble

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19
Q

Cholesterol cant be

A

stored

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20
Q

Fats are blank by bile salts

A

emulsified

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21
Q

Emulsified and digestive enzymes

A

need to make fats into smaller pieces before digestive enzymes Lipase, Cholesterol esterase can work on fats

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22
Q

Phospholipids have a

A

hydrophilic head and a hydrophobic tail

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23
Q

A cofactor of digestive enzymes is

A

Bile salts

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24
Q

Fats have to be what size to be used by digestive enzymes

A

1 mm small

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25
Q

If you have a stomach ache then Dr look at

A

pancreas for Pancreatitis; and increase in amylase can cause stomach issues

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26
Q

huge fats become

A

micelles

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27
Q

Micelles react with what to go into

A

Mucosal cells to go into ER

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28
Q

Smaller C FAs and medium C FA are less then blank and go through

A

10C and go directly through intestinal cells and into portal circulation

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29
Q

Albumin carries what to liver

A

Free fatty acids

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30
Q

Free fatty acids are absorbed by

A

enterocytes and then made into TGs and chylomicrons

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31
Q

TG and cholesterol in enterocytes are delivered to Interstines by chylomicrons and get into intestinal cells.

A
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32
Q

Only two percent of chylomicrons are

A

Proteins and do not separate on protein electrophoresis

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33
Q

Chylomicron is blank rich lipoprotein

A

TG and protein is Apo-B-48

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34
Q

Cylomicron is associated with

A

82% of TG
9% of cholesterol
7% of phospholipids

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35
Q

Increase in chylomicrons is associated with an

A

Increase in Exogenous TGs

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36
Q

HDL has blank and more blank charge

A

50% proteins and more negative charge

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37
Q

Intestines can make what

A

Phospholipids

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38
Q

Chylomicrons can be released for blank hours after a meal

A

14 hours from intestinal cells and Dr ask you to be fasted to minimize TG liver

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39
Q

Chylomicrons are transported to

A

All tissues

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40
Q

Chylomicron remnant is

A

Chylomicrons, after action of Lipoprotein lipase offloads TG and Chylomicrons are composed of the majority of Cholesterol.

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41
Q

Free fatty acids are

A

an important metabolic fuel

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42
Q

Acetate–> cholesterol involves what rate-limiting enzyme and what reaction

A

HMG-coA reductase and reaction is
B-hydroxy-B-methylglutaryl-CoA—–> Mevalonate

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43
Q

HMG coA reducatase is regulated by

A

Free cholesterol(Inhibited)

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44
Q

Neutral fats–> ethier what or what

A

Lipolysis and glycerol

lipolysis and fatty acids

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45
Q

Fatty acids to what or what

A

Acetyl Coenzyme A by Beta oxidation

Ketone by ketogenogenesis in the liver

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46
Q

ketone bodies to what or what

A

FA

Acetyl Co A

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47
Q

Acetyl co A to what or what

A

Cholesterol or krebs cycles

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48
Q

Cholesterol to what or what

A

Steroids or bile salts

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49
Q

IF acetyl co A is in excess then

A

FA made

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50
Q

Acetyl CoA—> what by what enzyme

A

7 malonyl coA by enzyme Acetyl coA carboxylase

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51
Q

Fatty acid synthesis

A

Acetyl coA + 7 malonyl coA + 14 NADPH + 14H+
——————>
Palmitic acid + 7CO2 + 8coA + 14 NADP + 6H20s

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52
Q

Acetyl coA carboxylase is dependent on

Inhibited by

Activated by

A

Biotin

Inhibited by long chain acyl coA

Activated by Citrate

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53
Q

The 14 NADPH for fatty acid syn are provided by the

A

pentose phosphate pathway and the Malic enzyme

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54
Q

Glucose 6-P + NADP—>

Then reaction 2 of PPP

A

Phosphoglucucono lactone + NADPH + H

2.) 6-phosphoglucuconate + NADP—> D-Ribulose-5-Phosphate + NADPH+ H+

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55
Q

By using H+ pyruvate can enter

A

mitochrondria

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56
Q

8 NADPH come from what

6 NADPH come from what

A

8 from Malic enzyme

6 from Pentose phosphate pathway( oxidation pathway)

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57
Q

Fatty acid synthase complex steps in words

A

1.) attachment of acetyl coA to enzyme
2.) addition of malonyl-CoA
3.) first reduction
4.) Elimination H20
5.) second reduction
6 Detached finished product

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58
Q

1st reaction in fatty acid synthase complex

A

Acetyl coA—> malonyl coA by enzyme acetyl transacylase

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59
Q

2nd reaction in fatty acid synthase complex

A

Malonyl coA—> Ketoacyl synthase by enzyme malonyl transacylase

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60
Q

3rd reaction in fatty acid synthase complex

A

Malonyl coA–> 3-ketoacyl-enzyme complex by ketoacyl synthase and loss of CO2

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61
Q

4th reaction in fatty acid synthase complex

A

3-ketoacyl-enzyme complex—> saturated acyl enzyme complex by enzymes ketoacyl reductase( NADPH to NADP) and hydratase( loss of water) and enoyl reductase

