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Metabolism of lipids

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Title: Metabolism of lipids


1
Metabolism of lipids
2
Course Content
  • Digestion and absorption of lipids
  • Triacylglycerol metabolism
  • Phospholipid metabolism
  • Cholesterol metabolism
  • plasma lipoprotein metabolism

3
Summary
  • Definition
  • Classes

fats triacylglycerols, TG
cholesterol, Ch
lipids
cholesteryl ester, CE
lipoids
phospholipids, PL
glucolipids, GL
  • Function

4
nomenclature
  • Fatty acids
  • Saturated fatty acids
  • 14?20C palmitic acid
  • 16C stearic acid 18C
  • Unsaturated fatty acids
  • Linolenic acid 18C three unsaturated
    bonds
  • Linoleate 18C two unsaturated bonds
  • Arachidonic acid 20C
    four unsaturated bonds
  • Essential fatty acids
  • required for the growth of mammals and they
    must be obtained from food. Including
    linoleate?linolenate, arachidonic acid amount
    unsaturated in plant

5
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6
Section I Digestion and absorption of lipids
  • digestion
  • small intestinebile?pancreatic
    lipase?colipase?phospholipase A2? cholesteryl
    esterase
  • product2-monoacylglycerol(MG)?FFA?Cholesterol?lys
    ophospholipid
  • absorption

7
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8
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9
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10
Absorption
11
Monoacylglycerol synthesis Pathway
12
Section II Triacylglycerol metabolism
13
Chemical Structure of Triacylglycerol
14
Fatty Acid Synthesis
  • Palmitic acid synthesis
  • Elongation of FA carbon-chainER
  • ER
  • --Mitochondrial
  • Synthesis of Unsaturated FA
  • Regulation of unsaturated FA

15
Biosynthesis of palmitic Acid
  • Tissuesliver(major site) ?kidney?
  • breast?adipose? lung ? brain
  • ---Cytosol
  • MaterialsAcetyl-CoA?NADPHH?ATP?HCO3- and Mn2
  • Pathway
  • ---Synthesis of malonyl-CoA
  • ---Synthesis of fatty acid

16
Citrate Pyruvate Cycle
17
malonyl-CoA Synthesis
???
18
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19
  • The overall reaction, which is spontaneous, may
    be summarized as
  • HCO3- ATP acetyl-CoA ? ADP Pi malonyl-CoA

20
  • Acetyl-CoA Carboxylase, which converts acetyl-CoA
    to malonyl-CoA, is the committed step of the
    fatty acid synthesis pathway.
  • The mammalian enzyme is regulated, by
  • phosphorylation
  • allosteric control by local metabolites.
  • Conformational changes associated with
    regulation
  • In the active conformation, Acetyl-CoA
    Carboxylase associates to form multimeric
    filamentous complexes.
  • Transition to the inactive conformation is
    associated with dissociation to yield the
    monomeric form of the enzyme (protomer).

21
AMP-Activated Kinase catalyzes phosphorylation of
Acetyl-CoA Carboxylase, causing inhibition.
  • The decreased production of malonyl-CoA prevents
    energy-utilizing fatty acid synthesis when
    cellular energy stores are depleted. (AMP is
    abundant only when ATP has been extensively
    dephosphorylated.)

22
  • The antagonistic effect of insulin, produced when
    blood glucose is high, is attributed to
    activation of Protein Phosphatase.

23
Regulation of Acetyl-CoA Carboxylase by local
metabolites
  • Palmitoyl-CoA (product of Fatty Acid Synthase)
    promotes the inactive conformation, diminishing
    production of malonyl-CoA, the precursor of fatty
    acid synthesis.
  • This is an example of feedback inhibition.

24
Citrate allosterically activates Acetyl-CoA
Carboxylase.
  • Citrate is high when there is adequate
    acetyl-CoA entering Krebs Cycle.
  • Excess acetyl-CoA is then converted via
    malonyl-CoA to fatty acids for storage.

25
  • Fatty acid synthesis from acetyl-CoA
    malonyl-CoA occurs by a series of reactions that
    are
  • in bacteria catalyzed by 6 different enzymes plus
    a separate acyl carrier protein (ACP)
  • in mammals catalyzed by individual domains of a
    very large polypeptide that includes an ACP
    domain.
  • NADPH serves as electron donor in the two
    reactions involving substrate reduction.
  • The NADPH is produced mainly by the Pentose
    Phosphate Pathway.

