Lipdid Biosyntheis Flashcards

(158 cards)

1
Q

fatty acid synthesis occurs with excess?

A

CHO, aa

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2
Q

fa synthesis occurs where?

A

liver and adipose

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3
Q

humans can synthesize what kind of fa?

A

sat and some unsat

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4
Q

fa synthesis main precursor?

A

acetyl-CoA

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5
Q

any substance (mainly CHO) that can be taken into acetyl-CoA can be?

A

stored as a fa

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6
Q

lipogenic

A

substance taken to acetyl-CoA and stored as a fa to be used as fuel

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7
Q

3 fs synthesis systems

A

cytoplasmic, mitochondrial, microsomal

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8
Q

cytoplasmic is?

A

major pathway

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9
Q

mitochondrial sys is used for?

A

longer fa

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10
Q

microsomal sys is located?

A

ER

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11
Q

microsomal sys is where _______ is made?

A

unsaturated fa

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12
Q

common cytoplasmic fa

A

palmitic 16C

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13
Q

palmitic : Overall

A

acetyl-CoA + 7malonyl-Coa +14NADPH+ 14H > fa synthase complex> 7CO2 + 8CoA + 6 H2O + 14 NADP

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14
Q

NADPH + H comes from?

A

pentose shunt

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15
Q

malonyl CoA formation

A

acetyl-Coa + HCO3- {acetyl-Coa carboxylase} malonyl-CoA

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16
Q

enzyme used in malyonl-CoA rxn

A

acetyl-CoA carboxylase

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17
Q

what activates acetyl-CoA carboxylase

A

Citrate

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18
Q

what does high CHO do to citrate

A

increase citrate and fa synthesis

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19
Q

what does low CHO do to citrate

A

decrease citrate and produce ketones (liver)

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20
Q

acetyl-CoA must get out of mitochondria as part of?

A

citrate

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21
Q

citrate important b/c? (2)

A

activates key enzyme (acetyl-CoA carboxylase) and transfers acetyl CoA to cytoplasm

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22
Q

biotin is a

A

coenzyme (vitamin) in the melyonal-CoA rxn

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23
Q

synthesis is?

A

anabolic

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24
Q

oxidation is?

