INTRODUCTION TO

BIOCHEMISTRY
PREPARED BY:
CHERRIE MAE V. PANGANIBAN, R.Ph
•BASIC ORANIC
CHEMISTRY
•LIPIDS
 ORGANIC
CHEMISTRY
DEFINITION OF TERMS
•CHEMISTRY
study of matter, its properties, how and
why substances combine or separate
to form other substances, and how
substances interact with energy.
FIVE BRANCHES OF CHEMISTRY
• Analytical chemistry uses qualitative and quantitative observation to
identify and measure the physical and chemical properties of substances.
In a sense, all chemistry is analytical.
• Physical chemistry combines chemistry with physics. Physical chemists
study how matter and energy interact. Thermodynamics and quantum
mechanics are two of the important branches of physical chemistry.
• Inorganic chemistry studies materials such as metals and gases that do not
have carbon as part of their makeup.
FIVE BRANCHES OF CHEMISTRY
• Organic chemistry specifically studies compounds that contain the
element carbon. Carbon has many unique properties that allow it to form
complex chemical bonds and very large molecules. Organic chemistry is
known as the “Chemistry of Life” because all of the molecules that make
up living tissue have carbon as part of their makeup.
• Biochemistry is the study of chemical processes that occur within living
organism
 • Organic chemistry is the
study of carbon-containing
compounds
• The field of organic
chemistry is very important
for a wide variety of reasons.
• A huge number of carbon-
containing compounds are
known.
• Most of the advances in the
pharmaceutical industry are
based on a knowledge of
organic chemistry.
Introduction • Life as we know it is based
on organic chemistry.
 • Most organic compounds
have a “skeleton” that is
composed of C-C bonds.
• The C-C bonds may be
single bonds, double bonds,
or triple bonds.
• Carbon forms a total of 4
bonds.

• The “skeleton” of an organic

compound has H’s attached
to it.

Introduction • other “heteroatoms” like O,

halogens, N, S, and P may
be present as well
 HYDROCARBONS
• Compounds composed of only carbon and
hydrogen atoms (C, H).
• Acyclic (without rings); Cyclic (with rings);
Saturated: only carbon-carbon single bonds;
Unsaturated: contains one or more carbon-carbon
double and/or triple bonds
• They represent a “backbone” when other
“heteroatoms” (O, N, S, .....) are substituted for H.
(The heteroatoms give function to the molecule.)
• Consider the bonding arrangements for (C, H, O,
and N). Particularly that each carbon has 4
bonds.
 C H O N
-
# of Valence e s 4 1 6 5

Total # of Bonds 4 1 2 3
(neutral atom)

Combinations of
bonds
(neutral atom):

# of single bonds 4 2 1 1 2 0 3 1 0

# of double bonds 0 1 0 0 0 1 0 1 0

# of triple bonds 0 0 1 0 0 0 0 0 1

Total Bonds 4 4 4 1 2 2 3 3 3

# of Free Pairs of 0 0 0 0 2 2 1 1 1
electrons
 HYDROCARBONS
• Alkanes contain only single ( ) bonds
and have the generic molecular formula:
[CnH2n+2]
• Alkenes also contain double ( + )
bonds and have the generic molecular
formula: [CnH2n]
• Alkynes contain triple ( + 2) bonds
and have the generic molecular formula:
[CnH2n-2]
• Aromatics are planar, ring structures
with alternating single and double bonds:
eg. C6H6
Some familiar organic
compounds:
Some familiar organic
compounds:
 • Organic compounds are
commonly classified and
named based on the type
of functional group
present.

• An atom or group of atoms

that influences the way the
molecule functions, reacts or
behaves.

• The center of reactivity in an

Introduction organic compound
 FUNCTIONAL GROUPS
Class of Compound Functional Group

Alkane None

Cycloalkane None

Alkyl halide

Alkene

Alkyne

Alcohol

Ether
FUNCTIONAL GROUPS
Class of Compound Functional Group

Aldehyde

Ketone

Carboxylic Acid

Ester
FUNCTIONAL GROUPS
Class of Compound Functional Group

Amine

Amide

Nitrile

Aromatic ring
 EMPIRICAL,
MOLECULAR
&
STRUCTURAL
FORMULAS
• empirical formula Empirical Molecular
Formula Formula
• simplest ratio of
atoms in a molecule CH4 CH4

• molecular formula CH3 C2H6

• actual numbers of CH2O C6H12O6
atoms in a molecule
CH2 C4H8

CH2 C8H16
structural formula
• unambiguously shows how the atoms are bonded
together

• can use condensed structural formulas

• bonds are omitted, repeated groups put together,
side chains put in brackets
• CH3CH2CH2CH2CH2CH3
• or even CH3(CH2)4CH3
• CH3CH(CH3)CH3
skeletal formula
• not accepted in the IB for answers but often used in
questions
• every “corner” represents a carbon
• hydrogens are implied
Isomers
• (structural) isomers: compounds with the
same molecular formula but different structure
(arrangement of atoms)
• different isomers are completely different
compounds
• have different physical properties such as
melting point and boiling point
Isomerism

Enantiomers Diastereomers
(Chiral: (Chiral:
Non-superimposable Non-superimposable
Mirror Images) Non-Mirror Images;
multiple chiral centers)
 Alkanes H H H
H C C C H
• Contain C-C single bonds
• no functional group
• Tetrahedral electron domain geometry
H H H propane
H H H H H
H
CH CH CH
H C C C H
H H C
C
H H H H C 3 H C2 H 3
C H
H
• sp3 hybridized carbons CH3CH2CH3 H H HH
HH H H
H H CC
H
C C H C
• Free rotation around single bonds H CH C CH C HC H
H H H
H
 Cycloalkanes
H H
• Contain C – C with at least 3 of H c
H
c H
the carbons arranged in a cyclic c
H c c H
(ring) structure
H H
• No functional group H

• Tetrahedral

• sp3 hybrid orbitals CH2CH2CHCH2CH3

 2 3 H
H H HH H
Alkyl Halides CH2=CHCH3
H H H H H C C C C H
• Contain C-halogen H H H H
H C C C
bond C H H Br H H
H C C C C H
• F, Cl, Br, or I
H Br H H H Br H H
CH3CH(Br)CH2CH3
CH3CH(Br)CH2CH3
Br
CH3CH(Br)CH2CH3 Br

Br
 H
C C
Alkenes H CH3
• Contain C=C (carbon-carbon double bonds)
• 1 sigma bond & 1 pi bond HH HH
CC CC H
HH C
CH
• Trigonal planar geometry CHH2=CHCH
H
3
3

CH2=CHCH3

H H
C C H
H C H
H 1-propene
• sp2 hybridized carbons CH2=CHCH3
Alkenes
• The C=C present in an alkene is composed of 1 sigma
(s) bond and 1 pi (p) bond.
H H
C C ethylene
H H

• Double bonds are rigid and cannot rotate freely.

• Rotation would cause loss of overlap of the p orbitals,
destroying the p bond.
 Alkynes
H C C H C C HCH 3
• Contain C
C C H
C triple bonds H
• 1 sigma bond
H C H
• 2 pi bonds
• Linear electron domain geometry
H C C C H
H H H H
C C H H
H C H
CH2=CHCH
H C
3
C C
H H
H
CH2=CHCH3 H C C CH3
C C
• sp hybridized carbons
 Ph
H

Aromatic Ring H CH
CCH3CHCH3
H
C
H C
H
H
CC CC H C
H C H C C H
• Planar ring system with alternating C benzene
C
H HCC H C C
single and double bonds C C H C H
H Ph
• does not react like an alkene C C H
C

H
• Trigonal planar CH3CHCH3
H C
C C H
CH3CHCH3 C C C
• sp2 hybridized carbons CH3CHCH3 C C H N
.. H
Ph
C C
C
H
• Benzene ring is a very common H PhC
Ph C C H
aromatic ring. N
C C C
C C H N
.. H
C
C
C pyridine H
H
Functional Groups
• Alkanes are often called saturated hydrocarbons
• Organic compounds composed of carbon and hydrogen that
contain the largest possible number of hydrogen atoms per
carbon atom.

• Alkenes, alkynes, and aromatic hydrocarbons are called

unsaturated hydrocarbons
• Organic compounds composed of carbon and hydrogen that
contain less hydrogen than an alkane having the same
number of carbon atoms
Functional Groups:
Alcohols (R-OH)
 Alcohols contain -OH groups.
 The names are derived from the hydrocarbon name with -
-ol in place of the -ane suffix. Example: ethane becomes
ethanol.
 Since the -O-H bond is polar, similar to H-O-H, alcohols
are quite soluble in water.
 CH3OH, methanol, is used as a gasoline additive and a
fuel. CH3CH2OH, ethanol is a legal recreational drug that
can be dangerous.
 CH3CH(OH)CH2CH(CH3)2

Alcohols CH3CH(OH)CH2CH(CH3)2

H
• Contain C-O-H bond H O H H H
• hydroxyl group H
H C C C C C H
H OH H H H
H H H
• Alcohols form hydrogen bonds. H C CH CC C
H C H

H HH HH

• Amphoteric OH H CH(CH
CH CH(OH)CH
C H)
3 2 3 2

H OH

H O H H H

H C C C C C H
Functional Groups:
Ethers (R-O-R)
 Like alcohols ethers have an oxygen atom with
two single bonds.
 But instead of a hydrogen atom being bonded to
the oxygen as in alcohols, ethers have oxygen
bonded to two carbons (R-).
 Ethers are commonly used as solvents.
 Certain ethers are biologically active. Some are
used as anesthetics.
 CH3CH2OC

Ethers
CH3CH(OH)CH2CH(CH3)2
H O (CH3CH2)2
O H H H H
H C C H H CH3CH2OCH2CH3
C
• Contain C-O-C
H
bond H
C H H C C O C C H
H H (CH
H CH
H )O
H
CH3CH(OH)CH HH H
CH(CH3)2H
3 2 2

• tetrahedral e.d. geometry

CH3CHO
CH3CH(OH)CH2CH(CH3)2
2

H C C O C C H
O
H CH CH2OCH2CH3
HH HH
H H H H
H CH3
CH2OCH2CH3
3
H H C C H OH O
C O C (CH3CH2)2O
H H H H (CH3CH2)2O
HH H H H H
H C C O C C H
H C C OOHC C H O
H H H HH
H H H
• bent molecular geo.
Compounds with a Carbonyl Group:
Aldehydes & Ketones
 The carbonyl functional group is C=O. Oxygen has a double bond.