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62
Q

5th reaction in fatty acid synthase complex

A

Saturated acyl enzyme complex–> palmitate by six cycles repeat

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63
Q

Thiel groups

A

oxidized and reduced group

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64
Q

Disulfide bonds bind

A

proteins

65
Q

fatty acid synthase complex is a

A

mirror image

66
Q

Palmithic acid is one of the most

A

common naturally occurring fatty acids

67
Q

Fatty acid utilization

A
68
Q

Triacylglycerol/ triglyceride–>

Adipose tissue to where

A

TG–>FFA by lipolysis

then FFA are transported in the blood to the liver and extrahepatic tissues by serum albumin complex

69
Q

In the liver( cytosol) FFA are converted to

A

acyl- CoA which is utillized for energy and biosynthesis

70
Q

In the liver(cytosol->mitochrondria) acyl-CoA–>

A

Carnithine acyltransferase–> acyl coA( synthesis of glycerolipids and sphingolipids

71
Q

In the mitochrondria acyl coA->

A

acyl-coA–>Acetyl CoA by B oxidation

72
Q

Short chain FA and medium chain FA are blanked

A

Diffuse into the Mitochrondria Short(2-4), medium( 4-12)

73
Q

Long chain FA require the

A

Carnitine cycle

74
Q

Beta oxidation step 1

A

Palmitoyl coA–> Trans-delta2 enoyl coA by enzyme acyl-coA dehydrogenase

75
Q

Beta oxidation step 2

A

Trans-delta2 enoly-CoA–> L-B-hydroxy-acyl-coA by enzyme enoyl-coA hydratase

76
Q

Beta oxidation step 3

A

L-B-hydroxy-acyl-coA–> B-ketoacyl-coA by enzyme D-hydroxyacyl-coA dehydrogenase (NAD–>NADH)

77
Q

Beta oxidation step 4

A

Beta-ketoacyl-coA–> acyl-coA and acetyl coA(2 carbons) by enzyme acyl-coA acetyltransferase (thiolase)

78
Q

Alternative FA oxidation pathway step one

A

Fatty acyl-coA cis-delta 3,cis delta 6—> fatty acyl-coA trans delta 2 and delta 6. by enzyme delta 3,2 enoyl-coA isomerase

79
Q

Alternative FA oxidation pathway step two

A

Fatty acyl-coA trans delta 2,6—> fatty acyl-coA cis 4 by B-oxidation and removes Acetyl coA

80
Q

Alternative FA oxi step three

A

Fatty acyl-coA- cis 4—> Fatty acyl-coA-trans-delta 2 and cis delta 4 by enzyme acyl-coA-dehydrogenase

81
Q

Alternative FA oxi step 4

A

Fatty acyl-coA trans delta 2 and cis delta 4—-> Fatty acyl-coA trans 3 by enzyme 2,4 dienoyl-coA reductase (nadph–> NADP)

82
Q

alternative FA oxi step 5

A

Fatty acyl-coA trans–> fatty acyl coA trans delta 2

83
Q

last step of Alternative FA oxi

A

fatty acyl coA trans delta 2–> 5 acytl coA by B-oxidation

84
Q

a-oxidation

A

Chorophyll—> phytol by hydrolysis

85
Q

Oxidation of odd number carbon FA

A

Bicarbonate + propionyl-coA—> D-methylmalonyl coA and enzme is propionyl-coA carboxylase( ATP–>ADP and is biotin dependent).

D-methylmalonyl coA—> L- methylmalonyl coA

L- methylmalonyl coA–> succinyl coA

86
Q

Assembly of HDL from cellular sources

A

Intestine liver macrophages–> Pre-B-HDL by APOA1/PL

Pre-B-HDL –> HDL-3 by LCAT and CETP transfer

HDL3–> HDL2 by CETP Ce transfer

87
Q

Saturated oxidation is more

A

energy efficient

88
Q

One double bond=

A

2 less ATPs produced

89
Q

The first carbon is

A

Alpha

90
Q

The second carbon is

A

B

91
Q

Alpha and beta carbon contain

A

single bonds

92
Q

Cant do cis double bond

A

oxidation in alternative FA oxidation

93
Q

Apoprotiens give proteins there

A

water solubilty

94
Q

Apoproteins recognize

A

Receptors

95
Q

B-100 receptor is associated with

A

TG offloading then size will change VLDL–> LDL

96
Q

genes from worst to better

A

E2, E4, E3

E2/E2 less recognized by cell

97
Q

5-10% of

A

VLDL

98
Q

15% of

A

LDL

99
Q

Cholesterol in MAC is

A

in Nucleus in Oxidized LDL and make Foam cells

100
Q

HDL can take cholesterol from

A

Macrophage

101
Q

How to write LDL/HDL ratio on test

A

If have 4.0- this ratio is in between average and twice average
- 2 decimal points

102
Q

Homozygous is what deficiency

A

Lcat defiecient

103
Q

Heterozygous is what deficiency

A

Fish eye deficiency

104
Q

Between alpha and beta carbons what happens

A

Oxidation

105
Q

Trans delta 2 enoyl coA

A

has 2 double bonds

106
Q

B-hydroxyl means

A

means beta carbon with a OH attached

107
Q

16 FA will equal what

A

8 acyl coA

108
Q

Enzymes in alternative oxidation pathway move

A

Double bonds to oxidative possible locations.