A

catabolic

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25
synthesis takes place?
cytoplasm
26
oxidation takes place?
mitochondria
27
NADPH is used in synthsis or oxidation?
synthesis
28
NAD, FAD are used in synthsis or oxidation?
oxidation
29
multi-enzyme complex? (syn/oxd)
synthesis
30
soluble enzymes? (syn/oxd)
Oxidation
31
fa synthesis needs?
ATP, CO2 , biotin, malonyl-CoA, citrate
32
fa oxidation needs?
carnitine
33
carnitine needed to?
get fa into mitoch
34
FA Synthase has how many sub units?
7
35
FA Synthase roughly what process?
reverse B-Oxidation
36
fa synthase multi-enzyme complex requires?
NADPH from pentose shunt and malanol-CoA
37
increase in glucose =
slows down KC and increased citrate leaves mitoch and goes to cytosol
38
citratel in cytosol is broken down into?
acetyl-CoA
39
microsomal system is in?
ER
40
Elongation promarily ?
C16- C18
41
what follows elongation?
unsaturation
42
humans can make?
monosaturated and polyunsaturated fa
43
fa humans can NOT make
Linolenic, a-linolenic Omega 3 and 6
44
FA humans can make
Palmitoleic, oleic, stearic, palmitic (Y-linolenic and Arachodonic)
45
Palmitic is made in the?
cytoplasm
46
steric, oleic is made in?
ER
47
cant make Y-Linolenic or Arachidonic w/o?
Linolenic acid
48
what is made form omega 3
PG3s
49
what is made from omega 6?
PG2s
50
PGs?
prostaglandins (local hormone-role in inflamation)
51
Regulation of FA SYnthase? (2)
Acetyl-Coa carboxylase | Malonyl-CoA
52
Acetyl-CoA carboxylase activated by?
citrate, insulin, and increased CHO decreased fat (get de novo synthesis)
53
(+) citrate means large amount of what are present?
OA and acetyl-CoA
54
large amts of OA and Acetyle-CoA means its a good time for?
fa synthesis
55
decrease of OA or acetyl-CoA will decrease?
fa synthesis
56
decrease of OA will favor?
ketone production
57
Acetyl-CoA Carboxylase is inhibited by?
palmitoyl-CoA (feed back mechanism)
58
Malonyl-CoA inhibited by
fa transfer into mitoch at carnitine step
59
TG location
liver adipose sm intestines
60
phosphoglyceride synthesis location
all cells (lipid bylayer)ch
61
need what to make TG?
3fa-CoA, glycerol, 7ATP
62
need what to make Phospoglycerides ?
lecithin, 2fa-Coa, glycerol, choline (7ATP--ATP, CTP)
63
why TG made in adipocytes? liver? sm intestines?
storage VLDLS Chylomicrons
64
cholesterol metabolism mostly in?
liver
65
800mg made per day to replace?
cholesterol lost as bile
66
as cholesterol intake increases feed back regulatoin does what?
decreases cholesterol production
67
what does it take to made cholesterol?
acetyl-CoA
68
cholesterol biosynthesis overall
acetyle-CoA, isoprene units, ATP, NADPH
69
HMG-CoA reductase ?
key regulatory enzyme (cholesterol) multiple levels of regulation
70
HMG-CoA long-term regulation: cholesterol intake causes?
decr. HMG-CoA reductase leves, decr. production, increases HMG-CoA reductase degradation
71
Short-term
phosphorylation/de-phosphorylation
72
HMG-CoA reductase : | P-form is
inactive
73
HMG-CoA reductase : | de-P-form is
active
74
de-P favors?
increased ATP/AMP
75
statins
competitive inhibitors of HMG-CoA reductase
76
is it a catabolic process to get rid of cholesterol?
no
77
what happens to cholesterol in liver?
excreted, converted to bile acids and packaged into VLDL
78
bile salt is a ?
bile acid conjugated with aa
79
reasons for lipid transport
1. transport diatary lipids 2.transport of tg, cholesterol to tissues 3. excretion of cholesterol in bile, 4. release of ffa during mobilization
80
lipoprotein diameter from smallest to largest
HDL,LDL,VLDL,chylomicron
81
B Apoprotein binds where?
at LDL receptor
82
LCAT adds fa from lecithin to?
cholesterol (in blood and sometimes associated with HDL)
83
VLDL increase with
CHO in diet
84
VLDL represents
transport of tg from liver to tissue
85
deposit of tg requires
lipoprotein lipase
86
lipoprotein lipase is found where
surface of capillary endothelial cells (breaks down tg to ffa + glycerol so it can be absorbed)
87
LDLs are remnats of?
VLDL
88
LDL loose?
tg, some spo-proteins and gain cholesterol
89
serum cholesterol is associated with?
LDL
90
LDL absorbed via
LDL receptor
91
LDL cholesterol is used for
membrane components and steroid precursors
92
2 types of LDL
larger (more cholesterol) smaller( incr. tg denser)~plaque
93
HDL first made as
phospholipid and protein
94
HDL prevent
