Lipo mechinisms Flashcards
1
Q
LCAT involves the transfer of what to what
A
Fatty acid from phospholipid to cholesterol
2
Q
LCAT is associated with
A
HDL
3
Q
HDL take LCAT to
A
Cholesterol
4
Q
HDL goes to
A
Peripheral tissue where cholesterol is being acclumulating
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.
6
Q
Is there a pathological disease caused by LCAT
A
Yes, Lcat deficiency will cause an accumulation of cholesterol.
7
Q
Acyl coA is a source of
A
FA’s for esterification
8
Q
Hyper lipid conditions are associated with
A
more LCAT
9
Q
TG’s store
A
Fatty acids
10
Q
Plasma TG’s are from
A
Intestines and liver
11
Q
Unsaturated Fatty acids
A
Have double bonds
12
Q
Saturated fatty acids have
A
no double bonds
13
Q
Vegatables contains more
A
Unsaturated fatty acids which are healthier and are liquid at room temperature
14
Q
meat contains more
A
saturated fatty acids which are solids at room temp and are unhealthier
15
Q
Lipids + sugar
A
glycolipids
16
Q
Prostaglandins
A
Do cell to cell communication and are synthesised as needed. They have a short half life
17
Q
PGA with subscript 2
A
Prostaglandin A with 2 double bonds
18
Q
Phospholipids are
A
water soluble
19
Q
Cholesterol cant be
A
stored
20
Q
Fats are blank by bile salts
A
emulsified
21
Q
Emulsified and digestive enzymes
A
need to make fats into smaller pieces before digestive enzymes Lipase, Cholesterol esterase can work on fats
22
Q
Phospholipids have a
A
hydrophilic head and a hydrophobic tail
23
Q
A cofactor of digestive enzymes is
A
Bile salts
24
Q
Fats have to be what size to be used by digestive enzymes
A
1 mm small
25
If you have a stomach ache then Dr look at
pancreas for Pancreatitis; and increase in amylase can cause stomach issues
26
huge fats become
micelles
27
Micelles react with what to go into
Mucosal cells to go into ER
28
Smaller C FAs and medium C FA are less then blank and go through
10C and go directly through intestinal cells and into portal circulation
29
Albumin carries what to liver
Free fatty acids
30
Free fatty acids are absorbed by
enterocytes and then made into TGs and chylomicrons
31
TG and cholesterol in enterocytes are delivered to Interstines by chylomicrons and get into intestinal cells.
32
Only two percent of chylomicrons are
Proteins and do not separate on protein electrophoresis
33
Chylomicron is blank rich lipoprotein
TG and protein is Apo-B-48
34
Cylomicron is associated with
82% of TG
9% of cholesterol
7% of phospholipids
35
Increase in chylomicrons is associated with an
Increase in Exogenous TGs
36
HDL has blank and more blank charge
50% proteins and more negative charge
37
Intestines can make what
Phospholipids
38
Chylomicrons can be released for blank hours after a meal
14 hours from intestinal cells and Dr ask you to be fasted to minimize TG liver
39
Chylomicrons are transported to
All tissues
40
Chylomicron remnant is
Chylomicrons, after action of Lipoprotein lipase offloads TG and Chylomicrons are composed of the majority of Cholesterol.