 Aldehydes must have at least one H atom attached to the carbonyl group:

O
C
R H
 Ketones must have two C atoms attached to the carbonyl group:
O
C
R R'
 H C C H

Aldehydes H O H H O
H C C H
H C C H
O
• Contain (-CHO) H H
C-H
CH3CHO
• Carbonyl (C=O) CH3CHO
• always on the 1st or last carbon in a CH3CHO
chain
H O OO
O O

H
H C C H
• trigonal planar geometry
H
H
H
C
C H
H H
• sp2 hybrid orbitals
H

CH CHO
 3 3

Ketones H
H

C
O

C
H

H C(O)CH
C CH
3 H3
H
• Contain H H
H O H
• Carbonyl attached to middle of chain
O H C C C H
CH3CHO
CH3C(O)CH3 CH3C(O)CH3
C-C-C H H
O HH
H O H H OH H H C
O H
C
H geo.
C C C H H HC C C CHH3CHO
• Trigonal planar e.d. H C H
H
H O H H C
H H C C H H
HH
H H H
• sp2 hybridized C
CH3CHO CH3CHO
H
Compounds with a Carbonyl Group:
Carboxylic Acids

 Carboxylic acids contain a carbonyl group with an -OH

attached.
 The “carboxylate” functional group is -COO-:
O
C
 Carboxylic acids are weak acids. R OH
 Carboxylic acids are found in spinach, vinegar, cleaners,
vitamin C, aspirin, and citrus fruits.
 Carboxylic acids are also used to produce polymers used
in fibers, paints, and films.
 N N

H O

Carboxylic Acids
H

CH3NH )3NH 3)3N H C C C O H

CH2 3NHCH NHCH3 (CH
3 CH3NHCH 3 (CH O
H
• Contain carboxyl group1o
2 3
o
1 2
o
2 H o
3H
o
O
3 H
o
O H
H H
H C C C O H
H C HC C
CO CH C O H
H H CH3CH2CO2H
-CO2-CO
H 2H -COOH
-COOH
H H H H
• Form hydrogen bonds CH CHCH COCHH CO H OH
CH3CH23CO2H
2
3
2
2 2
O
• trigonal planar
OH OH
HH
HO O
• sp2 hybridized carbon H C OH
C C
H O
Compounds with a Carbonyl Group:
Carboxylic Acid - Esters
 Some common esters are wintergreen oil, vegetable oil
and aspirin.
 Esters contain -COOR groups: O
C
R' OR
 Esters can be prepared by reacting a carboxylic acid with
an alcohol and a catalyst: (Esterification)
O H+
O
+ H2O
C + HO CH 2CH 3 C
H3C OH H3C OCH2CH3
Compounds with a Carbonyl Group:
Carboxylic Acid - Esters

 Most esters tend to have sweet, fruit like odors and are
used as food flavorings and scents.
 CH3COOCH2CH3
 Esters are named first using the alcohol part and then the
acid part; in the above example: ethyl from ethanol and
acetate from acetic acid.
 In the presence of a strong base, esters hydrolyze, the
ester molecule splits into an acid and an alcohol.
(saponification: the process used to make soap).
 H
H C OH
C C

Esters H O
H
H H O
H O HH HH
H HH OOH HH H
H

• Contain H C C HH
C C C CC CCC OOH CC
CO CC H
H
H C C C O C C H
H H HH HH HH H
H
-CO2R where R = alkyl
H group
H HH HH

CH3CH2COCH CHCH
CH CHCO
3CH
COCHCHCH CH3
CH3CH2CO2CH
2 3
2
CH
2 2
3
2
3 2 2 2 2 3

O
O
O
O
H H H O
H H HHHH H O O
H H H O
• trigonal planar H H
H C O C H
HH C
C HOO C CC C H CO C H
H C
C C C C C C H C H
C CH OH HH H
H HH
• sp2 hybridized H OO H HHHO
H H

-CO2R where R = alkyl group

-CORR=where
-CO R where R = alkyl group
alkyl group
Compounds with a Nitrogen atom:
Amines & Amides
 Amines are organic bases. They are weak bases.
 Just as alcohols can be thought of organic forms of water, amines can be thought of
organic forms of ammonia:

CH3CH2 NH2 (CH3)3N NH2

.
Ethylamine Trimethylamine Aniline
 Amides are composites of carbonyl and amine functionalities:
-

O
C
R N R'
H
 Amines H H H H
HH H HH H H
H H H H H
H
H
H
H C C C C H CHC N
H H HC C
C HH
C C N C H
• Contain C-N-R H
H CC C C C C C CC CN NC C
H
H
H H H H HH HH H
H H H H H
HH H H H H H HH HH HH H
R’
CH
CH3CH2CH2CH2CH CH2CH2CH2CH2NHCH3
NHCH
• R and R’ can be H or C CH
CH 2 3
CHCHCHCH3
CHCH
3 3 2 2 2 2 2
CHCH2NHCH
2 2NHCH3 3

H H
HH
N
• Primary and secondary amines N NN

form hydrogen bonds.

CH3NH2 CH3NHCH3 (CH3)3N
• Common organic bases 1
o
2
o
3
o

• lone pair of e- on N primary secondary tertiary

Amides H
H
H O
H O H
H H
H
H H O H HC CH CC CC N C
• Contain H N C C
C HH
C C C N C HHC HHH H HH HH
• where R and R’ = HH or C H
H H H H H
CH
CHCH
33
CH2CONHCH
2
CH
CONHCH2CH
2 3 3

CH3CH2CONHCH2CH3 H O
O
HH H O
• C=O is trigonal planar & H H
H NH O
H
H C O C H
sp2 hybridized HH H H C C C OOC C H H
H CH C C
O HH H
H C O C H
C C C H O HH
H
H O HH
-CO2R where R = alkyl group

-CO2R where R = alkyl group

 H H O H H H
H C O C H
C C
NitrilesC C N CC
H C C H H HH
H O HH
H H H H H H
• Contain H C O
C C
O O O
CH3CH2CONHCH2CH3 H H O
• CH
Linear
CNH2 CH3CNHCH3 CH3CN(CH3)2
3
N
• sp 1
o
hybridized C 2
o
3
o
O
HH H O
H CH3CNH2
H
H C O C H
HC C H CC C N CH3CN N o
1
H
H O HHH H

H H C C N
O O O
 “What family…?” quiz
Family names:
• cycloalkane • aldehyde
• alkene • ketone
• primary (1º) alcohol • carboxylic acid
• secondary (2º) alcohol • ester
• tertiary (3º) alcohol • ether
• phenol … are you ready?

5… 4… 3… 2… 1… GO!
What family does it belong to? (1)

H H
C C
H H
What family does it belong to? (2)

H
O
H C C
H
H
What family does it belong to? (3)

H
H O H

H C C C H

H H H
What family does it belong to? (4)

C O H

H
What family does it belong to? (5)

H H

H C O C H

H H
What family does it belong to? (6)

H
O
H
H C C

O C H
H

H
What family does it belong to? (7)

H O H

H C C C H

H H
What family does it belong to? (8)

O H
What family does it belong to? (9)

H H
O
H C C C
O H
H H
What family does it belong to? (10)
H

H C H
H

H C C O H

H H H
C
H
What family does it belong to? (11)

H H

C C H

H H
Answers: “What family?” quiz (1)

H H
C C
H H

alkene
Answers: “What family?” quiz (2)

H
O
H C C
H
H
aldehyde
Answers: “What family?” quiz (3)

H
H O H

H C C C H

H H H

secondary alcohol
Answers: “What family?” quiz (4)

C O H

primary alcohol
Answers: “What family?” quiz (5)

H H

H C O C H

H H

ether
Answers: “What family?” quiz (6)

H
O
H
H C C

O C H
H

ester
Answers: “What family?” quiz (7)

H O H

H C C C H

H H
ketone
Answers: “What family?” quiz (8)

O H

phenol
Answers: “What family?” quiz (9)

H H
O
H C C C
O H
H H

carboxylic acid
Answers: “What family?” quiz (10)
H

H C H
H

H C C O H

H H H
C
H
tertiary alcohol
Answers: “What family?” quiz (11)

H H

C C H

H H

cycloalkane
“Spot the functional groups” quiz

Functional groups:
 alkene • aldehyde
 primary (1º) alcohol • ketone
 secondary (2º) alcohol • carboxylic acid
 tertiary (3º) alcohol • ester
 phenol • ether
 arene (NEW!) … are you ready?