26
Mammalian fatty acid synthase
  • A dimer of two polypeptides of 240 kDa each
  • Each polypeptide contains eight domains that
    represent the seven catalytic centres plus an
    integral acyl carrier protein (ACP) domain

27
4' phosphopantetheine
28
The structure of the mammalian Fatty Acid
Synthase protein is summarized above KS
b-Ketoacyl Synthase (Condensing
Enzyme)---(Cys) AT Acyl transferase MT
Malonyl/Acetyl-CoA Transacylase DH
Dehydratase ER Enoyl Reductase KR b-Ketoacyl
Reductase TE Thioesterase ACP Acyl Carrier
Protein ---(Pant)
29
4. Reduction
5. Acyl transfer
3.Dehydration
1.Condensation
2.Reduction
30
  • Elongation of FA Carbon-chain
  • ER
  • Mitochondria
  • Synthesis of unsaturated FA
  • unsaturated FA ????Oleate?linoleate?linolenate?ar
    achidonic acid ( Essential FA )
  • Essential FArequired for the growth of mammals
    and they must be obtained from food. Including
    linoleate?linolenate, arachidonic acid

31
????
32
Regulation of FA synthesis
  • Dietary factors carbohydrate promotes synthesis
  • Hormone factors
  • insulin,store hormone,increase FA synthesis
  • Glucagon ,release hormon,inhibit FA
    synthesis

33
Important of polyunsaturated fatty
acids---prostaglandins (PG)? thromboxanes (TX)?
leukotrienes (LT)
  • Chemical structure and nomenclature of PG? TX? LT
  • Synthesis of PG?TX and LT
  • Physiological functions of PG?TX and LT

34
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35
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36
Thromboxane A2
Leukotriene A4(LTA4)
37
Synthesis of PG?TX and LT
38
Physiological functions of PG?TX and LT
  • PGPGE2 triggers inflammationPGE2?PGA2
    downregulates blood pressurePGF2promotes
    ovulation?delivery
  • TXTXA2 and PGE2 promotes coagulation and
    thrombosis
  • PGI2inhibiting coagulation and thrombosis
  • LTConstriction of bronchial smooth muscle
    cells,Slow reaction substances(SRS-A)are mixtures
    of LTC4?LTD4and LTE4

39
?????
  • ??????????????????????????????
  • ?????????????????????????????????

40
Synthesis of Triglycerides location
liver?adipose tissue and small
intestinal materialsglucose?dietary
fats pathwayAcylglycerol pathway
diacylglycerol pathway
41
Dietary (external)
Fat synthesis(internal)
CM
FFA
CM
VLDL
FFA mobilization
42
Diacylglycerol Pathway
43
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44
Degradation of Triacylglycerols
  • Lipolysis
  • Glycerol Metabolism
  • ß-Oxidation
  • Other oxydation modes of fatty acid
  • Formation and utilization of Ketone Bodies

45
Lipolysis
  • Concept
  • Committed enzymehormone-sensitive triglyceride
  • lipase (HSL)
  • Lipolysis hormonesadrenalin ?glucagon?ACTH and
    TSH
  • Anti-lipolysis hormonesInsulin?PEGE2 and
    Nicotinic Acid

46
PPi
ADP
HSL (active)
HSL (inactive)
P
Pi
47
Glucagon
Insulin
Committed enzyme
()
(-)
ATP
HSL
adenylyl cyclase
()
cAMP
Protein kinase
TG
DG
FFA
lipolysis
MG
FFA
glycerol
48
Glycerol metabolism
49
Experimental evidence for ß-Oxidation of fatty
acid
50
ß-Oxidation of fatty acid
  • ???????????ß-?????,???????????(acetyl-CoA)
  • StepsActivation of FAenter into mitochondria
  • ß-oxidation TAC(Tricarboxylic acid
    cycle)

51
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52
Activation of fatty acid Formation of Acyl-CoA
  • Locationcytosol

acyl-CoA
53
Carnitine
(Acyl-CoA)
(Carnitine)
54
Mitochondrion
55
Carnitine acyltransferase ?
???
CoASH
Carnitine acyltransferase ?
CoASH
56
Acyl CoA enter into mitochondrion
Committed enzyme
57
ß-Oxidation of fatty acid
  • locationmitochondrial matrix
  • ??????ß-???????????,????ß?????,dehydrogenation
    ???hydration?dehydrogenation ?thiolysis??,????????
    ?????????CoA(acyl-CoA)??????CoA(acetyl-CoA)

