Metabolism of Lipids

biochemistry and molecular

biology department

Concept
Lipids are substances that are
insoluble or immiscible in water, but
soluble in organic solvents.

Fats (Triglyceride or
triacylglycerole
)

To store and
supply
energy

Lipids
Phospholipids
Glycolipids
Lipoids
Cholesterol
Cholesterol ester

To be
important
membrane
components

Contents
Section 1 Fatty acids
Section 2

Metabolism of Triglycerids

Section 3 Metabolism of Phospholipids

Section 4 Metabolism of Cholesterols
Section 5 Metabolism of Plasma
Lipoproteins

Section 1 Fatty acids

1.1 Classification of fatty acids

Numerical Symbol

Common Name

Comments

14:0

Myristic acid

Saturated

16:0

Palmitic acid

Saturated

18:0

Stearic acid

Saturated

16:1 9

Palmitoleic acid

Unsaturated

18:1 9

Oleic acid

Unsaturated

18:2 9,12

Linoleic acid

EFA

18:3 9,12,15

Linolenic acid

EFA

20:4 5,8,11,14

Arachidonic acid

EFA

Essential Fatty Acids (EFA)

Linoleic, linolenic and arachidonic
acids are called essential fatty acids,
because they cannot be synthesized
by the body and must be obtained
through diet.

1.2 Important Derivatives of

Arachidonic acids
Arachidonic acids (AA) in turn gives rise
to biologically important substances
known as the eicosanoids.
Prostaglandins (PGs)
Thromboxanes (TXs)
Leukotrienes (LTs)

Section 2
Metabolism of Triglycerides

Triglyceride (TG) or triacylglycerol

(TAG)

Glycerol

O
O

CH2 O C R1

R2 C O C H
3

CH2 O C R3

Overview of triglycerides metabolism

Triglycerides
(fats)
Lipolysis

Esterification
Diet

Fatty acids

Lipogenesis
Carbohydrate
Amino acids

Steroids

-Oxidation
Acetyl-CoA

TAC
2CO2

Cholesterologenesis

Steroidogenesis
Cholesterol

Ketone bodies

 2.1 Degradation of TG
2.1.1 Fat catabolism (lipolysis)
2.1.2 -Oxidation of Fatty acids
2.1.3 Other Oxidations of Fatty acids
2.1.4 Ketone Bodies Formation and
Utilization

 2.1.1 Fat catabolism (lipolysis)

Fat mobilization
The triacylglycerol stored in the
adipocytes are hydrolyzed by lipases,
to produce free fatty acids (FFA) and
glycerol, which are released to the
blood, this process is called fat
mobilization.

 The fatty acids thus released

diffusively from the adipocyte into the
blood, where they bind to the serum
albumin.

Hormone sensitive lipase (HSL)

TG lipase is the rate-limiting enzyme in
the TG degradation in adipose tissue. It
is also named HSL because it is
regulated by some hormones.

Effect of hormones on lipolysis

Lipolytic Hormones:
epinephrine
norepinephrine
adrenocorticotropic hormone (ACTH)
thyroid stimulating hormone (TSH)
Glucagon etc.
Antilipolytic Hormones: insulin

glycerol metabolism
Place: liver, kidney, intestine

Note
In muscle cells and adipocytes, the
activity of glycerol kinase is low, so
these tissues cannot use glycerol as
fuel.

 2.1.2 -Oxidation of Fatty

acids
Fatty acids are one of the main
energy materials of human and other
mammalian.
Fatty acid catabolism can be
subdivided into 3 stages.

Stage 1 Activation of FAs

Acyl-CoA Synthetase (Thiokinase), which
locates on the cytoplasm, catalyzes the
activation of long chain fatty acids.

