( Komponen Lipid, Katabolisme Asam Lemak,

Biosintesis Asam Lemak)

COURSE CONTRACT
 COURSE TOPICS
Introduction of Lipids
Biosynthesis of Fatty Acids and Lipids
Catabolism of Fatty Acids (Beta Oxidation)
Catabolism of Lipids and Metabolism of ketone body
MIDTERM TEST (UTS)
Introduction of Vitamin and Mineral
Soluble Water Vitamin
Soluble Lipids Vitamin
Mineral
Introduction of Nucleic Acids (DNA & RNA)
DNA Duplication / Replication
Transkription & RNA Processing
Translation
 ASSIGNMENTS
• Groups divided into 12 groups.
• Each groups present in themes:
a. Biosynthesis of Fatty Acids and Lipids (weeks 7)
b. Catabolism of Fatty Acids and Lipids (weeks 7)
c. Vitamin and Mineral (weeks 2 after midterm test)
d. Nucleic Acids & DNA Replication (weeks 3 after
midterm test)
e. Transcription & RNA Processing (weeks 4 after
midterm test)
f. Translation (weeks 4 after midterm test)
• Each themes consist of 2 groups
 METABOLISME LEMAK
PENDAHULUAN :
LEMAK adalah SENYAWA ORGANIK YANG
TIDAK LARUT DALAM AIR, TETAPI LARUT
DALAM PELARUT NON POLAR ( ETER, ALKO-
HOL, BENZEN ); BERUPA ESTER DENGAN
ASAM LEMAK.
KEPENTINGAN :
1. Unsur penting dalam makanan
2. Sumber energi tubuh
3. Sebagai isolator ( organ, listrik, saraf )
4. Membran sel
5
5. Sebagai lipoprotein.
KLASIFIKAS
I : 1. LEMAK SEDERHANA : ( SIMPLE LIPID )
-. TRI ASIL GLISERIDA
-. MALAM

2. LEMAK CAMPURAN ( COMPOUND LIPID ) :

-. FOSFOLIPID -. SULFATIDA
-. GLIKOLIPID -. AMINO LIPID

3. LEMAK TURUNAN ( DERIVED LIPID ) :

. ASAM LEMAK . GLISEROL
. KOLESTEROL . BENDA KETON
TRIGLISERIDA O ASAM LEMAK O
O CH2-O-C-R1 H3C-CH2-CH2-CH2- ......-CH-C OH
R2-C-O-CH O O
6
 PHYSIOLOGICAL ROLE OF LIPIDS

 Energetic role (fuel

molecules)
 Components of membranes
(structural role)
 Precursors for many
hormones (steroids)
 Signal molecules
(prostaglandins)
 Protective role (lipids
surround important organs)
 Enzyme cofactors (vitamin K)
 Electron carriers (ubiquinone)
 Insulation against
temperature extremes
TRIACYLGLYCEROLS ARE HIGHLY
CONCENTRATED ENERGY STORES
•Triacylglycerols (TGs) and glycogen -
two major forms of stored energy
TGs which are more efficient energy
stores because:
(1) They are stored in an anhydrous form
(2) Their fatty acids are more reduced
than monosaccharides.
• 1 g of triacylglycerols stores more than six times
as much energy as a 1 g of glycogen
• Glycogen reserves are depleted in 12 to 24 hours
after eating, triacylglycerols within several
weeks.

•Fat breakdown
about 50 % of energy in liver, kidney and
skeletal muscles up to 95 % of energy cardiac
muscle
•Fats are the major source of energy for:
fasting animal organism in diabetes
• Fatty acids and glycerol -
substances that are directly used
as a fuel by mammalian organisms.
• Fatty acids (FA) and glycerol for
metabolic fuels are obtained
from triacylglycerols:
(1) In the diet
(2) Stored in adipocytes (fat
storage cells)
• Free fatty acids occur only in
trace amounts in cells

•For supplying of fatty acids as a fuel for organism, the

triacylglycerols have to be digested
 DIGESTION OF DIETARY LIPIDS
Lipids in diet:

•
triacylglycerols
• phospholipids
Digestion – in small intestine.
• cholesterol
Enzyme – pancreatic lipase.
Lipase catalyzes hydrolysis at the C1 and C3 positions of
TGs producing free fatty acids and 2-monoacylglycerol.
Colipase – protein which is present in the intestine and helps
bind the water-soluble lipase to the lipid substrates.
Colipase also activates lipase.
Bile salts (salts of bile acids) are required for lipids digestion.
Bile salts are synthesized in the
liver from cholesterol.
Taurocholate and glycocholate - the most abundant bile salts.
Amphipathic: hydrophilic (blue) and hydrophobic (black)
TGs are water insoluble and lipase is water soluble.
Digestion of TGs takes place at lipid-water interfaces.
Rate of digestion depends on the surface area of the
interface.
Bile salts are amphipathic, they act as detergent
emulsifying the lipid drops and increasing the surface area
of the interface.
Bile salts also activates the lipase.
Inadequate production of bile salts results in
steatorrhea.
 Dietary phospholipids are degraded by
phospholipases
Phospholipases are synthesized in the pancreas.
Major phospholipase is phospholipase A2 (catalyses the
hydrolysis of ester bond at C2 of glycerophospholipids
and lysophosphoglycerides are formed).

Lysophospho-
glycerides are
absorbed and in
the intestinal
cells are
reesterified
back to glycero-
phospholipids.
Lysophosphoglycerides can act as detergent
and therefore in high concentration can
disrupt cellular membranes.

Lysophosphoglyceride is normally present in

cells in low concentration.

Snake venom contain

phospholipase A2 and
causes the lysis of
erythrocytes
membranes.
 Dietary cholesterol
• Most dietary cholesterol is unesterified
• Cholesteryl esters are hydrolyzed in the intestine by
an intestinal esterase
• Free cholesterol is solublized by bile-salt micelles for
absorption
• After absorption in the intestinal cells cholesterol
react with acyl-CoA to form cholesteryl ester.
 LIPOPROTEIN PLASMA

. LEMAK TIDAK LARUT DALAM AIR

. MEDIA PELARUT DALAM TUBUH : AIR

TRANSPORTASI LEMAK HARUS DALAM BENTUK

EMULSI. UNTUK MEMBUAT EMULSI DIPERLUKAN
EMULGATOR  SENYAWA BIPOLAR : FOSFOLI –
PID ; KOLESTEROL ; PROTEIN.
== LIPOPROTEIN .
18
STRUKTUR LIPOPROTEIN :
. INTI  HIDROFOBIK : TG & KOLESTEROL ESTER
. LAPISAN KULIT  AMPIFATIK : APOPROTEIN ;
FOSFO– LIPID ( FOSFATIDIL KOLIN / SPINGOMIELIN ) ;
KOLESTE- ROL BEBAS.

MACAM LIPOPROTEIN :
1. KILOMIKRON
2. VLDL = VERY LOW DENSITY LIPOPROTEIN
3. LDL = LOW DENSITY LIPOPROTEIN
4. HDL = HIGH DENSITY LIPOPROTEIN

19
KOMPOSISI LIPOPROTEIN :

. MENGANDUNG PROTEIN, TG , FOSFOLIPID, KOLES –

TEROL dan KOLESTEROL ESTER DALAM JUMLAH
YANG BERBEDA.

. KANDUNGAN PROTEIN TERBANYAK  HDL

KANDUNGAN TG TERBANYAK  KILOMIKRON
dan VLDL
KANDUNGAN KOLESTEROL TERBANYAK  LDL

20
 TRANSPORT FORMS OF LIPIDS
• TGs, cholesterol and cholesterol esters are insoluble in water
and cannot be transported in blood or lymph as free molecules
• These lipids assemble
with phospholipids and
apoproteins
(apolipoproteins) to
form spherical
particles called
lipoprotein
Structure:
Hydrophobic core:
-TGs,
-cholesteryl esters
Hydrophilic surfaces:
-cholesterol,
-phospholipids,
-apolipoproteins
 The main classes of lipoproteins
1.Chylomicrons.
2.Very low density lipoproteins (VLDL).
3.Intermediate density lipoproteins (IDL).
4.Low density lipoproteins (LDL).
5.High density lipoproteins (HDL).
 Chylomicrons
• are the largest lipoproteins (180 to 500 nm in diameter)
• are synthesized in the ER of intestinal cells
• contain 85 % of TGs (it is the main transport form of dietary TGs).
• apoprotein B-48 (apo B-48) is the main protein component
• deliver TGs from the intestine (via lymph and blood) to tissues (muscle
for energy, adipose for storage).
• bind to membrane-bound lipoprotein lipase (at adipose tissue and
muscle), where the triacylglycerols are again degraded into free fatty
acids and monoacylglycerol for transport into the tissue
• are present in blood only after feeding