5… 4… 3… 2… 1… GO!
Spot both the functional groups (1)

OH phenol

OH

O
carboxylic acid
Spot all three functional groups (2)
O

ester
O
O
carboxylic acid
OH
arene
Spot both the functional groups (3)

O
OH
phenol
O
ester
Spot both the functional groups (4)

primary alcohols
OH
OH

OH
secondary alcohol
Spot all three functional groups (5)

O
ketone

tertiary
OH alcohol
alkene
Spot all three functional groups (6)

aldehyde
H
alkene

arene
Spot all three functional groups (7)

O
ketone

arene
OCH3

ether
LIPIDS
 DEFINITION
• A lipid is an organic substance
found in living systems that is
insoluble in water but is soluble in
organic solvents.

• Lipids vary widely in their structures.

They have mostly C,H and some have
a few polar atoms/ functional groups.
 IMPORTANCE
• Fat under skin serve as thermal
insulator against cold.
• Fat around kidney serve as
padding against injury.
• Fat serve as a source of energy
for man like carbohydrates.
 IMPORTANCE
• Energy storage
• Lipids are structural components of cell
membrane and nervous tissue.
• Some lipids serve as precursors for the
synthesis of complex molecules. For
example, acetyl-CoA is used for the
synthesis of cholesterol.
• Some lipids serve as hormones and fat-
soluble vitamins are lipids.
 IMPORTANCE
• Lipoproteins, which are complexes of
lipids and proteins are involved in the
transport of lipids in the blood and
components of cell membrane.
• Fats are essential for the absorption of
fat-soluble vitamins.
• Fats serve as surfactants by reducing
surface tension
• Eicosanoids which have profound
biological actions are derived from the
essential fatty acids
CHEMICAL NATURE OF
LIPIDS
• Greasy organic compounds
• Soluble in organic compounds
such as chloroform, ether,
benzene but insoluble in water
• Non-polar
• Hydrophobic
CLASSIFICATION OF
LIPIDS
1.SIMPLE
2.COMPOUND
3.DERIVED
 Lipids
1. Simple lipids: (Waxes, Fats & Oils) • Store energy
• insulation
2. Complex lipids (Glycerophospholipids) Cell membrane

3. Steroid (Cholesterol & steroid hormones) • Chemical

messenger
• Cell membrane
4. Eicosanoids Pain, fever, inflammation
 Lipids
Lipids can be categorized as:

1. Hydrolyzable lipids can be converted into

small molecules by aqueous hydrolysis.
 Lipids
Lipids can be categorized as:

2. Nonhydrolyzable lipids cannot be cleaved into

smaller molecules by aqueous hydrolysis.
 Hydrolysis
Most hydrolyzable lipids contain an ester.

Hydrolysis: reaction with water.

(breaking a bond and adding the elements of water)

O O
Heat
RCOR' + H2O H+ or enzyme RC- OH + H-OR'
An ester A carboxylic acid An alcohol
 CLASSIFICATION OF LIPIDS
Lipids are also classified according to their interaction with water.

Polar Lipids
They are further sub-divided into 3 sub-classes.
(a) Class one polar lipids are non-swelling water insoluble amphipathic molecules
(Amphiphiles) which forms thin lipid mono layer in water. They are tri- and
diacylglycerols,
long chain free fatty acids, free cholesterol and fat soluble vitamins.
(b) Class two polar lipids are swelling and water insoluble amphiphiles which forms
stable
lipid monolayer as well as laminated lipid water structure known as liquid crystals. They
are monoacylglycerols, ionized or dissociated free fatty acids and phospholipids.
(c) Class three polar lipids are water soluble amphiphiles, which contain strong polar
headgroups. These are water soluble only at low concentrations. They form mono-
layers as well as micelles. They are salts of long chain fatty acids and bile acids.
 CLASSIFICATION OF LIPIDS
Lipids are also classified according to their interaction with water.

Non-polar Lipids
They are insoluble in water. They are cholesterol esters, carotenes and hydrocarbons.
SIMPLE
LIPIDS
SIMPLE LIPIDS
• They are esters of
fatty acids with
alcohols. Fats and
waxes are example
for simple lipids.
• An ester is formed
when acid reacts
with alcohol
FATS • They are esters of fatty
acids with glycerol.
• They are also called
as triglycerides or
triacylglycerols
because all the three
hydroxyl groups of
glycerol are
esterified.
• Fats are also called as
neutral fats.
 FATS
Structure
• The chemical structure
of triglyceride or fat
consist of three
molecules of fatty acids
esterified with one
molecule of glycerol
 Fatty acids
Hydrolyzable lipids are derived from fatty acids.
Fatty acids are: COOH Stearic acid (18:0)
• Long-chain unbranched carbon (mp 70°C)
COOH Oleic acid (18;1)
attached to a carboxyl group (-COOH). (mp 16°C)

COOH Linoleic acid (18:2)

(mp-5°C)
• Typically 12-20 carbon atoms.
COOH Linolenic acid (18:3)
(mp -11°C)

• They have an even number of C atoms. COOH Stearic acid (1

(mp 70°C)
COOH Oleic acid (18;
(mp 16°C)

• Insoluble in water. Cis COOH Linoleic acid (1

(mp-5°C)
 Fatty acids
CH3(CH2)14COOH (palmitic acid)
polar portion = hydrophillic

nonpolar portion = hydrophobic

Hydrophobic portion is much bigger than hydrophilic portion. Insoluble in water

 Saturated and unsaturated Fatty acids
Saturated fatty acids have no double bonds in their long hydrocarbon
chains.
Stearic acid: CH3(CH2)16COOH

They are solids at room temperature.

Packed together  Maximum London dispersion forces

COOH
COOH
COOH
COOH
COOH
 Saturated and unsaturated Fatty acids
Unsaturated fatty acids have 1 or more double bonds (generally cis) in
their long hydrocarbon chains.

Oleic acid: CH3(CH2)7CH=CH(CH2)7COOH

They are liquids at room temperature.

They can not pack together  London dispersion forces 

COOH

COOH

COOH
COOH
COOH
 Fatty acids
• The human body is capable of synthesizing most fatty acids from
carbohydrates or other fatty acids.
• Humans do not synthesize enough amounts of fatty acids that
have more than one double bond.
• More than one double bond fatty acids are called essential fatty acids
and they must be provided by the diet.

Linoleic acid linolenic acid

 Essential Fatty acids
They are not systhesized in the body. So they must be obtained from diet. They
are also called as poly unsaturated fatty acids (PUFA). They are linoleic acid
(LA), linolenic acid (LNA) and arachidonic acid (AA).

Functions
1. They are essential for the synthesis of eicosanoids.
2. They are also required for membrane lipids.
Medical Importance
1. Dietary essential fatty acids has blood cholesterol lowering effect.
2. Deficiency status of essential fatty acids are rare with normal diet. However, deficiency
of these in rats causes poor growth, reproductive disorders and dermatitis.
3. Lipid transport may be impaired.
4. Infants consuming formula diets are susceptible to deficiency of essential fatty acids.
They may develop skin abnormalities.
 Essential Fatty acids
Omega-n acids n: the position of the first double bond
Linoleic acid is called an omega-6 acid, because of the position of
the first C=C in the nonpolar chain.
 Essential Fatty acids
Linolenic acid is called an omega-3 acid, because of the
position of the first C=C in the nonpolar chain.
CHEMICAL PROPERTIES
OF FATS
SAPONIFICATION
• When fats are boiled with bases like
KOH or NaOH glycerol and salts of
fatty acids are formed
• The salts of fatty acids act as soaps.
• Soaps are good cleansing agents,
germicides and detoxicants.
 SAPONIFICATION
- Is the process of forming “soaps” (salts of fatty acids).
- Is the reaction of a fat with a strong base (NaOH).
- Splits triacylglycerols into glycerol and the salts of fatty acids.
- With KOH or the oils that are polyunsaturated gives softer soaps (liquid
soaps).
- Soaps are typically made from lard (from hogs), tallow (from cows or
sheep), coconut oil, or palm oil.
- All soaps work in the same way, but have different properties depending
on the lipid source, length of C chain, and degree of unsaturation.
 O
SAPONIFICATION
CH2 O C (CH2)14CH3
O
+ 3NaOH
CH O C (CH2)14CH3

O
CH2 O C (CH2)14CH3
H
CH2 OH

O
Heat
H
CH OH + Na++--O C
3Na (CH2)14CH3
“soap”
Salt of fatty acid
CH2 OH
H
 Soaps Hydrophobic part: nonpolar

Hydrophilic part: polar (remains in contact with environment)

CH2 OH O
- +
CHOH + 3 RCO N a
CH2 OH
,3-Propanetriol Sodium soaps
lycerol; glycerin)
Soaps
When soap is mixed with dirt (grease, oil, and
…), soap micelles “dissolve” these nonpolar,
water-insoluble molecules.
 CHEMICAL PROPERTIES
OF FATS
HYDROGENATION
• It converts unsaturated fatty acids of
triglycerides into saturated fatty acids.
• Commercially hydrogenation is used to
convert liquid fats of plant origin to solid
cooking fats which are known as
margarines.
• Since hydrogenation converts liquid fat to
solid fat it is also called as hardening.
• Vanaspati (dalda) is obtained from
vegetable oils through this process.
 O
CH2 O C (CH2)5CH CH(CH2)7CH3
O Ni
_
CH O C (CH2)5CH _ CH(CH2)7CH3 + 3H2
O
CH2 O C (CH2)5CH CH(CH2)7CH3
O

glyceryl Trioleate CH2 O C (CH2)14CH3

(triolein) O
CH O C (CH2)14CH3
O
CH2 O C (CH2)14CH3

glyceryl tristearate
(tristearin)
Triacylglycerols are hydrolysis (split by water) in the presence of strong acid
or lipase (digestive enzyme).