58
a
ß
FAD
(dehydrogenation)
FADH
H2O
(hydration)
NAD
(dehydrogenation)
H
NADH
CoASH
(thiolysis)
59
(dehydrogenation)
(hydration)
(dehydrogenation)
(thiolysis)
60
???ß-Oxidation??
  • ?????????(cytosol),????ATP??????
  • Acyl-CoA?carnitine?????,???CAT-?
  • ß-Oxidation(mitochondrion) including
    dehydrogenation ?hydration ?dehydrogenation
    ?thiolysis four repeated steps

61
??????????
  • ????(C16)
  • 7?ß-??,??8????CoA?7??FADH2?7??NADH
  • ? 12 8 273 7131??ATP
  • ????????2??????
  • ???131-2129??ATP
  • formula12 5 ( -1) 2
  • ?????

62
Difference between synthesis and degradation of
palmitic Acid
difference synthesis degradation
location cytosol mitochondria
Acyl carrier ACP CoA
Two carbon- fragment Malonyl-CoA Acytel-CoA
reducing equivalents NADPH FAD?NAD
HCO3- and citrate needed Not needed
Energy alteration Consume 7ATP14NADPH Form 129ATP
63
Difference Between Fatty Acid Synthesis And
ß-Oxidation
Diffference Synthesis ß -Oxidation
Location Cytoplasm Mitochondrion
Thioester linkage ACP CoA
Two carbon-fragment Malonyl-CoA Acetyl-CoA
Electron carrier NADPH FADH?NADH
HCO3- and cytratre needed Nod needed
Energy alteration Consume 7ATP14NADPH Form 129ATP
64
Other oxydation modes of fatty acid
  • Oxydation of unsaturated FA
  • FA oxydation in peroxisomes
  • Oxydation of propionic acid

65
Formation and utilization of Ketone Bodies
  • Ketone BodiesAcetoacetate? ß-Hydroxybutyrate and
    Acetone
  • Ketogenesis
  • Utilization of Ketone Bodies
  • Physiology Significance of Ketogenesis
  • Regulation of Ketogenesis

66
ketone bodies(KB)
a
ß
?
ß-hydroxybutyrate
Acetoacetate
Acetone
67
CoASH
CoASH
???
CoASH
a
ß
NAD
CO2
NADH
H
68
Formation of Ketone Bodies
???
69
Utilization of Ketone Bodies
70
Liver Blood
Extrahepatic Tissues
?
?
Urine
?
?
?
Citric acid cycle
?
?
Citric acid cycle
Acetone Lungs
71
Major energy materials provided for tissues
Glucose FFA KB
Red Blood Cell
Brain
Muscle (exercise) (rest)
Liver
72
Concentration of energy materials of the blood in
full of eating or hungry (mmol/L)
Full(of eating) Hungry(5-6 weeks)
Glucose 5.0 4.49
ß-Hydroxybutyrate 0.02 6.67
Acetoacetate 1.17
73
Physiology Significance of Ketogenesis
  • Ketone bodies serve as a fuel for extrohepatic
    tissues.
  • Ketoacidosis results from prolonged
    ketosisHigher than normal quantities of ketone
    bodies present in the blood or urine constitude
    ketonemia or ketonuria, respectively.The overall
    condition is called ketosis.

74
Three Crucial Steps for Ketogenesis Regulation
  • Control of free fatty acid(FFA) mobilization from
    adipose tissue
  • The activity of carnitine acyltransferase (CAT-1)
    in liver,which determines the propotion of the
    fatty acid flux that is oxidized rather than
    esterified
  • Partition of acetyl-CoA between the pathway of
    ketogenesis and the citric acid cycle

75
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76
Regulation of Ketogenesis
77
???
  • ????
  • 1??????(lipolysis)
  • 2?????????????(HSL)
  • 3?????
  • 4?????ß-??(ß-oxidation)
  • 5?????(essential fatty acid)
  • 6???(ketone bodies)

78
  • ??
  • 1?????????????
  • 2?????????????
  • 3???????????????
  • 4???????????????CO2?H2O,??????ATP????????????