O
R

+ HSCoA
O

Fatty acid

AMP + PPi
O
Mg2+
R C
acyl-CoA
S CoA
synthetase
acyl-CoA

ATP

Key points of FA activation

1. Irreversible
2. Consume 2 ~P
3. Site: cytosol

Stage 2
Transport of acyl CoA into the
mitochondria
( rate-limiting step)
Carrier: carnitine

Rate-limiting enzyme
carnitine acyltransferase
CH3

OH

+
H3C N CH2 CH CH2 COO
CH3

Carnitine

CH3
+
H3C N CH2
CH3

SCoA
carnitine
acyltransferase

R
C

CH CH2 COO

Fatty acyl carnitine

HSCoA

Stage 3: -oxidation of FAs

-oxidation means -C reaction.
Four steps in one round
step 1: Dehydrogenate
step 2: Hydration
step 3: Dehydrogenate
step 4: Thiolytic cleavage

Step 1. Dehydrogenate

H3C

H
FAD

(CH2)n

SCoA
Fatty acyl-CoA

acyl-CoA dehydrogenase

FADH2
H3C

(CH2)n

C
H

SCoA

trans-2-enoyl-CoA

Step 2. Hydration
H3C

(CH2)n

Trans-2-enoyl-CoA

H
H2O

H3C

(CH2)n

SCoA

enoyl-CoA Hydratase

OH H

3-L-Hydroxyacyl-CoA

SCoA

Step 3. Dehydrogenate

H3C

OH H

H
NAD+

3-L-Hydroxyacyl-CoA

(CH2)n

NADH + H+

hydroxyacyl-CoA
dehydrogenase

O
H3C

(CH2)n

SCoA

O
CH2

SCoA

-Ketoacyl-CoA

Step 4. Thiolytic cleavage

O
H3C

(CH2)n

O
CH2

SCoA

-Ketoacyl-CoA
HSCoA

-Ketothiolase

O
H3C

(CH2)n

O
SCoA + CH3

Fatty acyl-CoA
(2C shorter)

SCoA

Acetyl-CoA

- oxidation of fatty acids

The -oxidation pathway is cyclic

Summary
one cycle of the -oxidation:
fatty acyl-CoA + FAD + NAD+ + HS-CoA
fatty acyl-CoA (2 C less) + FADH2 +
NADH + H+ + acetyl-CoA

The product of the

-oxidation is in
the form of FADH2,
NADH, acetyl CoA,
only after Krebs
cycle and
oxidative
phosphorylation,
can ATP be
produced.

Energy yield from one molecule of palmitic acid

palmitic acid
-2 ~P activation

72
respiratory chain

8 acetyl CoA + 7 FADH2 + 7 NADH + 7 H+

palmitoyl-CoA
7 turns of
-oxidation
TAC
respiratory chain
812
73

The net ATP production: 131 2 = 129

 2.1.3 Other Oxidations of Fatty

acids
1. Oxidation of unsaturated fatty acids
2. Peroxisomal fatty acid oxidation
3. Oxidation of propionyl-CoA

1. Oxidation of unsaturated fatty acid

Mitochondria
Isomerase: cis trans
Epimerase: D (-) L (+)

2. Peroxisomal fatty acid oxidation

Very long chain fatty acids
FAD

Acyl-CoA oxidase

shorter chain fatty acids

-oxidation

3. Oxidation of propionyl-CoA
propionyl-CoA
Carboxylase (biotin)
Epimerase
Mutase (VB12)
succinyl-CoA

 2.1.4 Ketone Bodies

Formation and Utilization
Ketone bodies are water-soluble
fuels normally exported by the liver
but overproduced during fasting or
in untreated diabetes mellitus,
including acetoacetate, hydroxybutyrate, and acetone.

The formation of ketone bodies

(Ketogenesis)
Location: hepatic mitochondria
Material: acetyl CoA
Rate-limiting enzyme: HMG-CoA
synthase

O
CH3

C S CoA

HSCoA

CH3
2 Acetyl-CoA

C S CoA

thiolase

O
CH3

C CH2 C S CoA
Acetoacetyl-CoA

HMG-CoA
synthase
OH

OH
CH3

OOC CH2

CH CH2 COO

HSCoA
O

C CH2 C S CoA

CH3
-Hydroxy--methylglutaryl-CoA
HMG-CoA

-Hydroxy-butyrate
NAD+

-hydroxybutyrate
dehydrogenase
NADH+H+

HMG-CoA
lyase

Acetyl-CoA

CH3 C CH3
Acetone

Acetyl-CoA

CH3
CO2

C CH2 COO
Acetoacetate

Utilization of ketone bodies (ketolysis) at

extrahepatic tissues
Succinyl-CoA
transsulfurase

HSCoA
ATP

AMP
PPi

Acetoacetate
thiokinase

Lack of succinyl-CoA transsulfurase

and Acetoacetate thiokinase in the liver.