excess cholesterol accumulation
95
HDL removes?
excess cholesterol
96
HDL transfers excess cholesterol where?
1. back into LDLs 2 delivered back to liver (reverse cholesterol transport)
97
reversi cholesterol transfer requires
enzyme: lecithen cholesterol acyl transferase (LCAT)
98
LCAT is able to add
fa to cholesterol
99
LCAT can add fa to cholesterol which can be enriched with
lipoprotein
100
chylomicrons carry?
dietary fats
101
chylomicrons formed with in?
mucosa
102
chylomicrons go through?
lymphatics and wnter blood via thoracic duct
103
the tg portion of the chylomicron is removed via?
LPLase
104
LPLase elaves what behind?
chylomicron remnant (picked up by liver)
105
serum albumen carries?
ffa released from adipose in mobilization ( not directly measured as blood lipids but some packaged in liver into VLDL)
106
transport of lipids from liver feedback mechanism?
incr. cholesterol: (-) HMG-CoA reductase, decr. LD receptors
107
tg synthesis balanced with
VLDL synthesis and release into blood
108
if tg and VLDL equilibrium is altered?
tg begin to deposit in liver = fatty liver
109
what decreases VLDL
decr. dietary protein and choline
110
what incereases tg synthesis
diabetess, starvation and ethanol
111
ethsnol in excess intake causes?
decr gluconeogenesis and hypoglycemia
112
ethonol metabolism: increased NADH-NAD inhibits
gluconeogenesis and lactate from going to pyruvate
113
water soluble vitamines primary function is?
as a coenzyme
114
Thiamine-B1 coemzyme form
Thiamine pyrophospate (TTP)
115
(B!): Thiamine pyrophosphate general role
oxidative decarboxylation
116
B1-Thiamine: oxidative decarboxylation pathwayL
pyruvate dehydrogenase and a-kg dehydrogenase (in KC)
117
no oxidative metabolism or no KC if no?
Thiamine
118
what rxn require thiamine and is part of the pentose shunt
transketolase
119
B1-thiamine deficiency
Beri-Beri: damage to nervous and cardiac systems
120
beriberi decreases aerobic CHO metabolish and you get elevated?
lactate and pyruvate because cant use pyruvate entry at PDH rxn (so both accumulate bc cant use aerobic metabolism)
121
Riboflavin-B2 coenzyme
FAD nucleotide
122
riboflavin-B2 general role
H+, e carrier (coenzyme for oxd/red rxn)
123
Riboflavin-B2 pathways
KC,ETS,B-ocidation (fa oxd & ) PDH rxn
124
Riboflavin-B2 deficiency
dermatitis and cheilosis (cracked mouth)
125
Niacin-B3 coenzyme
NAD & NADP nucleotide
126
Niacin-B3 general role
H+, e carrier (coenzyme for oxd/red rxn)
127
Niacin-B3 pathways
PDH, KC, ETS, B-Oxd, Pentose shunt, FA synthesis
128
Niacin-B3 deficiency
pellagra (low in tryptophan)
129
niacin precursor?
tryptophan
130
B6 coenzymes
PLP, PMP
131
B6 general role
coenzyme in amino acid metabolism, transamination (amino transer) Decarboxylations
132
Decarboxylation examples: Glutamate > ? | tryptophan >? glycine>?
GABA seritonin heme
133
lack of B6 causes disorders in
nervous sys (NT) and anemia (linked to heme)
134
panthothenic acid coenzyme
nucleotide part of Coenzyme A
135
panthothenic deficency
rare
136
folic acif coenzyme
tetrahdrofolate (THF)
137
fo\\the diff forms of folic acid are also
1C derivatives of folic acid
138
folic acid function
acts as coenzyme in 1C transfers like Purine Biosynthesis
139
Folic acid deficiency
megaloblastic anemia
140
B12 function
coenzyme in 1C transpositions and transfers
141
what accumulates if B12 deficient?
methyl and homocystine, methylmalonate
142
B12 deficiency
pernicious anemia or dietary deficiency
143
pernicious anemia
lack of intrensic factor
144
diatary deficiency
seen in vegitarians
145
SAM is a?
Methyl donar
146
Biotin function
coenzyme in carboxylations
147
which carboxylations in Biotin a coensyme in
Acetyl-CoA carboxylase, Pyruvate Carboxylase
148
Biotin Deficiency
none
149
Vit C function
collagen synthesis and cofactor for prolyl hydroxylase
150
Vit c invilved in collagen synthesis- required for?
hydroxylation of proline (also lysine)
151
Vit C deficiency
scurvy
152
Fat Soluble vit
A D E K
153
Vit A function
required for growth and maintenance of epithelial tissue
154
Vit A deficiency
xerophthalmia in children and night blindness in adults
155
Vit E function
antioxidant = protects against lipid perioxidation
156
Vit K function
cofactor for carboxylations of glutamic acid
157
vit K sensative enzyme or zymogen is?
prothrombin (II)
158
Vit K deficiency results in
hemorrhagic disease