41
Free fatty acids are
an important metabolic fuel
42
Acetate--> cholesterol involves what rate-limiting enzyme and what reaction
HMG-coA reductase and reaction is
B-hydroxy-B-methylglutaryl-CoA-----> Mevalonate
43
HMG coA reducatase is regulated by
Free cholesterol(Inhibited)
44
Neutral fats--> ethier what or what
Lipolysis and glycerol
lipolysis and fatty acids
45
Fatty acids to what or what
Acetyl Coenzyme A by Beta oxidation
Ketone by ketogenogenesis in the liver
46
ketone bodies to what or what
FA
Acetyl Co A
47
Acetyl co A to what or what
Cholesterol or krebs cycles
48
Cholesterol to what or what
Steroids or bile salts
49
IF acetyl co A is in excess then
FA made
50
Acetyl CoA---> what by what enzyme
7 malonyl coA by enzyme Acetyl coA carboxylase
51
Fatty acid synthesis
Acetyl coA + 7 malonyl coA + 14 NADPH + 14H+
------------------>
Palmitic acid + 7CO2 + 8coA + 14 NADP + 6H20s
52
Acetyl coA carboxylase is dependent on
Inhibited by
Activated by
Biotin
Inhibited by long chain acyl coA
Activated by Citrate
53
The 14 NADPH for fatty acid syn are provided by the
pentose phosphate pathway and the Malic enzyme
54
Glucose 6-P + NADP--->
Then reaction 2 of PPP
Phosphoglucucono lactone + NADPH + H
2.) 6-phosphoglucuconate + NADP---> D-Ribulose-5-Phosphate + NADPH+ H+
55
By using H+ pyruvate can enter
mitochrondria
56
8 NADPH come from what
6 NADPH come from what
8 from Malic enzyme
6 from Pentose phosphate pathway( oxidation pathway)
57
Fatty acid synthase complex steps in words
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
58
1st reaction in fatty acid synthase complex
Acetyl coA---> malonyl coA by enzyme acetyl transacylase
59
2nd reaction in fatty acid synthase complex
Malonyl coA---> Ketoacyl synthase by enzyme malonyl transacylase
60
3rd reaction in fatty acid synthase complex
Malonyl coA--> 3-ketoacyl-enzyme complex by ketoacyl synthase and loss of CO2
61
4th reaction in fatty acid synthase complex
3-ketoacyl-enzyme complex---> saturated acyl enzyme complex by enzymes ketoacyl reductase( NADPH to NADP) and hydratase( loss of water) and enoyl reductase
62
5th reaction in fatty acid synthase complex
Saturated acyl enzyme complex--> palmitate by six cycles repeat
63
Thiel groups
oxidized and reduced group
64
Disulfide bonds bind
proteins
65
fatty acid synthase complex is a
mirror image
66
Palmithic acid is one of the most
common naturally occurring fatty acids
67
Fatty acid utilization
68
Triacylglycerol/ triglyceride-->
Adipose tissue to where
TG-->FFA by lipolysis
then FFA are transported in the blood to the liver and extrahepatic tissues by serum albumin complex
69
In the liver( cytosol) FFA are converted to
acyl- CoA which is utillized for energy and biosynthesis
70
In the liver(cytosol->mitochrondria) acyl-CoA-->
Carnithine acyltransferase--> acyl coA( synthesis of glycerolipids and sphingolipids
71
In the mitochrondria acyl coA->
acyl-coA-->Acetyl CoA by B oxidation
72
Short chain FA and medium chain FA are blanked
Diffuse into the Mitochrondria Short(2-4), medium( 4-12)
73
Long chain FA require the
Carnitine cycle
74
Beta oxidation step 1
Palmitoyl coA--> Trans-delta2 enoyl coA by enzyme acyl-coA dehydrogenase
75
Beta oxidation step 2
Trans-delta2 enoly-CoA--> L-B-hydroxy-acyl-coA by enzyme enoyl-coA hydratase
76
Beta oxidation step 3
L-B-hydroxy-acyl-coA--> B-ketoacyl-coA by enzyme D-hydroxyacyl-coA dehydrogenase (NAD-->NADH)
77
Beta oxidation step 4
Beta-ketoacyl-coA--> acyl-coA and acetyl coA(2 carbons) by enzyme acyl-coA acetyltransferase (thiolase)
78
Alternative FA oxidation pathway step one
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
Alternative FA oxidation pathway step two
Fatty acyl-coA trans delta 2,6---> fatty acyl-coA cis 4 by B-oxidation and removes Acetyl coA
80
Alternative FA oxi step three
Fatty acyl-coA- cis 4---> Fatty acyl-coA-trans-delta 2 and cis delta 4 by enzyme acyl-coA-dehydrogenase
81
Alternative FA oxi step 4
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
alternative FA oxi step 5
Fatty acyl-coA trans--> fatty acyl coA trans delta 2
83
last step of Alternative FA oxi
fatty acyl coA trans delta 2--> 5 acytl coA by B-oxidation
84
a-oxidation
Chorophyll---> phytol by hydrolysis
85
Oxidation of odd number carbon FA
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
Assembly of HDL from cellular sources
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
Saturated oxidation is more
energy efficient
88
One double bond=
2 less ATPs produced
89
The first carbon is
Alpha
90
The second carbon is
B
91
Alpha and beta carbon contain
single bonds
92
Cant do cis double bond
oxidation in alternative FA oxidation
93
Apoprotiens give proteins there
water solubilty
94
Apoproteins recognize
Receptors
95
B-100 receptor is associated with
TG offloading then size will change VLDL--> LDL
96
genes from worst to better
E2, E4, E3
E2/E2 less recognized by cell
97
5-10% of
VLDL
98
15% of
LDL
99
Cholesterol in MAC is
in Nucleus in Oxidized LDL and make Foam cells
100
HDL can take cholesterol from
Macrophage
101
How to write LDL/HDL ratio on test
If have 4.0- this ratio is in between average and twice average
- 2 decimal points
102
Homozygous is what deficiency
Lcat defiecient
103
Heterozygous is what deficiency
Fish eye deficiency
104
Between alpha and beta carbons what happens
Oxidation
105
Trans delta 2 enoyl coA
has 2 double bonds
106
B-hydroxyl means
means beta carbon with a OH attached
107
16 FA will equal what
8 acyl coA
108
Enzymes in alternative oxidation pathway move
Double bonds to oxidative possible locations.