Lymphatic
exocytosis vessel
 VLDL
• are formed in the liver
• contain 50 % of TGs and 22 % of cholesterol
• two lipoproteins — apo B-100 and apo E
• the main transport form of TGs synthesized in the organism (liver)
• deliver the TGs from liver to peripheral tissue (muscle for energy,
adipose for storage)
• bind to membrane-bound lipoprotein lipases (triacylglycerols are again
degraded into free fatty acids and monoacylglycerol)

triacylglycerol

cholesteryl esters
Apo B
Apo E

phospholipids
cholesterol
Lipoproteinlipase – enzyme which is located within
capillaries of muscles and adipose tissue
Function: hydrolyses of TGs of chylomicrons and VLDL.
Formed free fatty acids and glycerol pass into the cells
Chylomicrons and VLDL which gave up TGs are called remnants
of chylomicrons and remnants of VLDL
Remnants are rich in cholesterol esters
Remnants of chylomicrons are captured by liver
Remnants of VLDL are also called intermediate density
lipoproteins (IDL)
Fate of the IDL:
- some are taken by the liver
- others are degraded to the
low density lipoproteins (LDL) (by the removal of more
triacylglycerol)
 LDL
LDL are formed in the blood from IDL and in liver from IDL
(enzyme – liver lipase)

LDL are enriched in

cholesterol and
cholesteryl esters
(contain about 50 % of
cholesterol)
Protein component - apo
B-100
LDL is the major
carrier of cholesterol
(transport cholesterol
to peripheral tissue)
Cells of all organs have LDL receptors
Receptors for LDL are localized in specialized regions called
coated pits, which contain a specialized protein called clathrin
Apo B-100 on the surface of an LDL binds to the receptor
Receptor-LDL complex enters the cell by endocytosis.
Endocytic vesicle is formed
LDL uptake by receptor-mediated endocytosis
 Familial hypercholesterolemia
 congenital disease when LDL receptor are not synthesized (mutation at a
single autosomal locus)
 the concentration of cholesterol in blood markedly increases
 severe atherosclerosis is developed (deposition of cholesterol in arteries)
 nodules of cholesterol called xanthomas are prominent in skin and tendons
 most homozygotes die of coronary artery disease in childhood
 the disease in heterozygotes (1 in 500 people) has a milder and more
variable clinical course

atherosclerosis

xanthomas
 HDL
 are formed in the liver and partially in small intestine
 contain the great amount of proteins (about 40 %)

 pick up the
cholesterol from
peripheral tissue,
chylomicrons and
VLDL
 enzyme
acyltransferase in
HDL esterifies
cholesterols,
convert it to
cholesterol esters
and transport to
the liver
 High serum levels of cholesterol
cause disease and death by
contributing to development of
atherosclerosis

Cholesterol which is present in the

form of the LDL is so-called "bad
cholesterol."

Cholesterol in the
form of HDL is
referred to as "good
cholesterol”

HDL functions as a
shuttle that moves
cholesterol
throughout the body
 LDL/HDL Ratio

The ratio of cholesterol in the form of LDL to that in the

form of HDL can be used to evaluate susceptibility to
the development of atherosclerosis

For a
healthy
person,
the
LDL/HDL
ratio is
3.5
Transport Forms of Lipids
LIPID METABOLISM:

MOBILIZATION OF
TRIACYLGLYCEROLS;
OXIDATION OF
GLYCEROL
 Storage and Mobilization of
Fatty Acids (FA)
• TGs are delivered to adipose
tissue in the form of
chylomicrones and VLDL,
hydrolyzed by lipoprotein
lipase into fatty acids and
glycerol, which are taken up
by adipocytes.
• Then fatty acids are
reesterified to TGs.
• TGs are stored in adipocytes.
• To supply energy demands
fatty acids and glycerol are
released – mobilisation of adipocyte
TGs.
At low carbohydrate and insulin concentrations (during
fasting), TG hydrolysis is stimulated by epinephrine,
norepinephrine, glucagon, and adrenocorticotropic
hormone.