O
CH2 O C (CH2)14CH3
O
CH O C (CH2)14CH3 + 3H2O

O
CH2 O C (CH2)14CH3
H
CH2 OH
O
+-
H +Na3H
CH OH O C (CH2)14CH3
H+ or Lipase

H
CH2 OH
 CHEMICAL PROPERTIES
OF FATS
LIPID PEROXIDATION
• When natural fats are exposed to
atmospheric oxygen, they develop bad
smell and taste. It is called as rancidity.
• Rancidity of fat develops even on
prolonged storing.
• It is due to formation of lipid peroxides.
• Atmospheric oxygen reacts with
unsaturated fatty acids of triglycerides and
forms lipid peroxides.
 ANTIOXIDANTS
• Like VITAMIN E AND
ASCORBIC acid prevent
peroxide formation. They are
added to food fats to improve
storage quality.
• In the body also lipid peroxides
are formed.
• Free radicals mediate lipid
peroxide formation in the body.
Diseases like cancer, diabetes,
atherosclerosis are due to the
formation of lipid peroxides in the
body.
 Metabolism of triacylglycerols
- Humans store energy as triacylglycerols in adipose cells below the surface of the
skin, in the breast area, and surrounding internal organs.

- The number of adipose cells is constant; weight gained or lost causes them to
swell or shrink, but not decrease or increase in number.

- To metabolize triacylglycerols for energy, the esters are hydrolyzed by enzymes

called lipases.

- Complete metabolism of a triacylglycerol yields CO2, H2O, and a great deal of

energy.
 Waxes
Because of their long nonpolar C chains, waxes are very hydrophobic.
O
Beeswax CH3(CH2)14 C O(CH2)29CH3
(myricyl palmitate)
hydrophobic hydrophobic
region region

They form protective coatings:

- In plants, they help prevent loss of water and damage from pests.

- In humans and animals, provide waterproof coating on skin and fur.

 Beeswax Carnauba
Coating

Jojoba

Lanolin from wool lotions

 Waxes
Hydrolysis reaction: like other esters, waxes are hydrolyzed.

Heat
 Triacylglycerols (Triglycerides)

Triacylglycerols are:

• Fats and oils (are stored in the body).

• Triesters of glycerol.

• Produced by Fischer esterification.

• Formed when the hydroxyl groups of

glycerol react with the carboxyl groups
of fatty acids.
 Esterification

glycerol three fatty acids triacylglycerol

O
CH2 OH HO C (CH2)14CH3
O
CH OH HO C (CH2)14CH3
O
CH2 OH HO C (CH2)14CH3 O
CH2 O C (CH2)14CH3
O
CH O C (CH2)14CH3 + 3H2O
Acid

O
CH2 O C (CH2)14CH3
 Triacylglycerols (Triglycerides)

CH2 OH

CH OH Glycerol

CH2 OH

O
G Fatty acid
CH2 O C (CH2)5CH CH(CH2)7CH3
L
O Y
C
CH O C (CH2)5CH CH(CH2)7CH3 Fatty acid
E
O R
CH2 O (CH2)5CH CH(CH2)7CH3 O
C L Fatty acid

Produced by esterification of glycerol (a trihydroxyl alcohol).

 Triacylglycerols (Triglycerides)

Simple triacylglycerols have three identical fatty acid side chains.

Mixed triacylglycerols have two or three different fatty acids.

 Triacylglycerols (Triglycerides)

Saturated triacylglycerols contain only saturated fatty acids.

Monounsaturated triacylglycerols have 1 C=C bond.

Polyunsaturated triacylglycerols have many C=C bonds.

Increasing the number of double bonds in the fatty acid chain

decreases the melting point of the triacylglycerol.
 Triacylglycerols (Triglycerides)

Fat: is a triacylglycerol that is solid at room temperature.

Made by more saturated fatty acids (Saturated triacylglycerols).

Meat, milk, butter and cheese (animal sources).

Oil: is a triacylglycerol that is liquid at room temperature.

Made by more unsaturated fatty acids (Unsaturated triacylglycerols).

Corn, cotton seed, safflower and sunflower (plant sources).

Both are colorless, odorless, and tasteless.

 Functions of
Triglycerides
• They function as storage lipids in animals and
in plants.
• In man adipose tissue or fat tissue found
under the skin, in the abdominal cavity and in
the mammary gland contain triacylglycerols.
The entire cytoplasm of adipocyte is replaced
by triacylglycerol.
• In other animals and plant cells also
triacylglycerols are found as tiny droplets in
cytosol.
• The fat stored under the skin serve as energy
store and as insulator against cold.
PHYSICAL PROPERTIES
OF TRIGLYCERIDES
• Pure fats have no colour, taste and odour.
• At room temperature, fat of plant origin
remains oil because it contains more
unsaturated fatty acids whereas animal fat
remain as solid, because it contains mostly
saturated fatty acids.
• Triglycerides containing asymmetric
carbon atom are optically active.
 Fat & Health

- Fats are used to build cell membranes, insulate the body, and
store energy for later use.

- It is recommended that no more than 20-35% of a person’s caloric

intake should come from lipids.

- A high intake of saturated triacylglycerols is linked to heart disease.

- Saturated fats stimulate cholesterol synthesis in the liver, which

can lead to cholesterol plaques building up inside arteries.

- The result is high blood pressure, heart attack, and even stroke.

- Unlike other vegetable oils, oils from palm and coconut trees are
very high in saturated fats.
 Fat & Health

- Unsaturated triacylglycerols (omega-3 fatty acids from fish) lower the risk
of heart disease by decreasing the level of cholesterol in the blood.

- However, if the double bond of the unsaturated triacylglycerol is

trans, the beneficial effect is lost.

- Trans fats, which are primarily synthesized instead of naturally

occurring, act like saturated fats and increase the cholesterol levels in the
blood.
SATURATED
FATTY ACIDS
• Name of
hydrocarbon
chain + ‘oic’
acid
UNSATURATED FATTY ACIDS
• Systemic name: Name of hydrocarbon chain + ‘enoic’ acid
• ω-end series: named according to the location of double
bonds(s) from ω-end.
• For example, palmitoleic acid containing a double bond
between 9 and 10 carbon atoms is named as ω-7 fatty
acid.
• Shorthand forms
PALMITOLEIC
ACID
COMPOUND
LIPIDS
COMPOUND LIPIDS
They are esters of fatty acids with alcohol containing nitrogenous bases
and additional groups.

I. Compounds lipids are also divided into:

a) phospholipids
b) glycolipids.

II. Based on alcohol compounds lipids are subdivided into:

(a) Glycerophospholipids
(b) Sphingolipids.
 PHOSPHOLIPIDS
Phospholipids are lipids that contain a P atom.

Two common types:

 PHOSPHOLIPIDS
1. Phosphoacylglycerols:

They are the main component of most cell membranes.

Structurally, they resemble a triacylglycerol, except the third fatty acid

has been replaced with a phosphodiester bonded to an alcohol.

Fatty acid

Fatty acid

Amino alcohol
 PHOSPHOLIPIDS
1. Phosphoacylglycerols:

There are 4 types of phosphoacylglycerols:

Serine Inositol
Ethanolamine Choline

Function: It is the major Function:phosphatidyl

phospholipid of cell inositol (PIP2) and inositol
membrane. It is also triphosphate (IP3) are
present in egg yolk and involved in signal
Cephalin
lipoproteins. transduction.
 PHOSPHOLIPIDS
2. Cardiolipin
• Structure: It is a double glycerophospholipid. It contains two phosphatidic acids
esterified to C-1 and C-3 of glycerol
• Function: It is present in inner mitochondrial membrane. It is also present in
heart muscle. It has immunological properties and used in the diagnosis of
syphilis.
3. Lysophospholipids
• Structure: They contain only one acyl group instead of two acyl groups
• Function: formed during biosynthesis of phospholipids. Lysolecithin is a
component of cobra venom and a strong hemolysing agent
4. Plasmalogens
• Structure: These compounds contain unsaturated fatty alcohol in place of fatty
acid at the C-1 position.
• Function: They are found in brain, heart and muscle. Plasmogen content is more
in cancer cells. Platelet activating factor, which causes aggregation of platelets is a
plasmalogen
 SPINGOLIPIDS
1. Sphingomyelins: They differ in two ways:

1. They do not contain a glycerol backbone, they have a sphingosine backbone instead.

sphingosine

2. They do not contain an ester; their single fatty acid is bonded to the backbone
by an amide bond.
 SPINGOLIPIDS
1. Sphingomyelins:

The myelin sheath, the coating that surrounds nerve cells, is rich in sphingomyelins.
 SPINGOLIPIDS

Nonpolar

O R Polar

Interact with both polar and nonpolar substances.

1. Most abundant lipids in cell membranes (semipermeable).

2. Combine with less polar triglycerides and cholesterol to make them soluble.
 Cell Membrane

Carbohydrate
Phospholipid
bilayer

Nonpolar
Hydrophobic

Polar
Hydrophilic

Semipermeable: selected nutrients can enter and waste products can leave.

Fluid mosaic model

 Cell Membrane

- Peripheral proteins are embedded within the membrane and

extend outward on one side only.

- Integral proteins extend through the entire bilayer.

- Sometimes carbohydrates are attached to the exterior of the cell

forming glycolipids and glycoproteins.
 Transport Across a Cell Membrane

Simple Diffusion: Small molecules like O2 and CO2 can diffuse through the cell
membrane, traveling from higher to lower concentration.