109
Beta carbon in cis form prevents what
Oxidation
110
Beta carbons cant
Be occupied by double bonds because oxidation will not take place
111
have to move double bonds from
beta carbon to alpha carbon and then beta carbon can be oxidizable
112
Populations that dont have enough alpha-hydroxylase
cant process plant-derived FA's= Refsums disease
113
A-hydrolase
do hydroxylation in A carbon so carbon 4 will be beta carbon and original beta carbon will become an alpha carbon
114
Cholesterol with tail is inside the
Middle
115
Cholesterol byitself is
outside region
116
Chylomicrons carry
TGs Exogenously
117
VLDL carry
TGs endogenously
118
Apoprotiens are complexed with what
lipids to form lipoproteins
119
Some VLDL, chylomicrons, LDL cells in different parts of body will have
Different receptors for different chylomicrons
120
HDL is going to clear peripheral what
IF cells don't have
Cholesterol back to the liver if cell don't have receptor that recognizes Apo-A1 then cholesterol will not be cleared
121
APo-A2 enhances
hepatic TG lipase activity so trading of cholesterol in HDL for TGs in chylomicrons in liver
122
Your body will not make one signal
VLDL
123
LDL is produced of the breakdown of
VLDL
TG offloading will cause cholesterol accumulation and make LDL
124
Chylomicrons produced in Intestines will offload TGs and become
Chylomicrons remnants
125
The starting to offload TG will produce what
Intermediate lipoproteins
126
Apo-B-100 will
Have same first 48 AA sequence as Apo- 48
VLDL, IDL, and LDL
127
Apo-48 is in
Chylomicrons
128
Protein content is same for VLDL and LDL but
Size is changing
129
Chylomicrons from
Intestines to liver
130
VLDL from
Liver to peripheral tissue
131
Isoforms
E2, E4, E3
E2 will be recognized less by LDL receptor, and therefore cholesterol will accumulate in blood and genes will be dimeric
132
Apo A competition will
inhibit plasminogen binding
133
B-VLDL is supposed to be in
Pre-Beta but can be seen in Beta fraction
134
IDL and what are similar
B-VLDL
135
Barbital is a
Alkaline buffer to keep electro-negativity
136
Isoelectrical point
at a certain point the net electrical charge will become zero
137
Beta is close to
negative electric side
138
Chylomicrons can be seen at
Point of application and 2 % is a protein
139
50%=
HDL protein
140
Macrophages have
Oxidized cholesterol
141
HDL can take cholesterol from
Macrophages
142
HDL is associated with Apo-A1 and A2 can activate
LCAT acitivity and take FA from phospholipid (lecithin) and give it to cholesterol to make cholesterol esters
143
Apo-A1 receptor where
The liver
144
LDL can bind to
Hepatocyte then liver will become fatty liver
145
HDL can trade cholesterol for
TG by enzyme Cholesterol ester transfer protein.
146
When LCAT does cholesterol esterification
More hydrophobic cholesterol gets in and HDL gets bigger
147
LDL receptors maintain
Cholesterol homeostatis
148
Defective receptor B-100
More endogenous cholesterol synthesis will occur
149
Modified LDL=
Oxidized LDL
150
Foam cells are hallmark of
151
Metabolic pattern in males and females are
Different so numbers for LDL/VlDL are different
152
Oxidized LDLs are trapped
trapped undernealth endotheliat and then gets larger and larger.
153
Fibrosis
Damage area closed and foam cells accumulation
154
Blood flows through
Smaller area and will be fast and will cause shear stress on endothelial cells
increase N0-
Increased oxidative damage
155
Fatty streaks
Scar damage
156
angina
Chest pain
157
Neurological activity is influenced by
FAT so increase Fat will damage neurological systems
158
Heterozygous tangiers=
MIld form No tonsilar enlargement and hepatosplenomegaly
159
Discoidal pre-Beta 1 in LCAT deficiency
2 dimensional electrophoresis
