LIPIDS

• Lipids are heterogenous groups of compounds soluble in

organic solvents such as benzene, alchol, ether and chloroform
e.t.c
• Contain non-polar( C-H) bonds and gives mainly fatty acids
and complex Alcohols on Hydrolysis
• Lipids also contain polar groups such as phosphoryl, amino,
sulfryl or Hydroxyl group and presence of both polar and non-
polar groups make lipids to have affinity for both water and
organic solvents
 FUNCTIONS OF LIPIDS
• Source of energy
• Thermal insulator

• Structural components of cell membrane

• Precursors for prostaglandin and steroid hormones

• Dissolve fat soluble vitamins

CLASSIFICATIONS OF LIPIDS

Simple lipids: Esters of fatty acids with different alcohols

 fats and Oils: These are esters of fatty acids with glycerol

 waxes: Esters of fatty acids with high molecular weight monohydric alcohols


Complex lipids: Esters of fatty acids and alcohols together with some other head groups

 phospholipids, glycolipids

 Amino lipids, lipoproteins

 sulpholipids


Derived lipids: Hydrolytic products of simple and complex lipids

Fatty acids, cholesterol etc

 TRIGLYCERIDES
• Triglycerides are a storage form of fatty acids
in mammals.
 Triglycerides from animals tend to have a higher proportion of
saturated fatty acids.

• Most are solids at room temperature and are called fats.

Examples include: butter, lard and bacon grease

 Triglycerides from plants tend to have a higher proportion of

unsaturated fatty acids.

• Most are liquids at room temperature and are called oils.

Examples include: corn oil, canola oil, peanut oil and olive oil.
6
• Triglycerides as primarily used as a form of stored energy.
• This is why when you eat more than you need to meet
your energy requirements, the excess energy is stored in
the form of fat.
• Fat can store almost twice as much energy per gram as
carbohydrates and proteins
• In mammals the fats are stored in the adipose tissue.

• Adipose tissue also functions to protect organs from shock

7
 Triglycerides…..
• Triglycerides are a combination of three 3 fatty
acid molecules with a glycerol molecule.

8
• Glycerol, which is also called glycerin,
is an alcohol with three hydroxyl groups.

– As with the waxes, the fatty acids can HO CH2

react with the hydroxyl groups to

form esters. HO CH

– Since there are three hydroxyl groups,

HO CH2
three fatty acids can react to form glycerol

three esters.
9
• For triglycerides, all three hydroxyls of the glycerol

have a fatty acid residue attached to it. O

CH3CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2C O CH2

O
CH3CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2C O CH

O
CH3CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2C O CH2
fatty acid glycerol
residues residue

10
 Lipoproteins
• Lipoproteins are used to
transport the water insoluble
lipids such as triglycerides,
phospholipids and cholesterol, in

the blood.

11
 – Lipoproteins contain lipids and proteins.
– They include:
• Chylomicrons transport primarily triglycerides from
the digestive track.
• LDLs (low density lipoproteins) transport cholesterol,
triglycerides and phospholipids from the liver to other
tissues.
• HDLs (high density lipoproteins) transport cholesterol
and phospholipids back to the liver.
 Lipoproteins…..
• The HDL and LDL levels in the blood can be used to assess
ones risk for atherosclerosis.
– High levels of HDL is considered good
• This is why HDL is sometimes referred to as “good
cholesterol”
• > 40 mg/dL is good.
– High levels of LDL is considered bad
• This is why LDL is sometimes referred to as “bad
cholesterol”
• > 100 mg/dL is bad. 13
 Fatty Acids
• Fatty acids contain a carboxylic acid group

– This should make them quite polar

• However, they also contain a long

hydrocarbon tail Which overall, makes them
nonpolar.
nonpolar polar

14
 PROPERTIES OF FATTY ACIDS
• Fatty acids are amphipathic, because of the Hydrophobic tail
and Hydrophilic (–COOH) head

• The longer the hydrocarbon chain the higher the melting point
of the fatty acid

• The greater the number of double bonds in the fatty acid the
lower the melting point of the fatty acid