109
Q

Beta carbon in cis form prevents what

A

Oxidation

110
Q

Beta carbons cant

A

Be occupied by double bonds because oxidation will not take place

111
Q

have to move double bonds from

A

beta carbon to alpha carbon and then beta carbon can be oxidizable

112
Q

Populations that dont have enough alpha-hydroxylase

A

cant process plant-derived FA’s= Refsums disease

113
Q

A-hydrolase

A

do hydroxylation in A carbon so carbon 4 will be beta carbon and original beta carbon will become an alpha carbon

114
Q

Cholesterol with tail is inside the

A

Middle

115
Q

Cholesterol byitself is

A

outside region

116
Q

Chylomicrons carry

A

TGs Exogenously

117
Q

VLDL carry

A

TGs endogenously

118
Q

Apoprotiens are complexed with what

A

lipids to form lipoproteins

119
Q

Some VLDL, chylomicrons, LDL cells in different parts of body will have

A

Different receptors for different chylomicrons

120
Q

HDL is going to clear peripheral what

IF cells don’t have

A

Cholesterol back to the liver if cell don’t have receptor that recognizes Apo-A1 then cholesterol will not be cleared

121
Q

APo-A2 enhances

A

hepatic TG lipase activity so trading of cholesterol in HDL for TGs in chylomicrons in liver

122
Q

Your body will not make one signal

A

VLDL

123
Q

LDL is produced of the breakdown of

A

VLDL

TG offloading will cause cholesterol accumulation and make LDL

124
Q

Chylomicrons produced in Intestines will offload TGs and become

A

Chylomicrons remnants

125
Q

The starting to offload TG will produce what

A

Intermediate lipoproteins

126
Q

Apo-B-100 will

A

Have same first 48 AA sequence as Apo- 48

VLDL, IDL, and LDL

127
Q

Apo-48 is in

A

Chylomicrons

128
Q

Protein content is same for VLDL and LDL but

A

Size is changing

129
Q

Chylomicrons from

A

Intestines to liver

130
Q

VLDL from

A

Liver to peripheral tissue

131
Q

Isoforms

A

E2, E4, E3

E2 will be recognized less by LDL receptor, and therefore cholesterol will accumulate in blood and genes will be dimeric

132
Q

Apo A competition will

A

inhibit plasminogen binding

133
Q

B-VLDL is supposed to be in

A

Pre-Beta but can be seen in Beta fraction

134
Q

IDL and what are similar

A

B-VLDL

135
Q

Barbital is a

A

Alkaline buffer to keep electro-negativity

136
Q

Isoelectrical point

A

at a certain point the net electrical charge will become zero

137
Q

Beta is close to

A

negative electric side

138
Q

Chylomicrons can be seen at

A

Point of application and 2 % is a protein

139
Q

50%=

A

HDL protein

140
Q

Macrophages have

A

Oxidized cholesterol

141
Q

HDL can take cholesterol from

A

Macrophages

142
Q

HDL is associated with Apo-A1 and A2 can activate

A

LCAT acitivity and take FA from phospholipid (lecithin) and give it to cholesterol to make cholesterol esters

143
Q

Apo-A1 receptor where

A

The liver

144
Q

LDL can bind to

A

Hepatocyte then liver will become fatty liver

145
Q

HDL can trade cholesterol for

A

TG by enzyme Cholesterol ester transfer protein.

146
Q

When LCAT does cholesterol esterification

A

More hydrophobic cholesterol gets in and HDL gets bigger

147
Q

LDL receptors maintain

A

Cholesterol homeostatis

148
Q

Defective receptor B-100

A

More endogenous cholesterol synthesis will occur

149
Q

Modified LDL=

A

Oxidized LDL

150
Q

Foam cells are hallmark of

A
151
Q

Metabolic pattern in males and females are

A

Different so numbers for LDL/VlDL are different

152
Q

Oxidized LDLs are trapped

A

trapped undernealth endotheliat and then gets larger and larger.

153
Q

Fibrosis

A

Damage area closed and foam cells accumulation

154
Q

Blood flows through

A

Smaller area and will be fast and will cause shear stress on endothelial cells

increase N0-

Increased oxidative damage

155
Q

Fatty streaks

A

Scar damage

156
Q

angina

A

Chest pain

157
Q

Neurological activity is influenced by

A

FAT so increase Fat will damage neurological systems

158
Q

Heterozygous tangiers=

A

MIld form No tonsilar enlargement and hepatosplenomegaly

159
Q

Discoidal pre-Beta 1 in LCAT deficiency

A

2 dimensional electrophoresis

Clinical Chemistry II - 4378 (28 decks)

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