79
???
  • 1?????? ? ? ? ? ? ? ? ? ?
  • A? ? ? ? ? ? ? ? ? ?
  • B? ? ? ? ? ? ? ? ? ? ?
  • C? ? ? ? ? ? ? ? ? ? ? ?
  • D? ? ? ? ? ? ? ? ? ? ? ?
  • E? ? ? ? ? ? ? ? ? ? ? ?

(A?B)
80
???
  • 2?? ? ? ? ? ? ?, ? FAD ? ? ? ? ? ? ?
  • A? ? ? ? ? ? ? ? CoA
  • B? ß-? ? ? CoA ? ?
  • C? ? ? ? ? ? ?
  • D? ? ? CoA ? ?
  • E? ß-? ? ? ? ?

(D)
81
???
  • 3????14 ???????ß-?????CoA
  • A?????????2 ???????
  • B???????7?ß-?????7????CoA
  • C???6 ??FADH2 ?6 ??NADH H
  • D??????????????ß-??????

(A?C)
82
???
  • 4??????????????????????
  • A?????? B???CH3COCoA
  • C?ß????????RCH2CH2CH2COCoA
  • D???????RCH2CHOHCH2COCoA
  • E??????NAD?NADH

(A)
83
???
  • 5?????1?????CoA(180)????????O2?
  • A?23 B?26 C?30
  • D?16 E?32

(B)
84
???
(A?B?C?D)
  • 6???????????
  • A?????????????ß-???
  • B??????????
  • C??????????
  • D???????????

85
???
  • 7????????CO2?H2O????
  • A??? B????
  • C?? D??

(A?C)
86
  • ?????
  • ??????????????????????????????
  • ?????????????????????

87
Section II Phospholipid Metabolism
88
Classification of Phospholipids
  • phosphoglyceride
  • Phosphatidylcholine (PC)
  • Phosphatidylethanolamine (PE)
  • Phosphatidylserine (PS)
  • Phosphatidylglycerol (PG)
  • Diphosphatidylglycerol (DPG)
  • phosphatidyl inositol(PI)
  • Sphingomyelin

89
  • Chemical Structure of Phosphoglyceride

Most phospholipids have a saturated fatty acid on
C-1 and an unsaturated fatty acid (Arachidonic
Acid )on C-2 of the glycerol backbone.
90
Structure of Phospholipid
91
Classification of phosphoglyceride-1
  • X-OH X-
    name

92
Classification of phosphoglyceride-2
X-OH X-
name
93
Glycerophospholipid synthesis
  • Site liver,kidney,intestine
  • endoplasmic reticulum, ER
  • SourcesFA,glycerol,phosphate,nitrogenous base
    (choline,ethanolamine,serine,inostol,etc),ATP,
    CTP
  • CDP- nitrogenous base
  • CDP-diacylglycerol

94
CDP-choline?CDP- diacylglycerol
95
Diacylglycerol Pathway
96
Diacylglycerol PathwayPE, PC
97
CDP- Diacylglycerol PathwayPI?PS?DPG
98
Synthesis of CDP- nitrogenous base
99
Phosphoglycerol degradation
100
Metabolism of Sphingolipids
Sphingomyelins and Glycosphingolipids
XPhosphorylcholin or phosphoethanolamine
XMono-or Poly- saccharin
Sphingomyelin
Glycosphingolipid
101
Synthesis and Degradation of
Sphingomyelin
  • Site brain---ER
  • Soucespalmitoyl-CoA,
  • Serine,NADPHH,FAD
  • Pathway

102
Degradation of Sphingomyelin
  • Sphingomyelinase (PLC )
  • -----Defects in the enzymes
    result in
  • genetic diseases such as
    Niemann-
  • Pick disease

103
?????
  • ????????????????????CTP????????????????

104
???
  • 1?????????(??)
  • ??????????,????????????
  • ???????????????
  • 2?????????????????????????(??)
  • 3??????????????????
  • 4????????????????

105
???
  • ????1?????CoA(180)????????O2?
  • A?23 B?26 C?30
  • D?16 E?32

(B)
106
???
  • 1????????????????
  • A?????CoA
  • B?????????CoA
  • C????????
  • D??NADH????
  • E????????????