• Unsaturated fatty acids have substantially lower melting points

than saturated fatty acids
• Based on the bonds that exist within the hydrocarbon chains,
fatty acids can be saturated or unsaturated.
• Saturated fatty acid is a long-chain carboxylic acid
containing only C-C single bonds.
• Unsaturated fatty acid is a long-chain carboxylic acid
containing one or more C-C double bonds
• Unsaturated fatty acids occur mostly in cis form e.g oleic
acid rather than trans form e.g elaidic acid
 Fatty Acids…..
• Some fatty acids contain double bonds

• saturated

• monounsaturated

• polyunsaturated

• polyunsaturated
17
Linolenic acid is one of the omega-3 fatty acids. 18
 ESSENTIAL AND NON-ESSENTIAL
FATTY ACIDS
• Essential fatty acids are the ones that cannot be
synthesized in the body and thus are obtained
from the diet e.g. ω-3 and ω-6 fatty acids.
• Non-essential fatty acids can be synthesized in
the human system and therefore do not come
only from diet
• Fatty acids can be represented by the general formula R-
COOH, where R is an alkyl chain.
• The fatty acid chain lengths varies and are commonly
classified as short chain (2-4 carbon atoms), medium chain
(6-10 carbon atoms) or long chain (12-26 carbon atoms).
• Those of importance in human nutrition and metabolism
are the long chain class that contains an even number of
carbon atoms.
 FATTY ACID NOMENCLATURE
 Δ-Numbering system: starting from the carboxyl terminal
end
• fatty acids are abbreviated according to the number of
carbon atoms, number of double bonds and position(s) of
double bond
 ω-Numbering system: starting from terminal methyl end.
• In addition the carbon atoms may be labeled with Greek
symbols, with α being adjacent to the carboxyl group and ω
being farthest away.
• Carbon atoms 2 and 3 are often referred to as α and β,
respectively. The methyl carbon atom at the distal end of the
chain is called the ω-carbon atom
 Geneva or Systematic classification: based on the parent
name of hydrocarbon
• For example, linoleic acid would be written as
C18:2⁹ ² which contains 18 carbon atoms and two
double bonds between carbons 9 and 10 and carbons
12 and 13.
• Using the η or ω system, linoleic acid would be
abbreviated as C18:2n-6 where the first carbon
forming the unsaturated pair is written````~~
 DIGESTION, ABSORPTION
AND TRANSPORT OF DIETARY
LIPIDS
 DIGESTION AND ABSORPTION
• Digestion is the process of break down of food substances
in intestinal tract to simple products the body can use

• Absorption is the process of transportation food products

or nutrients into circulatory system and then to the cell

• Utilization involves metabolic reactions in the cell to

utilize nutrients absorbed to produce materials needed for
our existence
 DIGESTION AND ABSORPTION…