Facilitated Transport: Larger polar molecules (glucose) and ions (Cl- and
HCO3-) travel through integral protein channels.

Active Transport: Other ions, Na+, K+, and Ca2+, move against the concentration
gradient; this required energy input.
 SPINGOLIPIDS
1. Sphingomyelins:
Structure:
-In sphingomyelins, fatty acid is linked to sphingosine by an amide bond and
phosphorylcholine is esterified to C-1 hydroxyl of sphingosine. Because of
the phosphorous
•sphingomyelins are called as sphingo phospholipids.
Functions:
1. They are simple and most abundant sphingolipids.
2. They are present in most of animal membranes.
3. Myelin sheath of nerve cells is rich in sphingomyelins.
4. Grey matter also contain sphingomyelins.
 SPINGOLIPIDS
2. Glycolipids
Subdivided into:
1. Cerebrosides
•They contain sphingosine, fatty acid and sugar. The
combination of sphingosine and fatty acid is called as ceramide.
•Named according to the sugar present (glucocerebroside,
galactocerebroside)
•In some cerebrosides, sulfate is attached to sugar then they are
called as sulfatides or sulfolipids
•Functions: Cerebrosides occur in large amounts in white
matter of brain and in myelin sheath of nerves. Some
cerebrosides are present in non-neural tissue.
, growth, differentiation and carcinogenesis.
 SPINGOLIPIDS
2. Glycolipids
2. Gangliosides
•They are highly complex sphingolipids. They contain
ceramide, oligosaccharide and sialic acid.
•Functions
1. They are abundant in grey matter of brain.
2. They are also found in non-nerval tissues.
3. They are components of hormone receptors.
4. They also function as receptors for toxins of cholera,
influenza and tetanus.
5. They are also involved in cell-cell recognition, growth,
differentiation and carcinogenesis.
DERIVED
LIPIDS
 STEROIDS
Steroids have:

• A steroid nucleus which is

4 carbon rings.

• Attached groups that make the

different types of compounds.
‘cyclopentanoperhydrophenanthrene’
‘sterane’ ring
• No fatty acids.
 CHOLESTEROL
Cholesterol:

• Is the most abundant steroid in the body.

• Insoluble in water (need a water soluble carrier).

• Has methyl CH3- groups, alkyl chain, and -OH CH3 CH3
attached to the steroid nucleus. CH3
CH3
CH3

HO
 CHOLESTEROL

Functions
1. Cholesterol and its esters are important components of cell membrane and
lipoproteins.
2. Steroids with diverse physiological functions are derived from cholesterol.
Some of them are given below:
(a) Vitamin D 7-dehydrocholesterol derived from cholesterol is provitamin
of vitamin D.
(b) Bile acids They are required for the formation of bile salts.
(c) Hormones of adrenal cortex They are cortisol, corticosterone and
aldosterone. They are derived form cholesterol.
(d) Female sex hormones They are progesterone and estrogen.
(e) Male sex hormones They are testosterone and androsterone.
 CHOLESTEROL
Cholesterol:

• Is obtained from meats, milk, and eggs.

• Is synthesized in the liver from fats, carbohydrates

and proteins.

At artery clogged by
• Is needed for cell membranes, brain and nerve tissue, cholesterol plaque
steroid hormones, and Vitamin D.

• Clogs arteries when high levels form plaque (because it

is insoluble in blood).

• No cholesterol in vegetable and plants.

Gallstones form in gallbladder

Other Noteworthy Steroids
1. Ergosterol provitamin of vitamin D found
in yeast and plants.
2. Sitosterol present in plants.
3. Cardiac glycosides like ouabain and
streptomycin an antibiotic.
4. Coprostanol found in feces is derived from
cholesterol.
5. Wool fat sterols like agnosterol and
 LIPOPROTEINS
Water-soluble form of lipids
Triacylglycerols
(soluble in blood)

Spherical particles

Polar surface and nonpolar inner

Transporting lipids through the bloodstream to tissues where they are stored,
Used for energy, or to make hormones.
 CLASSIFICATION OF LIPOPROTEINS
BASED ON DESNSITY (can be separated by ultra centrifugation)
**Density of a lipoprotein is inversely related to the lipid content. The greater
the lipid content, Lower is the density.
1. CHYLOMICRONS
2. VLDL
3. LDL
4. HDL

BASED ON DIFFERENCES IN ELECTROPHORETIC MOBILITIES (can be separated

by electrophoresis)
1. a-lipoproteins
2. pre-beta-lipoproteins
3. beta-lipoproteins
4. chylomicrons
 LIPOPROTEINS
VLDL: very-low-density lipoprotein Triglycerides and Cholesterol

LDL: low-density lipoprotein (bad Cholesterol) Cholesterol

HDL: high-density lipoprotein (good Cholesterol) Cholesterol

Recommended levels are: HDL > 40 mg/dL, LDL < 100 mg/dL, total serum cholesterol < 200 mg/dL.

Chylomicrons Triglycerides and Cholesterol

VLDL

Fat storage Heart and

Liver cells muscles
Intestine Energy
and HDL
elimination
LDL
 Functions of Lipoproteins

Lipoproteins are involved in the transportation of lipids in the

body.
1. Chylomicrons They transport dietary or exogenous
triglycerides from intestine to liver.
2. Very low density lipoproteins (VLDL) They are involved
in the transport of endogenous triglycerides from liver to extra
hepatic tissues.
3. Low density lipoproteins (LDL) LDL is the major vehicle
for the transport of cholesterol from liver to extra hepatic
tissues.
 STEROID HORMONES
A hormone is a molecule that is synthesized in one part of an
organism, which then elicits a response at a different site.

Two types of steroids hormones:

1. Sex hormones Estrogens & progestins in females

Androgens in males

2. Adrenal Cortical Steroids

 SEX HORMONES
Estrogens (Female Sex Hormones):

The estrogens estradiol and estrone control development of secondary

sex characteristics, regulate the menstrual cycle, and are made in the
ovaries.
 SEX HORMONES
Progestins (Female Sex Hormones):

The progestin progesterone is called the “pregnancy hormone”; it is

responsible for the preparation of the uterus for implantation of a fertilized
egg.
 SEX HORMONES
Androgens (Male Sex Hormones):

Testosterone and Androsterone are androgens made in the testes.

They control the development of secondary sex characteristics in males.

 SEX HORMONES
- Synthetic androgen analogues, called anabolic steroids, promote
muscle growth.

- They have the same effect as testosterone, but are more stable, so
they are not metabolized as quickly.

- They have come to be used by athletes and body builders, but

are not permitted in competitive sports.

- Prolonged use of anabolic steroids can cause physical and

psychological problems.
 SEX HORMONES
Some examples of anabolic steroids:

(THG or the Clear)

 ADRENAL CORTICAL STEROIDS
Aldosterone regulates blood pressure and volume by controlling the
concentration of Na+ and K+ in body fluids.

Cortisone and cortisol serve as anti-inflammatory agents, which also

regulate carbohydrate metabolism.

aldosterone
cortisone

cortisol
 ADRENAL CORTICAL STEROIDS
Cortisone are used to suppress organ rejection after transplant surgery
and to treat many allergic and autoimmune disorders.

Prolonged use of these steroids can have undesired side effects,

including bone loss and high blood pressure.

Prednisone, a synthetic alternative, has similar anti-inflammatory

properties but can be taken orally.
 VITAMINS
They are organic compounds required in small quantities for normal
metabolism.

They must be obtained from the diet (our cells cannot synthesize them).

Vitamins are either water soluble or fat soluble.

The four fat-soluble vitamins (A, D, E, and K) are lipids and

nonpolar.

They are found in fruits, vegetables, fish, liver, and dairy products.

Excess vitamins are stored in adipose cells to be used when needed.

 VITAMINS
Vitamin A
It is found in liver, fish, and dairy products, and is made from β-carotene
(the orange pigment in carrots).

It is needed for vision and for healthy mucous membranes.

Vitamin A deficiency causes night blindness and dry eyes and skin.
 VITAMINS
Vitamin D

Vitamin D can be synthesized from cholesterol.

It can be obtained in the diet from many foods, especially milk, and
helps regulate Ca and P metabolism.

A deficiency of vitamin D causes rickets (bone malformation).

 VITAMINS
Vitamin E

Vitamin E is an antioxidant, protecting unsaturated side chains in

fatty acids from unwanted oxidation.

Deficiency of vitamin E causes numerous neurological problems,

although it is rare.
 VITAMINS
Vitamin K

Vitamin K regulates the synthesis of clotting proteins (prothrombin),

and deficiency of this leads to excessive or fatal bleeding.
 EICOSANOIDS
Prostaglandins, Leukotrienes, Prostacyclins,
Thromboxanes and Lipoxins are types of eicosanoids (20
C atoms derived from the fatty acids).

- All eicosanoids are very potent compounds, which are

not stored in cells, but rather synthesized in response to
external stimulus.

- Unlike hormones they are local mediators, performing

their function in the environment in which they are
synthesized.
 PROSTAGLANDINS
Prostaglandins are carboxylic acids that contain a five-membered ring
and have a wide range of biological activities.
 PROSTAGLANDINS
Prostaglandins are responsible for inflammation.

- Aspirin and ibuprofen relieve pain and inflammation by blocking the

synthesis of these molecules.

- Prostaglandins also decrease gastric secretions, inhibit blood

platelet aggregation, stimulate uterine contractions, and relax
smooth muscles.