Biological Significance
Ketone bodies replace glucose as the
major source of energy for many
tissues especially the brain, heart and
muscles during times of prolonged
starvation.

Normal physiological responses to

carbohydrate shortages cause the
liver to increase the production of
ketone bodies from the acetyl-CoA
generated from fatty acid oxidation.

Plasma concentrations of metabolic

fuels (mmol/L) in the fed and starving
states

Ketosis consists of ketonemia, ketonuria

and smell of acetone in breath

Causes for ketosis

Severe diabetes mellitus
Starvation
Hyperemesis (vomiting) in early
pregnancy

 2.2 Lipogenesis

 2.2.1 Synthesis of fatty acid

O
C-S-CoA
H3C
palmitic acid (C16:0)

palmitoylCoA

O
C-S-CoA
H3C
stearic acid (C18:0)

stearoylCoA

O
C-S-CoA

9
oleic acid (C18:1 9)
18

H3 C

1
oleoylCoA

1. Palmitic Acid Synthesis

Location: cytosol of liver, adipose tissue,
kidney, brain and breast.
Precursor: acetyl CoA
Other materials: ATP, NADPH, CO2

Citrate-pyruvate cycle

The sources of NADPH are as follows:

Pentose phosphate pathway
Malic enzyme

Cytoplasmic isocitrate dehydrogenase

Process of synthesis:
(1) Carboxylation of Acetyl CoA
(2) Repetitive steps catalyzed by fatty
acid synthase

(1) Carboxylation of Acetyl CoA

O
CH3 C SCoA + HCO3
acetyl-CoA

ATP

ADP + Pi
biotin

acetyl-CoA
carboxylase

O
OOC CH2 C SCoA
malonyl-CoA

Malonyl-CoA serves as the donor of twocarbon unit.

Acetyl-CoA Carboxylase is the rate

limiting enzyme of the fatty acid
synthesis pathway.
The mammalian enzyme is regulated, by
phosphorylation
allosteric regulation by local
metabolites.

glucagon
ATP

insulin
ADP + Pi

acetyl-CoA + HCO3 + H+
malonyl-CoA
acetyl-CoA carboxylase
(biotin)
long chain acyl-CoA
citrate
isocitrate

(2) Repetitive steps catalyzed by

fatty acid synthase
Fatty acid synthesis from acetyl-CoA &
malonyl-CoA occurs by a series of
reactions that are:
in bacteria catalyzed by seven separate
enzymes.
in mammals catalyzed by individual
domains of a single large polypeptide.

Fatty acid synthase complex

(multifunctional enzyme)

Acyl carrier protein (ACP)

Acetyl-CoA-ACP transacetylase (AT)
-Ketoacyl-ACP synthase (KS)
Malonyl-CoA-ACP transferase (MT)
-Ketoacyl-ACP reductase (KR)
-Hydroacyl-ACP dehydratase (HD)
Enoyl-ACP reductase (ER)
Thioesterase (TE)

ACP contains 4-phosphopantotheine.

The overall reaction of synthesis:

acetyl-CoA + 7 malonyl-CoA + 14 NADPH + 14H+

palmitate + 7 CO2 + 14 NADP+ + 8 HSCoA + 6H2O

Routes of synthesis of other fatty acids

2. Elongation of palmitate
Elongation beyond the 16-C length of
the palmitate occurs in mitochondria
and endoplasmic reticulum (ER).

 Fatty acid elongation within

mitochondria uses the acetyl-CoA as
donor of 2-carbon units and NADPH
serves as electron donor for the final
reduction step.
Fatty acids esterified to coenzyme A
are substrates for the ER elongation
machinery, which uses malonyl-CoA as
donor of 2-carbon units.

3. The synthesis of unsaturated

fatty acid
Formation of a double bond in a fatty
acid involves several endoplasmic
reticulum membrane proteins in
mammalian cells

Desaturases introduce double bonds at

specific positions in a fatty acid chain.