• Digestion of food includes processes such as

mechanical process of chewing of food and
chemical reactions such as hydrolysis or
splitting of food with water and facilitation of
digestion process by enzymes
 DIGESTION
• Digestion of lipid starts from mouth by the
enzyme lingual lipase then continue in the
stomach by gastric lipase. How ever due to
low solublity of lipids there is low digestion of
lipids in the mouth and stomach.
 DIGESTION…..
• Entry of fats to the small intestine leads to production of
cholecystokinin which stimulate gallbladder to release
bile into intestine which leads to emulsification that
increases surface area for digestion of triglycerides by
Pancreatic enzymes such as pancreatic lipase and
colipase produced from pancreas by the action of
cholecytokinin
 DIGESTION……
• phospholipaseA2 and cholesterol esterase are
released from pancrease hydrolyzes
phospholpids and cholesterol esters
respectively
 ABSORPTION AND TRANSPORT
• Products of triglycerides including free fatty acids and
glycerol with other lipids which are produced by enzymatic
digestion such as Lysophospholipids and cholesterol with
lipid soluble vitamins form MICELLES with bile acids in
intestine lumen
• Micelles are tiny micro droplets formed by emulsification of
digestion products of lipids by bile acids
 ABSORPTION AND TRANSPORT….
•Micelles interacts with enterocyte membrane and allow
diffusion of lipid soluble components into cells, where as
bile acids will go down and reabsorbed from ileum and enter
into enterohepatic circulation
•Short and medium chain C4 to C12 fatty acids will directly
transported to intestinal ephitelial cells without forming
micelles and transported to liver by binding to Albumin
• Intestinal ephitelial cells produce triacylglycerols from
mono acyl glycerols and free fatty acids and forms
asoluble lipoproten called chylomicron with apoprotein-
48, phospholipids and cholesterol esters.
• chylomicrons are secreted to lymph and entered to
circulation in which dietary lipids are transported to
different parts of the body
METABOLISM OF
FATTY ACIDS
 METABOLISM OF FATTY ACIDS….
• Fatty acids are major source of fuel for cardiac
muscle, skeletal muscle and liver during overnight
fasting.
• Increased demands such as during exercise and when
energy need arise between meals fatty acids are
major source of energy
• Limited energy supply in the body leads to release of hormones
such as glucagon and Epinephrine (adrenaline) to adipocytes.
• Binding of hormones to plasma membrane of adipocytes
stimulate synthesis of cyclic AMP.
• cAMP activates protein kinase which phosphorylate and
activates hormone sensitive triacyl glycerol lipase that hydrolze
triacylglycerol at position 1 and 3 to produce diacylglycerol and
fatty acids whichi s rate limiting step of hydrolysis
• Diacylglycerol lipase hydrolyze diacyle glycerol to
monoacylglycerol and fatty acids and monoacyleglycerol lipase
again hydrolyze monoacylglycerol to glycerol and fatty acids
• Free fatty acids pass plasma membrane of adipose cells and
endothelial cells of blood capillaries by difussion bind to albumin
in blood plasma which are transported to pheripheral tissue
• Glycerol is taken by liver and metabolized by glycolysis or
gluconeogenesis pathway
• Fatty acid binding proteins transport fatty acids from
blood plasma and also additional fatty acid binding
proteins will transport intracellularly to mitochondoria
• Fatty acids first be activated by CoA which converts to
fatty acyl CoA derivatives by ACYL CoA synthatases
found im cytosols and mithocondoria
• Carnitine acyle transferase I: transfers activated fatty acyle
from CoA to carnitine forming fatty acyle carnitine and
cross inner mithochondorial membrane with the aid of
translocase

• Carnitine acyle transferase II: transfers fatty acyle to CoA

from carnitine then carnitine released will return back to
cytosolic side of mitochondorial membrane by the first
translocase that brings fatty acyl carnitine
 METABOLISM OF FATTY ACIDS….
• Long chain fatty acyl CoA becomes substrate β-
oxidation

• Carnitine is obtained from the diet or synthesized

from the side chain of lysine by a pathway that begins
in skeletal muscle, and is completed in the liver
Β-OXIDATION….
Β-OXIDATION….
 Β-OXIDATION….
• Thus, an even chain fatty acid such as
palmitoyl CoA, which has 16 carbons, is
cleaved seven times, producing 7 FAD (2H), 7
NADH, and 8 acetyl CoA
FATTY ACID SYNTHESIS
 FATTY ACID SYNTHESIS
• Denovo synthesis of fatty acids occurs in cytosol of liver, mammary