TG
hydro-
lysis is
inhibited
by insulin
in fed
state
•Lipolysis - hydrolysis of
triacylglycerols by lipases.
•A hormone-sensitive lipase
converts TGs to free fatty
acids and monoacylglycerol
•Monoacylglycerol is
hydrolyzed to fatty acid
and glycerol or by a
hormone-sensitive lipase or
by more specific and more
active monoacylglycerol
lipase
Transport of Fatty Acids and Glycerol
• Fatty acids and glycerol diffuse
through the adipocyte membrane and
enter bloodstream.
• Glycerol is transported via the blood
in free state and oxidized or converted
to glucose in liver.
• Fatty acids are traveled bound to
albumin.
• In heart, skeletal muscles and liver
they are oxidized with energy release.
 Oxidation of Glycerol
Glycerol is absorbed by the liver.
Steps: phosphorylation, oxidation and isomerisation.
Glyceraldehyde 3-phosphate is an intermediate in:
 glycolytic pathway
 gluconeogenic pathways
Isomerase
 LIPID
METABOLISM:

FATTY
ACID
OXIDATION
 Stages of fatty acid oxidation
(1) Activation of fatty acids takes place
on the outer mitochondrial membrane

(2) Transport into the mitochondria

(3) Degradation to two-carbon

fragments (as acetyl CoA) in the
mitochondrial matrix (β-oxidation
pathway)
 (1) Activation of Fatty Acids
• Fatty acids are converted to CoA thioesters by
acyl-CoA synthetase (ATP dependent)
• The PPi released is hydrolyzed by a
pyrophosphatase to 2 Pi
• Two phosphoanhydride bonds (two ATP equivalents)
are consumed to activate one fatty acid to a
thioester
(2) Transport of Fatty Acyl CoA into Mitochondria
• The carnitine shuttle
system.
• Fatty acyl CoA is first
converted to acylcarnitine
(enzyme carnitine
acyltransferase I (bound to
the outer mitochondrial
membrane).
• Acylcarnitine enters the
mitochondria by a
translocase.
• The acyl group is transferred
back to CoA (enzyme -
carnitine acyltransferase II).
(3) The Reactions of β oxidation
• The β-oxidation pathway (β-carbon atom
(C3) is oxidized) degrades fatty acids two
carbons at a time

α
β
1. Oxidation of acyl
CoA by an acyl CoA
dehydrogenase to
give an enoyl CoA

Coenzyme - FAD
2. Hydration of the
double bond between
C-2 and C-3 by enoyl
CoA hydratase with
the 3-hydroxyacyl
CoA (β-hydroxyacyl
CoA) formation
3. Oxidation of
3-hydroxyacyl CoA to
3-ketoacyl CoA by
3-hydroxyacyl CoA
dehydrogenase

Coenzyme – NAD+
4. Cleavage of
3-ketoacyl CoA by
the thiol group of
a second molecule
of CoA with the
formation of
acetyl CoA and an
acyl CoA
shortened by two
carbon atoms.

Enzyme -
β -ketothiolase.
The shortened acyl
CoA then
undergoes another
cycle of oxidation

The number of
cycles: n/2-1,
where n – the
number of carbon
atoms
 Fatty acyl CoAof
β-Oxidation
saturated fatty
acids
• One round of β oxidation: 4 enzyme steps
produce acetyl CoA from fatty acyl CoA
• Each round generates one molecule each of:
FADH2
NADH
Acetyl CoA
Fatty acyl CoA (2 carbons shorter each round)

Fates of the products of β-oxidation:

- NADH and FADH2 - are
used in ETC - acetyl CoA - enters the
citric acid cycle - acyl CoA –
undergoes the next cycle of oxidation
 ENERGI β-OKSIDASI :
ENERGI YANG DIHASILKAN dari β-OKSIDASI BILA DIKAIT-
KAN dengan OKSIDASI BIOLOGI dan S.A.S adalah :
- TAHAP OKSIDASI I ( FAD ) = 2 ATP
- TAHAP OKSIDASI II ( NAD ) = 3 ATP +
SETIAP SIKLUS β-OKSIDASI = 5 ATP
- DARI S.A.S. PER MOL. ASETIL-KoA = 12 ATP
- PADA TAHAP AKTIVASI, HUTANG = 2 ATP
KALAU JUMLAH ATOM C dari ASAM LEMAK =N  MAKA TERDAPAT ½
N MOL. ASETIL-KoA dan ( N/2 – 1 ) SIKLUS OKSIDASI