(B)
107
???
  • 2??????????CoA?
  • A???????
  • B??????????????????
  • C???????????
  • D??????,???CoA???
  • E??????????

(B)
108
???
  • 3??????????????
  • A???? B????
  • C???? D????

(B)
109
???
  • 4???????????????
  • A?TDP-?? B?ADP-??
  • C?UDP-?? D?GDP-??
  • E?CDP-??

(E)
110
Section IV Cholesterol(Ch) Metabolism
111
Cholesterol Structure
Cholesterol(Ch)
Cholesterol Ester(CE)
??????
112
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113
Roles of Cholesterol
  • Membrane component
  • Steroid synthesis
  • Bile acid/salt precursor
  • Vitamin D precursor

114
Sources of Cholesterol
Cholesterol synthesized in extrahepatic tissues
De novo synthesis
Diet
Liver cholesterol pool
Free cholesterol In bile
Conversion to bile salts/acids
Secretion of HDL and VLDL
115
Dietary Cholesterol
  • Animal products eggs
  • Absorb about 50
  • Increase intake decreased absorption
  • Excrete 1 g/day (bile acids)

116
Dietary Cholesterol
  • Assume 400 mg intake / day
  • 200 mg is absorbed
  • 1000 mg is excreted
  • 800 mg from de novo synthesis
  • Lowering cholesterol in diet has very little
    effect on blood cholesterol !!!

117
Cholesterol Synthesis
  • 80 in liver, 10 intestine, 5 skin
  • Occurs in cytosol
  • Requires 18Acetyl-CoA?16NADPH?36ATP
  • Similar to ketogenic pathway
  • Highly regulated

118
Cholesterol Synthesis-1
???
119
Cholesterol Synthesis -2
120
Cholesterol Synthesis Summary
121
Regulation of Cholesterol Synthesis
  • rate-limiting enzymeHMGCoA reductase
  • Regulation factors
  • Famine and saturation famine (-), fasting (-)
  • cholesterol inactivate HMGCoA reductase
  • Hormons insulin/thyroxin induce activity of
    HMGCoA reductase glucagon/cortisol/Epi
    inactivate HMGCoA reductase

122
HMG CoA reductase - Phosphorylation
HMG CoA reductase OH (active)
HMG CoA reductase P (inactive)
AMP-Activated Protein Kinase (high
activity)
()
AMP
phosphatase
kinase
()
()
AMP-Activated Protein Kinase (low activity)
increase cAMP
Insulin
Glucagon/epi
123
Conversion of Cholesterol
  • Bile acid liver (2/5)
  • Steroids adrenal cortex, testicle,ovary
  • Vitamin D skin(7-dehydrocholeterol and
  • Vitamin D3)

124
?????
  • ????????????????????????????????????
  • ????????????????????????????

125
Section IV Metabolism of Plasma Lipoproteins
  • Plasma lipids
  • Plasma lipoproteins
  • Apolipoproteins
  • Metabolism of Plasma Lipoproteins
  • Medical implications

126
  • Plasma Lipids ----Lipids in plasma
  • TG100mg/dl
  • PL 200mg /dl
  • lecithins
    70
  • nerve sphingomyelin 20
  • cephalin
    10
  • Ch and CE200mg /dl
  • Ch55mg /dl CE145mg /dl
  • FFA15mg /dl
  • Origin of plasma lipids
  • Exogenous dietary lipids
  • Endogenous synthetized by liver, adipose
    tissue and
  • other tissues

127
Plasma Lipoproteins
  • Classes
  • electrophoresisCM (Chylomicron) ?ß? pro-ß?a
  • ultracentrifugation
  • CM?VLDL(very low density lipoprotein)?LDL?HDL

128
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129
Compositions of plasma lipoproteins
130
Structure of plasma lipoprotein
131
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132
Apolipoproteins (apo) -1
Type Association Function
B48 Chylomicron Carry cholesterol
esters Lacks LDL recpt binding
domain B100 VLDL,IDL,LDL Binds LDL
recpt. C-II Chyl. VLDL, IDL, HDL Activates
LPL C-III Chyl. VLDL, IDL, HDL
Inhibits LPL E Chyl. Remnant,
VLDL, IDL Binds LDL recpt HDL A-1 HDL/Chyl
omicron LCAT activator (lecithincholestero
l acyltransferase) A?
HDL
HL()??HDL A?
HDL,CM
LPL()
133
Apolipoprotein (apo) -2
Type Association Function
D HDL
transports CE J
HDL binds and transports
lipids CETP HDL
transports CE,TG PTP
HDL transports PL
134
Major Enzymes for Lipoprotein Metabolism
  • lipoprotein lipase,LPL
  • hepatic lipase,HL
  • lecithin cholesterol acyltransferase, LCAT
  • acyl-CoA cholesterol acyltransferase, ACAT