glands, renal cortex and adipose tissue

• When excess calorie is ingested in the body fatty acid is synthesized

• The major source of carbon for synthesis of fatty acid comes from

dietary carbohydrates

• Excess dietary protein also results in synthesis of fatty acids

• The carbon skeleton of amino acid is either converted
into acetyl CoA or intermediates of tri-carboxyclic-
cycle.
• When excess carbohydrate is ingested it will be
converted into pyruvate then acetyl CoA which forms
citrate with oxaloacetate and transported to cytosol
• Fatty acid is synthesized from cytosolic acetyl-CoA
• When acetyl CoA is high in mitochondria, pyruvate
dehydrogenase is inhibited and pyruvate carboxylase activity
is stimulated and synthesis of oxaloacetate will increase
• When Oxaloacetate condensed with acetyl coA to form citrate
the level of acetyl coA will decrease and causes activation of
pyruvate dehydrogenase
• Through such reciprocal regulation citrate is synthesized and
transported across the inner mitochondorial membrane
 FATTY ACID SYNTHESIS…
• IN MITOCHONDORIA oxaloacetate condenses with
acetyl coA to form citrate
• Citrate is then transported to the cytosol across the inner
mitochondorial membrane
• In cytosol citrate is cleaved by citrate lyase into
oxaloacetate and acetyl coA
• In cytosol oxaloacetate is converted to malate by NAD ⁺
dependent malate dehydrogenase then pyruvate is produced
by oxidative decarboxylation of malate by NADP ⁺
dependent malate dehydrogenase or malic enzyme
• NADPH produced, during decarboxylation of malate to
pyruvate by malic enzyme and NADPH produced by
pentose phosphate pathway are used in the synthesis of fatty
acid
• Acetyl coA carboxylase is inactivated by
phosphorylation by AMP dependent protein kinase
• Citrate allostrically activates acetyl coA
carboxylase
• Palmitoyl coA produced from palmitate inhibits
acety carboxylase activity
 FATTY ACID SYNTHESIS…
• The generation of cytosolic acetyl coA from pyruvate
is stimulated by elevated levels of insulin/glucagon
ration due to high carbohydrate meal
• Acetyl coA is converted to malonyl CoA by acetyl
carboxylase
 FATTY ACID SYNTHESIS
• Fatty acid synthase complex is the enzyme
complex that synthesizes saturated fatty acids
from acetyl CoA, malonyl CoA and NADPH
• Fatty acid synthase sequentially adds acetyl CoA
to the growing fatty acyl chain to form palmitate
• The acetyl moiety from acetyl CoA and malonyl moiety from
malonyl CoA transferred to acyl carrier protein by acetyl
transferase and malonyl transferase
• The acetyl moiety and malonyl moiety condenses with release of
malonyl carboxyl group as CO2 which result in formation of four
carbon α-keto-acyl ACP (aceto acyl-ACP) by keto acyl synthase
• Series of three reaction then reduces 4 carbon keto acyl to alcohol
which remove water to form double bond and reduces the double
bond
• Then keto acyl-ACP reduced to 3-hydroxybutryl-ACP by keto acyl-ACP-reductase

• 3-hydroxybutryl-ACP then dehdrated and forms enoylCoA by3-hydroxyl acyl ACP

dehydratase

• Enoyl-ACP reductase converts Enoyl CoA ACP to butryl-ACP and at this stage the

fatty acid elongated by two carbons

• The four carbon acyl group is then condenses with malonyl CoA again to repeat the

cycle

• This step (cycle of two carbon additions) continues until 16 carbon palmitate is formed

• NADPH provides the reducing equivalents for reduction reactions

• Malonyl CoA prevents new synthesized fatty acids from oxidation by inhibiting the

action of carnitine acyl transferass

 De Novo synthesis Elongation of fatty Desaturation of
of fatty acids acids fatty acids
• Saturated fatty • Acetyl or malonyl • Double bonds are
acids are fragments are introduced into
synthesized from added to the the fatty acids
acetyl CoA existing fatty acids • Occur in
derived from • Occur in both microsomes
glucose microsomes and
• Occur in mitochondria by
cytoplasm elongase enzyme

SYNTHESIS OF FATTY ACIDS

 Acetyl CoA C-2

De novo synthesis

Palmitic C-16 fatty acid

acid
Elongation

Stearic C-18 fatty acid

acid
Desaturation

Oleic acid C-18 fatty acid, Unsaturated ∆9

 Definition
De novo synthesis of fatty acid is
the synthesis of saturated fatty
acids from acetyl CoA that is
primarily derived from glucose

DE NOVO SYNTHEISS OF FATTY ACIDS

• Occurs mainly in LIVER, ADIPOSE TISSUE and
LACTATING MAMMARY GLAND

• DE NOVO synthesis means new synthesis from

amphibolic compounds

• In FA biosynthesis acetyl-CoA used as PRIMER

DE NOVO SYNTHESIS OF FATTY ACIDS

• carbohydrate intake  - acetyl CoA  - fatty
acids synthesis
• Occurred in cytosol
• Need - acetyl CoA
- NADPH ( from HMP shunt )

DE NOVO SYNTHESIS OF FATTY ACIDS

DE NOVO SYNTHESIS OF FATTY ACIDS
 SYNTHESIS DEGRADATION
Intermediates Linked to SH in Linked to CoASH
Proteins
(Acyl Carrier Proteins)

Site Cytosol Mitochondria

Enzymes Components of single Separate Polypeptides

Peptide

Redox NADP+ / NADPH NAD+ / NADH

Coenzymes

FATTY ACID SYNTHESIS VS DEGRADATION

Phase I Transport of substrates into cytosol
Carboxylation of acetyl-CoA to malonyl-CoA