ENERGI : ½ N X 12 + (½ N – 1 ) X 5 - 2 MOL.ATP
MISAL : ASAM PALMITAT ( 16 ATOM C )
16/2 x 12 + ( 16/2 -1 ) X 5 - 2 = 129 MOL. ATP
53
LIPID METABOLISM:
FATTY ACID
OXIDATION
β-OXIDATION OF ODD-CHAIN FATTY ACIDS

• Odd-chain fatty acids

occur in bacteria and
microorganisms
• Final cleavage product is
propionyl CoA rather
than acetyl CoA
• Three enzymes convert
propionyl CoA to succinyl
CoA (citric acid cycle
intermediate)
Propionyl CoA Is Converted into Succinyl CoA

1. Propionyl CoA is carboxylated to yield the D

isomer of methylmalonyl CoA.
The hydrolysis of an ATP is required.
Enzyme: propionyl CoA carboxylase
Coenzyme: biotin
2. The D isomer of methylmalonyl CoA is
racemized to the L isomer
Enzyme: methylmalonyl-CoA racemase
3. L isomer of methylmalonyl CoA is converted
into succinyl CoA by an intramolecular
rearrangement
Enzyme: methylmalonyl CoA mutase
Coenzyme: vitamin B12 (cobalamin)

Ke siklus Asam sitrat

 OXIDATION OF FATTY ACIDS IN
PEROXISOMES
Peroxisomes - organelles containing
enzyme catalase, which catalyzes
the dismutation of hydrogen
peroxide into water and molecular
oxygen Acyl CoA
dehydrogenase
transfers electrons
to O2 to yield H2O2
instead of capturing
the high-energy
electrons by ETC,
as occurs in
mitochondrial β-
oxidation.
 KETOGENESIS & KETOLISIS

PADA KEADAAN TERTENTU ( KELAPARAN; DIABETES M.)

MOBILISASI AS. LEMAK ↑ OKSIDASI-β ↑ ENERGI
KETOGENESIS

KETOGENESIS = SINTESIS BENDA KETON

KETOLISIS = KATABOLISME BENDA KETON

KETOGENESIS terjadi di HEPAR, dengan TUJUAN UNTUK

PENGHEMATAN ENERGI ( TIDAK SEMUA AS.LEMAK DI OK-
SIDASI + SAS, TAPI DIBENTUK MENJADI BENDA KETON )

BENDA KETON : β-HIDROKSI BUTIRAT, ASETOASETAT dan

ASETON.
60
 HEPAR DARAH
(BENDA KETON)
OTOT SKELET
ENERGI

OTAK
ENERGI ( sebagai peng-
ganti glukosa,
melalui : glucose-fatty
acids-keton bodies
BENDA KETON bersifat ASAM cycle )
GANGGUAN ASAM BASA DARAH ( KETOASIDOSIS )
terutama pada - DIABETES MELLITUS
- KELAPARAN  masih dapat diatasi
oleh tubuh dengan SISTEM BUFFER
61
 FFA
KETOGENESIS ( MOBILISASI dari ADIPOSA )

GLISEROL-P TG
ASIL-KoA FOSFOLIPID
Membran Mitokondria

ASIL-KoA
( ASETIL-KoA )n OKSIDASI - β KOLESTEROL

H3C-CO-CH2-CO~SKoA
ASETOASETIL-KoA CH2-COO-

KoA-SH H3C-COH-CH2-CO-SKoA
HMG-KoA
H2O
HMG-KoA
CH3-CO-SKoA Liase
ASETIL-KoA
CH3-CO-SKoA ASETOASETAT
NADH + H+
NAD+
ASIL-KoA 3β-HIDROKSI BUTIRAT
SAS 62
( paling dominan )
KETOGENESIS HANYA TERJADI DI HEPAR, KATABOLISME NYA
TERJADI DI LUAR HEPAR SEBAGIAN BESAR DI OTOT SKELET