 2.2.2
Synthesis of Triacylglycerol
Monoacylglycerol pathway (small
intestine)
Diacylglycerol pathway (liver, adipose
tissue)

1. Monoacylglycerol pathway
O

CH2

HSCoA
OH acyl CoA

R2 C O C H
CH2

OH

acyl CoA
transferase

O
O

CH2

R2 C O C H
CH2

acyl CoA
transferase

C R1

OH

1,2-diacylglycerol

2-monoacylglycerol
HSCoA
acyl CoA

CH2 O C R1

R2 C O C H

CH2 O C R3

triacylglycerol

2. Diacylglycerol pathway
glycolysis

Summary
Places:
tissue

small intestine, liver, adipose

Materials:
Endogenous: glucose amino acid
glycerol
Exogenous: free fatty acid and
monoacylglycerol

Adipose tissue generate fat mainly from

glucose
In adipose tissue, the acetyl CoA for the
synthesis of fatty acid is mainly from
glucose.
The lack of glycerol kinase make the only
source of glycerol 3-phosphate in
adipose tissue is glucose.

Obesity results from an imbalance between

energy input and output
Food
adipose
tissue

Work
or
Growth

fatty acids
& triacylglcerols
ADP
ATP

Heat
CO2 + H2O

Obesity

Section 3 Metabolism of
Phospholipids

 Phospholipid refers to phosphorouscontaining lipids.

Glycerophospholipids
Phospholipids
Sphingolipids

 3.1 Classification and Structure of

Glycerophospholipids

Glycerophospholipids are lipids with a

glycerol, fatty acids, a phosphate group
and a nitrogenous base.

glycerol

fatty acids
nitrogenous base

Phosphatidylcholine


glycerol

CH2 O

O
R2

fatty acyl group

C
CH2

R1

fatty
acyl group

O
O

O X Nitrogenous
base

OH

The basic structure of glycerophospholipid

In general, glycerophospholipids
contain a saturated fatty acid at C-1 and
an unsaturated fatty acid (usually
arachidonic acid) at C-2.

The major
function of
phospholipids
is to form
biomembrane.

 Hydrophobic tail = fatty acids

Polar head = nitrogenous base

Some common glycerophospholipid

Some common glycerophospholipid

(continue)

 3.2
Synthesis of Glycerophospholipid
Location:
All tissue of body, especially liver &
kidney
Endoplasmic reticulum
Pathways:
CDP-diacylglycerol pathway
Diacylglycerol pathway

The system of synthesis

a. FA
Glycerol

from carbohydrate

b. poly unsaturated fatty acid from plant oil

c. choline
ethanolamine
serine
inositol

from food or synthesis

in body

d. ATP, CTP
e. Enzymes and cofactors

Diacylglycerol pathway
CO2
HO CH2 CH COOH

HO CH2 CH2 NH2

3 SAM

HO CH2 CH2 N(CH3)3

Choline

Ethanolamine

NH2

Serine

ATP

ATP

ADP

ADP

P O CH2 CH2 N(CH3)3

P O CH2 CH2 NH2

Phosphocholine

Phosphoethanolamine
CTP

CTP

PPi

PPi

CDP O CH2 CH2 NH2

CDP O CH2 CH2 N(CH3)3

CDP-choline

CDP-ethanolamine
CO2

Phosphatidyl
serine

DG

DG

CMP

CMP

Phosphatidyl
ethanolamine

3 SAM

Phosphatidyl
choline

CDP-Diacylglycerol pathway
Dihydroxyacetone
phosphate

Glycerol 3-phosphate
Phosphotidate
CTP

PPi
Inositol
CMP

CDP-diacylglycerol
Serine

Phosphatidyl glycerol
CMP

CMP
Phosphatidyl inositol

Diphosphatidyl glycerol
(cardiolipin)
Phosphatidyl serine

Phosphatidylcholine (Lecithin)

Phosphatidylethanolamine (Cephalin)

CDP-diacylglycerol

Phosphatidylserine

Phosphatidylglycerol

Diphosphatidyl glycerol
(Cardiolipin)

Phosphatidylinositol

 3.3 Degradation of
glycerophospholipids by
phospholipase
A1
O
A2
O
R2

CH2
C
CH2

R1
D

O
O

P
OH
C

O
O

CH2
HO

C
CH2

R1
R2

B1 O
O

OH
Lysophospholipid-1

OH

CH2

O
O
B2

C
CH2

O
O

P
OH

Lysophospholipid-2

Actions of phospholipases on
lecithin
PLA1: fatty acid + lysolecithin
PLA2: fatty acid + acyl
glycerophosphoryl choline
PLC: 1,2 diacylglycerol + phosphoryl
choline
PLD: phosphatidic acid + choline

Lysophospholipids, the products of

Phospholipase A hydrolysis, are
powerful detergents.
O

O
O
R2

CH2
O

O C

CH2O

P
O

phospholipid

R1 H2O

R2

O
O

CH2

HO
O X

PLA2

O
H

CH2O

R1

O X

O
Lysophospholipid

Section 4 Metabolism of
Cholesterol

 4.1 Structure and function of

cholesterol
1. Function of cholesterol:
(1) It is a constituent of all cell
membranes.
(2) It is necessary for the synthesis of all
steroid hormones, bile salts and
vitamin D.