Phase Utilization of substrate to form palmitate

II By enzyme complex fatty acid synthase

Phase Elongation and desaturation of palmitate

III To generate different fatty acids

PHASES OF DE NOVO FA SYNTHESIS

Phase I
Transport of substrates into cytosol
Carboxylation of acetyl-CoA to malonyl-CoA

PHASES OF DE NOVO FA SYNTHESIS

 Mitochondria Cytosol

Citrate Citrate ACETYL-CoA

ACETYL-CoA

Oxaloacetate

Oxaloacetate PHASE- I

Malate

Pyruvate Pyruvate
 Phase I
Transport of substrates into cytosol
Carboxylation of acetyl-CoA to malonyl-CoA

ATP ADP + Pi
BIOTIN
Acetyl-CoA Malonyl-CoA
Acetyl-CoA carboxylase

CO2
Phase II
Utilization of substrate to form palmitate
By enzyme FATTY ACID SYNTHASE COMPLEX

PHASES OF DE NOVO FA SYNTHESIS

 Acetyl transacylase
• Is a polypeptide
containing seven Malonyl transacylase
ACP
enzyme activities 3-ketoacyl synthase

and acyl carrier 3-ketoacyl reductase

protein (ACP) 3-hydroxyacyl hydratase
segment Enoyl reductase

Thioesterase

FATTY ACID SYNTHASE MULTIENZYME COMPLEX

FATTY ACID SYNTHESIS……..
1. Replacement of CoA with Acyl Carrier Protein (ACP)

ACP CoASH

Transacylase

Malonyl-CoA Malonyl-ACP
ACP CoASH

Transacylase
Acetyl-CoA Acetyl-ACP
 FATTY ACID SYNTHESIS……

2. Joining of 2 Carbons from Malonyl-ACP to Growing Acyl Chain

3-Ketoacyl ACP Synthase

 FATTY ACID SYNTHESIS……..

3. Reduction of Ketone on Beta Carbon

OH is in D-Configuration,
in Contrast to L-Form in
Beta Oxidation

3-Ketoacyl ACP Reductase

 FATTY ACID SYNTHESIS……..

4. Removal of Water, Creating a Trans Double Bond

3-Hydroxyacyl ACP Dehydrase

 FATTY ACID SYNTHESIS……..

5. Reduction of Double Bond Fatty Acid has Grown by 2 Carbons

and Becomes Template for Next Cycle

Enoyl ACP Reductase

Cycle of 2 Carbon Additions Continues Until 16 Carbons Reached
- Palmitic Acid
 FATTY ACID SYNTHESIS……..

6. Release of Palmitic Acid at End of Cycle

Thioesterase Palmitic Acid

ACP
Palmitoyl-ACP
 Acetyl CoA Acetyl CoA

CO2 CoASH Acetyl transacylase

Biotin
ATP Acetyl CoA Acetyl S-enzyme

Fatty acid synthase multienzyme complex

carboxylase Malonyl CoA
Malonyl transacylase
ADP + Pi CoASH
Acetyl malonyl S-enzyme
Malonyl CoA
CO2 3-ketoacyl synthase
3-ketoacyl S-enzyme
NADPH+H+
3-ketoacyl reductase
NADPH
3-Hydroxyacyl S-enzyme
H2O Dehydratase

2,3-Unsaturated acyl S-enzyme

NADPH+H+
Enoyl reductase
NADPH
Acyl S-enzyme
 Fatty acid synthase multienzyme complex
Acyl S-enzyme 4 Carbon

After cycling through steps

2 - 5 seven times

Palmitoyl S-enzyme
Fa

H2O
tty
aci

Thioesterase
ds
yn
tha
se

Palmitic acid 16 Carbon

 Enzymes • Acetyl CoA carboxylase

Metabolites • Citrate
End • Palmitoyl CoA
products
• Insulin
Hormones
• Glucagon

Diet • High carbohydrate diet

REGULATION OF FATTY ACID SYNTHESIS

 REGULATION OF FA SYNTHESIS
Acetyl-CoA carboxylase

High carbohydrate diet Insulin

+ +
+
FATTY ACID SYNTHESIS

- - -
High fat diet Starvation Diabetes mellitus
ELONGATION
OF
FATTY ACIDS
Elongation of fatty
acids
• Acetyl fragments
(from malonyl
CoA) are added
to the existing
fatty acids
• Occur in both
ER and
mitochondria
DESATURATION OF FA
KETONE BODY METABOLISM
 Ketone bodies are