- There are two different cylcooxygenase enzymes responsible

for prostaglandin synthesis called COX-1 and COX-2.
 PROSTAGLANDINS
COX-1 is involved in the usual production of prostaglandins.

COX-2 is responsible for additional prostaglandins in inflammatory

diseases like arthritis.

- Nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin and

ibuprofen inactivate both COX-1 and -2, but increase risk for stomach
ulcer formation.

- Drugs sold as Vioxx, Bextra, and Celebrex block only the COX-2
enzyme without affecting gastric secretions.
 LEUKOTRIENES
Asthma is characterized by chronic inflammation, so inhaled
steroids to reduce this inflammation are commonly used.

Leukotrienes are molecules that contribute to the asthmatic

response by constricting smooth muscle of the lung.

New asthma drugs act by blocking the synthesis of leukotriene C4,

which treat the disease instead of just the inflammation symptoms.
 FUNCTIONS OF EICOSANOIDS

They function as local hormones. They act on several organs and produce
physiological as well as pharmacological effects:
1. Heart. PGE class prostaglandins increases cardiac output and myocardial
contraction.
2. Blood vessels. Prostaglandins (PGE) maintain blood vessel tone and arterial
pressure.
3. Blood pressure. PGA and PGE class prostaglandins lower blood pressure.
So they may be useful as anti hypertensive agents.
4. Brain. PGE class prostaglandins produce sedation and tranquilizing effect in cerebral
cortex.
5. Kidney. PGA and PGE class prostaglandins increases excretion of Na+, K+ and CI-.
They may increase urine volume by increasing plasma flow.
6. Lungs. Prostaglandins dilate bronchi, so they are useful in the treatment of asthma.
7. Nose. Prostaglandins releive nasal congestion.
8. Stomach. Prostaglandins decreases acid secretion in stomach. So they are useful in
 FUNCTIONS OF EICOSANOIDS

9. Uterus. Prostaglandins induces contraction of uterine muscle. So they are used in the
termination of pregnancy. Prostaglandins also has role in fertility.
10. Metabolism. Prostaglandins influences several metabolism by altering cAMP level.
For example, they inhibit lipolysis in adipocyte by increasing cAMP level.
11. PGE class prostaglandins are involved in inflammation.
12. Prostacylins inhibit platelet aggregation.
13. Thromboxanes causes platelet aggregation and clot formation.
14. Leukotrienes are involved in the regulation of neutrophil and eosinophil function.
They act as mediators of immediate hyper sensitivity reaction. The slow reacting
substance of anaphylaxis (SRS-A) is a leukotriene. Some leukotrienes act as chemotactic
agents. Lipoxins are vasoactive and immuno-regulatory substances.
15. Thromboxane A2 regulates acquired immunity. It causes construction of smooth
muscle cells. It is a mitogen.
 LIPID LAYERS,
MICELLES AND
LIPOSOMES
1. Amphipathic
Molecules
2. Lipid monolayer
3. Micelles
4. Lipid Bilayer
 Liposomes
• Structure
- When a lipid bilayer closes on itself a
spherical vesicle called as ‘liposome’ is
formed
• Functions
1. Liposomes are used as a carrier of
certain drugs to specific site of body
where they act. They can deliver drugs
directly into cell because they easily
fuses with cell membranes.
2. They are used in cancer therapy to
deliver drugs only to cancer cells.
3. In gene therapy also they are used as
vehicles for genes.
LIPID
DEFICIENCIES
• Hyperlipidemia
• Atherosclerosis
• Fatty liver
• Fabry’s disease
• Farber’s disease
• Gangliosidoses
• Gaucher disease
• Niemann- Pick disease
• Tay-Sach’s Disease
• Vitamin deficiency
 HYPERLIPIDEMIA
• Increase cholesterol in the blood
• CAUSE: Foods that have cholesterol, saturated
fat, and trans fats can raise
your blood cholesterol level. These include:
• Cheese
• Egg yolks
• Fried and processed foods
• Ice cream
• Pastries
• Red meat
 HYPERLIPIDEMIA
• SIGNS AND SYMPTOMS
• chest pain (at a young age)
• heart attack (at a young age)
• cramping in the calves while walking
• sores on the toes that don’t heal properly
• stroke symptoms, including trouble
speaking, drooping on one side of the face,
or weakness in the extremities
 HYPERLIPIDEMIA
• RISKS
• eating foods with saturated and trans fats
• eating animal protein, like meat and dairy
• not getting enough exercise
• not eating enough healthy fats
• obesity
• large waist circumference
• smoking
• drinking alcohol excessively
 HYPERLIPIDEMIA
• RISKS
• kidney disease
• diabetes
• polycystic ovary syndrome
• pregnancy
• underactive thyroid
• inherited conditions
• birth control pills
• diuretics
• some depression medications
 HYPERLIPIDEMIA

• DIAGNOSIS
• LIPID PROFILE
 HYPERLIPIDEMIA

• TREATMENT
• LIFESTYLE
MODIFICATION
• MEDICATION
What is the classification
of Hyperlipidemia

Hyperlipidemias are classified according to the


Fredrickson classification which is based on the
pattern of lipoproteins on electrophoresis or
ultracentrifugation. It was later adopted by the
World Health Organization (WHO). It does not
directly account for HDL, and it does not
distinguish among the different genes that may
be partially responsible for some of these
conditions.
 GROUPS OF HYPERLIPIDEMIA

Primary or familial hyperlipoproteinaemia
Secondary hyperlipoproteinaemia
The current classification of hyperlipidemias is based
on the pattern of lipid abnormality in the blood.
 Primary familial
hyperlipoproteinaemia

• Subclassified into six phenotypes
I , IIa , IIb, III, IV, and V based on lipoproteins and lipids
were elevated.

•current literature, however, favour the more descriptive

classifications and subclassification
see table 30.2 in foy’s book
Hyperlipoproteinemia Synonyms Increased Treatment
lipoprotein
Type I (rare) ''Buerger-Gruetz syndrome'', Chylomicro Diet control
''Primary hyperlipoproteinaemia'', ns by
or ''Familial reduced LPL
hyperchylomicronemia''

Type IIa ''Polygenic hypercholesterolaemia'' LDL+TG Bile acid

or ''Familial hypercholesterolemia sequestrants,
statins,
niacin
Type IIb ''Combined hyperlipidemia'' LDL and Statins,
VLDL niacin,
fibrate
Type III (rare) ''Familial dysbetalipoproteinemia'' IDL Fibrates,
statins

Type IV ''Familial hyperlipidemia'' VLDL Fibrate,

niacin],
statins
Type V (rare) ''Endogenous VLDL and Niacin,
hypertriglyceridemia Chylomicro fibrate
ns
Several different classes of drugs are used to
treat hyperlipidemia. These classes differ not
only in their mechanism of action but also in
the type of lipid reduction and the magnitude of
the reduction.
 CLASSIFICATION
S.No. Class Example

1) HMG CoA Reductase Lovastatin, Simvastatin, Metastatin,

inhibitors Pravastatin, Fluvastatin, Atorvastatin,
Pitavastatin, Rosuvastatin

2) Fibric acid derivatives Clofibrate, Fenofibrate, Gemfibrozil,

Ciprofibrate, benzaffibrate, Fluvestatin.

3) Bile acid sequestrants Cholestyramine, Colestipol

4) LDL oxidation Probucol

inhibitor
5) Pyridine derivatives Nicotinic acid, Nicotinamide

6) Cholesterol absorption Ezetimibe

inhibitors
7) Miscellaneous agents β-Sitosterol, Dextrothyroxine
 Target: HMG-CoA Reductase (HMGR)
 The enzyme that HO
CH3
catalyzes the conversion C
of HMG- Co Ato H 2C
CH2 C SCoA
mevanolate. C
 O
O O
HMG-CoA
2NADPH
 This reaction is the rate- HMG-CoA
determining step in the 2NADP+ Reductase
+ HSCoA
synthetic pathway of HO
cholesterol. CH3
C
H 2C H2
CH2 C OH
3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) C
O mevalonate
O
HMG-CoA reductase inhibitors

28
 Statins
 Lovastatin was isolated from Aspergillus terreus.


Today, there are two classes of statins:
Natural Statins: Lovastatin(mevacor), Pravastatin (pravachol),
Simvastatin (Zocor).
Synthetic Statins: Atorvastatin (Lipitor), Fluvastatin (Lescol).