3-HIDROKSI BUTIRAT
NAD
NADH + H+

ASETO ASETAT
SUKSINIL-KoA SITRAT
KoA-Transferase SIKLUS ASAM SITRAT

SUKSINAT OKSALO ASETAT

ASETO ASETIL-KoA

Tiolase

ASETIL-KoA

63
BAHAN BAKU : ASETIL-KoA

PRINSIPNYA : PENGGANDENGAN ASETIL-KoA

ASETIL-KoA BERASAL DARI - KH  glikolisis

- PROTEIN / AS.AMINO

CARA SINTESIS :1. SISTEM MITOKONDRIA

2. SISTEM EKSTRA MITOKONDRIA

64
SINTESIS ASAM LEMAK SISTEM MITOKONDRIA :

►MERUPAKAN SISTEM UNTUK MEMPERPANJANG ASAM

LEMAK YANG SUDAH ADA atau UNTUK KONVERSI SATU
ASAM LEMAK KE JENIS ASAM LEMAK YANG LAIN
► LEBIH SERING DIPAKAI UNTUK SINTESIS ASAM LEMAK
TIDAK JENUH = UNSATURATED FATTY ACIDS = UFA

► BAHAN BAKU : ASAM PALMITAT ( 16 C )

atau ASAM LEMAK TIDAK JENUH YANG
ADA DALAM TUBUH.
► PRINSIP REAKSINYA merupakan KEBALIKAN DARI
OKSIDA-SI β ( ENZIMNYA SAMA, KECUALI ENZ. TIOLASE
DIGANTI DENGAN ENZ. ENOIL-KoA REDUKTASE.

►BERLANGSUNG DALAM SUASANA ANAEROB

65
 SINTESIS ASAM LEMAK SISTEM MITOKONDRIA

CH3-(CH2)n-CH2-CO-S-KoA
FAD+

FADH + H+
CH3-(CH2)n-1-CH=CH-CO-S-KoA
H2O
OH
CH3-(CH2)n-1-CH-CH2-CO-S-KoA
NAD+
NADH + H+
O
CH3-(CH2)n-1-C-CH2-CO-S-KoA
KoA-SH

O
CH3-(CH2)n-1- C-S-KoA + CH2-CO-S-KoA

ASETIL-KoA 66
SINTESIS ASAM LEMAK SISTEM EKSTRA MITOKONDRIA :
67
★ SINTESIS ASAM LEMAK “DE NOVO”
DENGAN BAHAN DASARNYA :
ASETIL-KoA + CO2
★ SISTEM INI SERING DIGUNAKAN dan AKTIF DI
JARINGAN- JARINGAN HEPAR, ADIPOSA dan
KELENJAR MAMMAE YANG SEDANG LAKTASI

★ DIKATALISA OLEH KOMPLEKS ENZIM : “ FATTY ACID

SINTHASE COMPLEX “  YANG MENGANDUNG GUGUS
PROTEIN PENGEMBAN ASIL ( ACYL CARRIER PROTEIN
= ACP )
 CO2 SINTESA
CH3-CO-SKoA OOC-CH2-CO-SKoA
-

ASETIL-KoA BIOTIN MALONIL-KoA ASAM

LEMAK
HS-PAN- -Cys-HS SISTEM
KoA KoA EXTRA
HS-Cys- -PAN-HS
O
MITOKON

=
ENZIM -- -Cys-S-C-CH3
O
-- -PAN-S-C-CH2-COO DRIA
-ENZ-ASIL ( ASETIL MALONIL )
3-KETOASIL SINTASE CO2
- -CyS-SH
O O
- -PAN-S-C-CH2-C-CH3 ENZ-3-KETOASIL ( ENZ ASETOASETIL )
NADPH + H+
NADP+ 3-KETO ASIL REDUKTASE
- -CyS-SH
PENGHASIL NADPH : O O
- -PAN-S-C-CH2-CH-CH3 ENZ.-3-HIDROKSI ASIL
- JALUR HMP HIDRATASE
- ISOSITRAT DEHIDRO H2O
GENASE - - -Cys-SH
ENZIM MALAT - -PAN-S-C-CH=CH-CH3 ENZ.-2,3-ASIL TAK JENUH
NADPH + H+
NADP+
- -Cys-SH
7X
- -PAN-S-C-CH2-CH2-CH3
( Cn )
PALMITAT ENZIM-ASIL 68
SINTESIS ASAM LEMAK SISTEM MIKROSOM
☺ JARANG DILAKUKAN
☺ FUNGSI : SEPERTI SISTEM MITOKONDRIA :
 MEMPERPANJANG RANTAI AS. LEMAK
☺ REAKSINYA MIRIP DENGAN SISTEM EKSTRA MITOKON

DRIA, YAITU MEMERLUKAN ADANYA MALONIL-KoA

69