2. Structure of cholesterol
All steroids have cyclopentano penhydro
phenanthrene ring system.
H3C 21
18 CH3
19 CH3
2
3

HO

A
4

10
5

11

12

B 8
6

13
14

20

22

23

24

25

CH3

27 CH3

17

D 16
15

26

Cholesterol ester

O
R

 4.2 Synthesis of cholesterol

Location:
All tissue except brain and mature red
blood cells.
The major organ is liver (80%).
Enzymes locate in cytosol and
endoplasmic reticulum.
Materials:
Acetyl CoA, NADPH(H+), ATP

Acetyl-CoA is the direct and the only carbon

source.

Acetyl-CoA

HMG-CoA

Acetoacetyl-CoA

HMG CoA reductase is the rate-limiting enzyme

The total process of cholesterol de novo synthesis

Regulation of cholesterol synthesis

fasting

HMG CoA

Glucagon

HMG CoA reductase

after meal

insulin

MVA

thyroxine

cholesterol

bile acid

 4.3 Transformation and excretion

of cholesterol
Bile acids
Steroid
hormones

Vitamin D
Cholesterol

1. Conversion of Cholesterol into

bile acid
(1) Classification of bile acids
The primary bile acids are synthesized in
the liver from cholesterol. The 7hydroxylase is rate-limiting enzyme in
the pathway for synthesis of the bile
acids.

The secondary bile acids are products

that the primary bile acids in the
intestine are subjected to some further
changes by the activity of the intestinal
bacteria.

Classification of bile acids

Classification

Primary bile
acids

Secondary
bile acids

Free bile
acids

Conjugated bile acids

Cholic acid

Glycocholic
acid

Taurocholic acid

Chenodeoxycholic acid

Glycochenodeoxycholic
acid

Taurochenodeoxycholic acid

Deoxycholic
acid

Glycodeoxycholic acid

Taurodeoxycholic acid

Lithocholic
acid

Glycolithocholic acid

Taurolitho-cholic
acid

(2) Strcture of bile acids

OH

COOH

COOH

12

HO

H
cholic acid

OH

OH

HO

OH

glycocholic acid

HO

OH
H
chenodeoxycholic acid

CONHCH2COOH

HO

OH

CONHCH2CH2SO3H

OH

taurocholic acid

OH

HO

H
deoxycholic acid

COOH

COOH

HO

H
lithocholic acid

(3) Enterohepatic Cycle of bile

acids
Conversion to bile salts, that are
secreted into the intestine, is the only
mechanism by which cholesterol is
excreted.
Most bile acids are reabsorbed in the
ileum , returned to the liver by the portal
vein, and re-secreted into the intestine.
This is the enterohepatic cycle.

(4) Function of bile acids

Bile acids are amphipathic, with
detergent properties.
Emulsify fat and aid digestion of fats &
fat-soluble vitamins in the intestine.
Increase solubility of cholesterol in
bile.

2. Conversion of cholesterol into

steroid hormones
Tissues: adrenal cortex, gonads
Steroid hormones: cortisol (glucocorticoid), corticosterone and aldosterone
(mineralocorticoid), progesterone,
testosterone, and estradiol

Steroids derived from cholesterol

3. Conversion into 7-dehydrocholesterol

cholesterol
in skin
25-hydroxylase
(microsome
in the liver)

ultraviolet
light
7-dehydrocholecalciferol (VD3)
cholesterol

25-OH-D3

1-hydroxylase
(mitochondria
in the kidney)

1,25-(OH)2-D3
active Vit D3

 4.4 Esterification of cholesterol

in cells
SHCoA
acyl CoA
O

HO

cholesterol

acyl CoA
cholesterol R C O
acyl transferase
cholesteryl ester
(ACAT)

in plasma

Section 5
Plasma lipoprotein

 5.1 blood lipid

Concept: All the lipids contained in
plasma, including fat, phosphalipids,
cholesterol, cholesterol ester and fatty
acid.
Blood lipid exist and transport in the
form of lipoprotein.