DEFINITION
metabolic products
that are produced in
excess during
excessive breakdown
of fatty acids.
 SIGNIFICANCE
Alternate sources to
glucose for energy

Production of ketone bodies under

conditions of cellular energy deprivation

Utilization of ketone
bodies by the brain
 Ketone
bodies are
synthesized
only in liver

SITE OF KETOGENESIS
 Acetyl-CoA Acetyl-CoA

CoA-SH Thiolase

Acetyl-CoA Acetoacetyl-CoA
HMG-CoA synthase H 2O
CoA-SH
HMG-CoA
NADH+H+
Acetyl-CoA HMG-CoA lyase
β-Hydroxybutyrate
dehydrogenase
CO2 Acetoacetate
NAD

Acetone β-Hydroxybutyrate
 INSULIN
GLUCAGO
Level Lipolysis
N 1

Entry of fatty Level

acid to
mitochondria 2 CAT-I

OXALOACETATE
Level Oxidation of
3 acetyl CoA

REGULATION OF KETOGENESIS
 KETOLYSIS

Ketone bodies are not oxidized in the liver.

Utilized in extrahepatic tissues such as brain, heart, skeletal
muscle and kidney
β-Hydroxybutyrate Acetoacetate
Succinyl CoA

CoA transferase

Succinate
Acetoacetatyl CoA
KETOLYSIS
CoA-SH
Thiolase

Acetyl-CoA 2
 KETOSIS

Ketosis is a disorder of
excessive production of
ketone bodies
 CAUSES OF KETOSIS
Prolonged starvation

• Carbohydrate deprivation
Uncontrolled diabetes mellitus

• Impaired uptake of glucose by the peripheral

tissues
CHOLESTEROL
METABOLISM
CHOLESTEROL
No vegetable oil contains any cholesterol.

Cholesterol is the major sterol in animal tissues.

Only a little portion of the body cholesterol is derived

from diet.

The bulk of it is synthesized in the body.

 Cholesterol Synthesis
• Perhydrocyclopentanophenanthrene structure consists
of four fused rings
• Cholesterol contains a hydroxyl group at C3, double
bond between C5 & C6, eight-membered hydrocarbon
chain at C17, & methyl groups at C10 & C13
Fig.2
Fig. 1

Perhydrocyclopentanophenanthrene Cholesterol
FUNCTIONS OF CHOLESTEROL
 CHOLESTEROL SYNTHESIS
• All the carbon atoms of
cholesterol are derived from
acetyl CoA

• Liver and Intestine are major

sites of cholesterol
 STEPS OF DE NOVO CHOLESTEROL
SYNTHESIS

• Step 1—Biosynthesis of Mevalonate

• Step 2—Formation of Isoprenoid Units
• Step 3—Six Isoprenoid Units Form Squalene
• Step 4—Formation of Lanosterol
• Step 5—Formation of Cholesterol
 Cholesterol Synthesis
Stage I: Acetyl CoA to Mevalonate

A. B. C.

Fig.3

Rate limiting step

Cholesterol Synthesis Stage 2: Mevalonate to 2
Activated Isoprenes

• Transfer 3 ATP to Mevalonate in

order to activate C5 & OH-
group of C3
• Phosphate group at C3 &
Carboxyl group of C1 leave,
which produces a double bound
• This allows for two active
isoprenes
Fig.5
 Cholesterol Synthesis Stage 3:
Condensation of Isoprenes to for Squalene
• 1) Head to tail attachment of
isoprenes to form Geranyl
pyrophosphate
• 2) Head to tail condensation of
Geranyl pyrophosphate and
isopentenylpyrophosphate to form
Farnesyl pyrophosphate
• 3) Head to head fusion of two
Farnesyl pyrophosphate to form
squalene
Fig.6
Cholesterol Synthesis Stage 4: Squalene to Four-
Ring Steroid Nucleus

Fig. 7
• Squalene monooxygenase adds oxygen to form an epoxide
• Unsaturated carbons (double bonds) are aligned to allow cyclization and
formation of lanosterol
• After many reaction get cholesterol
 Fates of Cholesterol
• Membranes
• Cholesterol Ester
• Biliary Cholesterol
• Bile Acids
 K Y O U
T H A N