135
lipoprotein lipase,LPL
  • hepatic lipase,HP

136
lecithin cholesterol acyltransferase, LCAT
137
acyl-CoA cholesterol acyltransferase,ACAT
138
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139
(No Transcript)
140
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141
CM Metabolism
apoC???LPL
142
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143
VLDL Metabolism
apoC???LPL
144
CE
145
LDL Metabolism
146
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147
HDL Metabolism
148
Function of plasma lipoproteins
  • CMTransport dietary from intestine to
  • liver (exogenous)
  • VLDL Transport lipids from liver to peripheral
  • tissues (endogenous
  • LDLendogenous Cholesterol transport
  • HDLreverse Cholesterol transport

149
Clinical importance for disease
  • Hypertriglyceridemia and CHD Risk Associated
    Abnormalities
  • Accumulation of chylomicron remnants
  • Accumulation of VLDL remnants
  • Generation of small, dense LDL
  • Association with low HDL
  • Increased coagulability
  • - ? plasminogen activator inhibitor (PAI-1)
  • - ? factor VIIc
  • - Activation of prothrombin to thrombin

150
Genetic Disease
  • LPL Deficiency
  • LDL receptor Deficiency

151
?????
  • ????????????????????????????
  • ????????????????LDL???????????????????

152
???
  • ??????
  • 1???2??????3?????
  • ????
  • 1????????????
  • 2???????????(?????????)?????????

153
????? ???
154
1. ?????????( )
A ????????(HSL) B ??? C ?????? D ????? E ???
155
2. ??????????????( )
A ????? B ???? C ACTH D ????? E ???
156
3. ????????????,??????????( )
A ??? B ?? C ?? D ??? E ???
157
4. ????????????( )
A ??CoA??? B ???????I C ???????II D
??CoA??? E ?-????
158
5. ??????-??????????( )
A ??,??,???,?? B ??,??,???,?? C ??,???,??,
?? D ??,??,??,??? E ??,??,??,???
159
6. ?????,???????????( )
A ???? B ?????? C ?????? D ???? E ????
160
7. ?????????????( )
A ??? B ??? C ??? D ???? E ??
161
8. ????HMG-CoA????????????( )
A ?????????? B ????????????? C ??????????? D
?????????? E ???????????
162
9. ?????????????????????( )
A ??????B B ?VLDL??LDL?? C ???LDL?????? D
??HMG-CoA??????? E ??????????(ACAT)????
163
10. ????????????????( )
A ????????????? B ?????????????????CoA C
???????? D ??ATP E ??NADPH??
164
11. The organ having the strongest ability of
fatty acid synthesis is ( )
A fatty tissue B lacteal gland C liver D
kidney E brain
165
12. Which one transports cholesterol from outer
to inner of liver?
A CM B VLDL C LDL D HDL E IDL
166
13. Which one is essential fatty acid?
A palmitic acid B stearic acid C oleinic acid D
octadecadienoic acid E eicosanoic acid
167
14. The main metabolic outlet of body
cholesterol is ( )
A change into cholesterol ester B change into
vitamine D3 C change into bile acid D change
into steroid hormone E change into
dihydrocholesterol
168
15. ????????????????( )
A ??? B ?????? C ???????? D ??? E ??

169
16. ??????????????( )
A ?? B ??? C ?? D ??? E ???
170
17. ?????????????( )
A ????????(HSL) B ??????(LPL) C ????(HL) D
???????????(LCAT) E ???????????(ACAT)

171
18. ???????( )

A ???????? B ?????????????? C ???????? D CM
VLDL?????????? E LDL HDL??????????
172
19. Which can be the source of acetyl CoA?

A glucose B fatty acid C ketone body D
cholesterol E citric acid
173
20. The matters which join in synthesis of
cholesterol directly are ( )
A acetyl CoA B malonyl CoA C ATP D NADH E
NADPH
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