TG
cholesterol

blood lipids

free
ester
lecithin
phospholipids sphingolipids
cephalin
FFA

 5.2 Classification of plasma

lipoproteins
1. electrophoresis method:
- Lipoprotein
pre -Lipoprotein
-Lipoprotein
CM (chylomicron)

fast

slow

2. Ultra centrifugation method

high density lipoprotein (HDL)
high
low density lipoprotein ( LDL)
very low density lipoprotein ( VLDL)
CM (chylomicron )
low

electron microscope

Separation of plasma lipoproteins by

electrophoresis on agarose gel

 5.3 Structure

 5.4 Composition of lipoprotein

CM

VLDL

LDL

HDL

<1.006

0.951.006

1.0061.063

1.0631.210

Protein

10

23

55

Phospholipids

18

20

24

Cholesterol

Cholesteryl esters

12

37

15

TG

85

50

10

Density(g/ml)

 5.5 Apolipoproteins

Functions of apolipoproteins
a . To combine and transport lipids.
b . To regulate lipoprotein metabolism.
apo A II activates hepatic lipase HL
apo A I activates LCAT
apo C II activates lipoprotein
lipase LPL
c. To recognize the lipoprotein receptors.

 5.6 Metabolism of plasma

lipoprotein

1. CM
Chylomicrons are formed in the
intestinal mucosal cells and secreted
into the lacteals of lymphatic system.

structure of CM

Cholesterol

Apolipoproteins

phospholipids
Triacylglycerols and
cholesteryl esters

Metabolic fate of CM

summary of CM
Site of formation: intestinal mucosal
cells
Function: transport exogenous TG
key E: LPL in blood
HL in liver
apoC is the activator of LPL
apo E and apo B-48 will be recognized
by the LRP receptor

2. VLDL
Very low density lipoproteins (VLDL)
are synthesized in the liver and
produce a turbidity in plasma.

Nascent
VLDL

Metabolic fate of VLDL and production of LDL

Summary of VLDL
Formation site: liver
Function: VLDL carries endogenous
triglycerides from liver to peripheral
tissues for energy needs.
key E: LPL in blood
HL in liver

3. LDL
Most of the LDL particles are derived
from VLDL, but a small part is directly
released from liver. They are
cholesterol rich lipoprotein molecules
containing only apo B-100.

LDL
receptors
Cholesterol
ester
protein

Cholesterol

LDL

Cholesteryl
oleate

Amino acids
LDL binding

Internalization

Lysosomal hydrolysis

Michael Brown and

Joseph Goldstein
were awarded Nobel
prize in 1985 for their
work on LDL
receptors.

Summary of LDL
Formation site: from VLDL in blood
Function: transport cholesterol from
liver to the peripheral tissues. LDL
concentration in blood has positive
correlation with incidence of
cardiovascular diseases.

Fates of cholesterol in the cells

1. Incorporated into cell membranes.
2. Metabolized to steroid hormones.
3. Re-esterified and stored. The reesterification is catalyzed by ACAT.
4. Expulsion of cholesterol from the cell,
esterified by LCAT and transported by
HDL and finally excreted through liver.

4. HDL
LDL variety is called bad cholesterol
whereas HDL is known as good
cholesterol .

Liver

Heart
VLDL

Good
Excretion

BAD
LDL
Cholesterol
Deposit

HDL

Forward and reverse cholesterol

transport

Reverse cholesterol transport

Cholesterol from tissues reach liver,
and is later excreted. This is called
reverse cholesterol transport by HDL.

Metabolism of HDL in reverse cholesterol transport

CETP
Cholesterol ester transfer protein
(CETP) transfer cholesterol ester in
HDL to VLDL and LDL.

Summary of HDL
Formation site: liver and intestine
Function: transport cholesterol from
peripheral tissues to liver

summary of lipoprotein metabolism

 5.7 Hyperlipidemias
classification

Lipoprotein

Blood lipids

CM

TAG CH

LDL

CH

LDL, VLDL

CH TAG

IDL

CH TAG

VLDL

VLDL, CM

TAG
TAG CH