Statins are competitive inhibitors of HMG-CoA reductase. They

are bulky and “stuck” in the active site.
This prevents the enzyme from binding with its substrate, HMG-
CoA.
 HO O
HO O

O
O O
O


O
H3 C H H O
CH3 H3 C H H
CH3

H3 C
MEVASTATIN
LOVASTATIN (MEVACOR)

HO O
HO
COOH
O
OH
O
O

O
O
H3 C CH3 H
H3 C H H
CH3
CH3

HO
SIMVASTATIN (ZOCOR)
PRAVASTATIN (PRAVACHOL)
 DRUG ADR USES

Lovastatin Increased creatinine phosphokinase, Flatulence, Antihyperlipoproteinemi c agent

Nausea

Simvastatin Headache, nausea, flatulence, heartburn, Antihyperlipdemic agent

abdominal pain

Pravastatin GI disturbances, headache, insomnia, Antihyperlipoproteinemi c agent

chest pain, rash

Atorvastatin Headache, flatulence, diarrhea Primmary hyperlipidemia

and secondary hyper
cholesterolemia

Rosuvastatin Headache, dizziness, constipation, nausea, High LDL, total

vomiting cholesterol, TGs
 SAR of HMG-CoA
reductase inhibitors
The structure should contain
a. lactone ring (sensitive to stereochemistry of it, ability of ring
to hydrolyzed, length of bridge)
b. Bicyclic rings ( could be replaced with other lipophlic rings,
size and shape of it are important for activity)
c. Ethylene bridge between them
 FIBRIC ACID
DERIVATIVES
CH3
CH3 CH3
O (CH2)3 C COOH Cl O C COOEt

CH3 CH3
H3C
GEMFIBROSIL(LOPID) CLOFIBRATE (ATROMID-S)
Cl

CH3

iPrO2C C O

CH3 O

F E N O F I B R AT E ( T R I C OR )
 Overview
agents, widely used in the
•Fibrates are antihyperlipidemic
treatment of different forms of hyperlipidemia and
hypercholesterolemia
•Fibrates are 2-phenoxy-2-methyl propanoic acid derivatives.
•these drugs stimulate β-oxidation of fatty acids in mitochondria
•This group of drugs is therefore known for decreasing plasma
levels of fatty acid and triacylglycerol
Mechanism of Action = works in a variety ways

• Decrease plasma TGs levels more than C levels

• Fibrates lower blood triglyceride levels by reducing the

liver's production of VLDL (the triglyceride-carrying
particle that circulates in the blood) by activation of
lipoprotein lipase and speeding up the removal of TGs
from the blood. It is supported by PPAR-α.

• Fibrates also are modestly effective in increasing blood

HDL cholesterol; however, fibrates are not much
effective in lowering LDL cholesterol.
 SAR of Fibric acid
derivatives
aromatic ring]-O-[spacer group]-C(CH ) -CO-OH

3 2

Fibric acid
 They are classified as analogues of isobutyric acid
derivatives (essential for activity)
 SAR

Fenofibrate gemfibrozil

• Fenofibrate contain ester (prodrug)

• Para-subtitution with Cl or Cl containing isopropyl ring
increase half-lives.
• n-propyl spacer result in active drugs (gemfibrozil )
 DRUG ADR USES

Clofibrate Cholecystitis, gall stone, Type III

eosinophilia, pneumonia Hyperlipoproteinemias

Gemfibrozil Myositis syndrome, Hyperlipidemia

Cholelithiasis, GI disturbances,
rash and headache.

Fenofibrate Headache, dizziness, asthaenia, More potent

fatigue, arrhythmia hypercholesterolemic
and triglycerides
lowering agent
 Bile Acid Sequestrants
 cholestyramine (Questran)
 
colestipol hydrochloride (Colestid)
 colesevelam (tablet form)
 Also called bile acid–binding resins and
ion-exchange resins
Cholestyramine (Questran)


• is a non-absorbed bile acid sequestrant that is
used as a therapy of hyperlipidemia and for the
pruritis of chronic liver disease and biliary
• obstruction.
• is a large, highly positively charged anion
exchange resin that binds to negatively
• charged anions such as bile acids.
• The binding of bile acids to cholestyramine
creates an insoluble compound that cannot be
reabsorbed and is thus excreted in the feces.
• Moderately effective with excellent safety record
• Large MW polymers containing Cl-


• Resin binds to bile acids and the
acid-resin complex is excreted
– prevents enterohepatic cycling of bile acids
– obligates the liver to synthesize
replacement bile acids from
cholesterol.
The levels of LDL-C in the serum are
• reduced as more cholesterol is delivered
• to the liver
Little effect on levels of HDL-C and TG.
Excellent choice for people that cannot
tolerate other types of drugs
 Colesevalam

 A third generation drug of this class……resemble the
previous ones but don’t contain chloride ions.
 Strictly speaking, it is not an anion exchange resin.
 Selectivity for hydroxylated form of bile acids shows
a reduced side effect………reduced constipation.
 Adverse effects
• Constipation 
• Heartburn, nausea, bloating
• These adverse effects tend to disappear over
time.
 Therapeutic Uses

•

Type IIa hyperlipoproteinemia.

• Relief of pruritus associated with partial biliary

obstruction (cholestyramine).
 Ezetimibe (Zetia)
 OH
OH

N
F
O

EZETIMIBE

is a drug that lowers plasma cholesterol levels. It

acts by decreasing cholesterol absorption in the
intestine
Mechanism of action Cholesterol Absorption
Inhibitor
•

lowers plasma cholesterol levels by inhibiting the
absorption from intestine
• This cause a decrease in the cholesterol delivery to the
liver which in turn clears more cholesterol from the
blood

• selective in its action (( not interfere with TGs, lipid-

soluble vitamins absorption))

• The levels of LDL-C in the serum are reduced as in bile

acid sequestrants.
 Therapeutic uses

• as monotherapy or in combination with HMGRI for
reduction of elevated total cholesterol.
Niacin (Nicotinic
Acid)
 NICOTINIC ACID
(Niacin)
COOH

N 
NICOTINICACID(NIACIN)
A water soluble vitamin of the B family;
Once converted to the amide, it is
incorporated into NAD

In order to be effective, it has to be dosed at the rate of 1.5 to 3.5

gm daily.
A sustained release dosage form is available
 Niacin (Nicotinic Acid)
 Vitamin B 3

 Lipid-lowering properties require much higher doses than
when used as a vitamin

 Effective, inexpensive, often used in combination with

other lipid-lowering drugs
 Niacin (Nicotinic Acid)
Mechanism of action

 Increases activity of lipase, which breaks down lipids
 Reduces the metabolism of cholesterol and triglycerides

Indications
 Effective in lowering triglyceride, total serum cholesterol,
and LDL levels
 Increases HDL levels
 Effective in the treatment of types IIa, IIb, III, IV, and V
hyperlipidemias
 Niacin (Nicotinic Acid)

Adverse effects

 Flushing (due to histamine release)

 Pruritus
 GI distress
 Liver dysfunction and jaundice. Serious liver
damage is the most important risk.
LDL oxidation inhibitor: Probucol


• Molecule has two tertiary butylphenol groups linked

by a dithiopropylidene bridge, giving it a high
lipophilic character with strong antioxidant
properties.
LDL oxidation inhibitor: Probucol


ADR: GI disorders and prolongation of GI intervals.

Use: It is used as antihyperlipoproteinemic agent.
 Miscellaneous agent
β-Sitosterol


 Sitosterol is a plant sterol, whose structure is identical with

that of cholesterol, except for the substituted ethyl group on
C-24 of its side chain.
 
 Sitosterols are absorbed poorly from the mucosal lining and
appear to compete with cholesterol for absorption sites in
the intestine.
ADR: Diarrhoea, constipation, GI disturbances
Use: Anti cholesteremic agent and treatment of prostatic edema.
ATHEROSCLEROSiS
A T H E R O S C L E R O S iS

• Atherosclerosis (also known as Arteriosclerotic

Vascular Disease or ASVD)
• the condition in which an artery wall thickens as the
result of a build-up of fatty materials such as
cholesterol
• affecting arterial blood vessels, a
chronic inflammatory response in the
walls of arteries
• due to the accumulation of macrophage white
blood cells and promoted by Low-density
lipoproteins without adequate removal of fats and
cholesterol from the macrophages by functional
high density lipoproteins
• It is commonly referred to as a hardening or furring of
the arteries.
• It is caused by the formation of multiple plaqueswithin
the arteries.
• It can restrict blood flow. These plaques can also burst,
causing a blood clot.
• Although atherosclerosis is often considered a heart
problem, it can affect arteries anywhere in your body.
• Atherosclerosis is a preventable and treatable
condition.
 TERMS
• Arteriosclerosis is a general term describing any
hardening (and loss of elasticity) of medium or large arteries
• Arteriolosclerosis is any hardening (and loss of
elasticity) of arterioles (small arteries);
• Atherosclerosis is a hardening of an artery specifically
due to an atheromatous plaque.
• Atherogenic is used for substances or processes that
cause atherosclerosis.
• Atherogenesis is the developmental process of
atheromatous plaques
Causes
Atherosclerosis starts with damage or injury to
the inner layer of an artery. The damage may
be caused by:

• High blood pressure

• High cholesterol
• An irritant, such as nicotine
• Certain diseases, such as diabetes
Pathophysiology
• Atherosclerosis develops as a chronic
inflammatory response of the arterial wall to
endothelial injury.
• Lesion progression occurs through interactions
of modified lipoproteins, monocyte-derived
macrophages, T-lymphocytes, and the normal
cellular constituent of the arterial wall.
• The contemporary view of atherosclerosis is
expressed by the response-to-injury hypothesis.
Micrograph of an artery that supplies the heart With
significant atherosclerosis and marked luminal narrowing
Symptoms
• Atherosclerosis develops gradually, typically
begins in early adolescence, and is usually
found in most major arteries. There are usually
no atherosclerosis symptoms until an artery is
so narrowed or clogged that it can't supply
adequate blood to your organs and tissues.
Sometimes a blood clot completely obstructs
blood flow, or even breaks apart and causes
blood clots that can trigger a heart attack or
stroke.
Symptoms
Atherosclerosis symptoms depend on which arteries are
affected. For example:
• Atherosclerosis in heart arteries, have symptoms similar
to those of a heart attack, such as chest pain (angina).
• Atherosclerosis in the arteries leading to brain, have
symptoms such as sudden numbness or weakness in your
arms or legs, difficulty speaking or slurred speech, or
drooping muscles in your face.
• Atherosclerosis in the arteries in arms and legs, produces
decreased blood flow is called peripheral artery occlusive
disease (PAOD).have symptoms such as leg pain when
walking
• Sometimes atherosclerosis causes erectile dysfunction in
men.
 Physiologic factors that increase risk
Various anatomic, physiological & behavioral risk factors for atherosclerosis are
known. These can be divided into various categories:, modifiable and non-
modifiable.
1. Modifiable
• Having diabetes or Impaired glucose tolerance (IGT)
• Dyslipoproteinemia (unhealthy patterns of serum proteins
carrying fats & cholesterol):
– High serum concentration of low-density lipoprotein (LDL, "bad if elevated
concentrations and small"), and / or very low density lipoprotein (VLDL) particles, i.e.,
"lipoprotein subclass analysis"
– Low serum concentration of functioning high density lipoprotein (HDL "protective if
large and high enough" particles), i.e., "lipoprotein subclass analysis"
– An LDL:HDL ratio greater than 3:1
• Tobacco smoking, increases risk by 200% after several pack
years
• Having high blood pressure, on its own increasing risk by 60%
• Elevated serum C-reactive protein concentrations
Physiologic factors that increase risk
2. Non modifiable 3. Lesser or uncertain
• Being obese (in particular central
• Advanced age obesity,
• A sedentary lifestyle
• Male sex • Postmenopausal estrogen deficiency
• High carbohydrate intake
• Having close relatives • Elevated serum levels of
who have had some triglycerides
complication of • Elevated serum levels of uric acid
(also responsible for gout)
atherosclerosis (eg. • Elevated serum fibrinogen
coronary heart disease concentrations
• Elevated serum lipoprotein
or stroke) concentrations
• Genetic abnormalities, • Stress or symptoms of clinical
depression
e.g. familial • Hyperthyroidism
hypercholesterolemia • Elevated serum insulin levels
• Short sleep duration Chlamydia
• pneumoniae infection
Table 1.Conditions That Accelerate the Progression of Atherosclerosis and the Mechanisms
Responsible.
Condition Mechanism
Male gender (and females Estrogen increases cholesterol removal by the liver, and the progression of
after menopause) atherosclerosis is less rapid in premenopausal women that in men

Family history of Probably multiple genetic mechanisms.

ischemic heart disease,
stroke
Primary hyperlipidemia Inherited disorders causing lipoprotein lipase deficiency (type I), defective LDL
receptors (type IIa), abnormal apoprotein E (type III), deficiency of apoprotein C (type
V), or unknown cause (types IIb and IV).
Secondary Increased circulating triglycerides produced by diuretics, b-adrenergic blocking drugs,
hyperlipidemia excess alcohol intake.

Cigarette smoking Probably carbon monoxide-induced hypoxic injury to endothelial cells.

Hypertension Increased shear stress, with damage to endothelium.
Diabetes mellitus (types 1 Decreased hepatic removal of LDL from the circulation; increased glycosylation of
and 2) collagen, which increases LDL binding to blood vessel walls.
Obesity, particularly Unsettled, but obesity is associated with type 2 diabetes, hypertriglyceridemia,
abdominal obesity hypercholesterolemia, and hypertension, all of which are risk factors in their own right.
Nephrotic syndrome Increased hepatic production of lipids and lipoprotein (a).
Hypothyroidism Decreased formation of LDL receptors in the liver.
Elevated plasma Unsettled. Probably increased homocysteine provides more H2O2 and other reactive
homocysteine oxygen molecules that foster formation of oxidized LDL.
 Complications
The complications of atherosclerosis depend on the
location of the blocked arteries. For example:
• Coronary artery disease. When atherosclerosis
narrows the arteries close to your heart, you may
develop coronary artery disease, which can cause
chest pain (angina) or a heart attack.
• Carotid artery disease. When atherosclerosis
narrows the arteries close to your brain, you may
develop carotid artery disease, which can cause a
transient ischemic attack (TIA) or stroke.
 Complications
• Peripheral artery disease. When atherosclerosis narrows the arteries
in your arms or legs, you may develop circulation problems in your
arms and legs called peripheral arterial disease. This can make you
less sensitive to heat and cold, increasing your risk of burns or
frostbite. In rare cases, poor circulation in your arms or legs can cause
tissue death (gangrene).
• Aneurysms. Atherosclerosis can also cause aneurysms, a serious
complication that can occur anywhere in your body. An aneurysm is a
bulge in the wall of your artery. Pain and throbbing in the area of an
aneurysm is a common symptom. If an aneurysm bursts, you may face
life-threatening internal bleeding. Although this is usually a sudden,
catastrophic event, a slow leak is possible. If a blood clot within an
aneurysm dislodges, it may obstruct an artery at some distant point.
 Tests and diagnosis
Doctors may find signs of narrowed, enlarged or hardened
arteries during a physical exam. These include:
• A weak or absent pulse below the narrowed area of the
artery
• Decreased blood pressure in an affected limb
• Whooshing sounds (bruits) over the arteries, heard with a
stethoscope
• Signs of a pulsating bulge (aneurysm) in the abdomen or
behind knee
• Evidence of poor wound healing in the area where blood
flow is restricted
 Tests and diagnosis
Depending on the results of the physical exam, doctors
may suggest one or more diagnostic tests, including:
• Blood tests.
• Doppler ultrasound
• Ankle-brachial index.
• Other imaging tests.
• Angiogram.
• Electrocardiogram (ECG).
 Tests and diagnosis
• Blood tests. Lab tests can detect increased levels of cholesterol and
blood sugar that may increase the risk of atherosclerosis.
• Doppler ultrasound. Uses a special ultrasound device (Doppler
ultrasound) to measure blood pressure at various points along arm or
leg. These measurements can help doctor gauge the degree of any
blockages, as well as the speed of blood flow in the arteries.
• Ankle-brachial index. This test can tell if one have atherosclerosis in
the arteries in your legs and feet. Doctor may compare the blood
pressure in ankle with the blood pressure in the arm. This is known as
the ankle-brachial index. An abnormal difference may indicate
peripheral vascular disease, which is usually caused by
atherosclerosis.
 Tests and diagnosis
• Electrocardiogram (ECG). An electrocardiogram records electrical
signals as they travel through your heart. An ECG can often reveal
evidence of a previous heart attack or one that's in progress. If signs
and symptoms occur most often during exercise,
• Angiogram. To better view blood flow through heart, brain, arms or
legs, doctor may inject a special dye into your arteries before an X-
ray. This is known as an angiogram. The dye outlines narrow spots
and blockages on the X-ray images.
• Other imaging tests. doctor may use ultrasound, a computerized
tomography (CT) scan or a magnetic resonance angiogram (MRA) to
study the arteries. These tests can often show hardening and
narrowing of large arteries, as well as aneurysms and calcium deposits
in the artery walls.
 Treatments and drugs
Lifestyle changes, such as eating a healthy diet and exercising,
are often the first line of defense in treating atherosclerosis.
But sometimes, medication or surgical procedures may be
recommended as well.
Various drugs can slow — or sometimes even reverse — the
effects of atherosclerosis. Here are some common choices:
• Cholesterol medications. Aggressively lowering low-
density lipoprotein (LDL) cholesterol, the "bad" cholesterol,
can slow, stop or even reverse the buildup of fatty deposits
in arteries. Boosting your high-density lipoprotein (HDL)
cholesterol, the "good" cholesterol, may help, too.
cholesterol medications includes drugs known as statins and
fibrates.
 Treatments and drugs
• Anti-platelet medications. Doctors may prescribe anti-
platelet medications, such as aspirin, to reduce the
likelihood that platelets will clump in narrowed arteries,
form a blood clot and cause further blockage.
• Anticoagulants. An anticoagulant, such as heparin or
warfarin (Coumadin), can help thin blood to prevent
clots from forming.
• Blood pressure medications. Medications to control
blood pressure — such as beta blockers, angiotensin-
converting enzyme (ACE) inhibitors and calcium
channel blockers — can help slow the progression of
atherosclerosis
 Treatments and drugs
Other medications. doctor may suggest certain
medications to control specific risk factors for
atherosclerosis, such as diabetes. Sometimes
medications to treat symptoms of atherosclerosis,
such as leg pain during exercise, are prescribed.
Sometimes more aggressive treatment is needed. If
you have severe symptoms or a blockage that
threatens muscle or skin tissue survival, you may be
a candidate for one of the following surgical
procedures:
 Treatments and drugs
• Angioplasty. In this procedure, your doctor inserts a
long, thin tube (catheter) into the blocked or narrowed
part of your artery. A wire with a deflated balloon is
passed through the catheter to the narrowed area. The
balloon is then inflated, compressing the deposits against
your artery walls. A mesh tube (stent) is usually left in
the artery to help keep the artery open. Angioplasty may
also be done with laser technology.
• Endarterectomy. In some cases, fatty deposits must be
surgically removed from the walls of a narrowed artery.
When the procedure is done on arteries in the neck (the
carotid arteries), it's known as carotid endarterectomy.
 Treatments and drugs

• Thrombolytic therapy. If you have an artery

that's blocked by a blood clot, your doctor
may insert a clot-dissolving drug into your
artery at the point of the clot to break it up.
• Bypass surgery. Your doctor may create a
graft bypass using a vessel from another part
of your body or a tube made of synthetic
fabric. This allows blood to flow around the
blocked or narrowed artery.
 Lifestyle and home remedies
Lifestyle changes can help prevent or slow the
progression of atherosclerosis.
• Stop smoking.
• Exercise most days of the week.
• Eat healthy foods
• Manage stress
• manage the condition of high cholesterol, high
blood pressure, diabetes or other chronic
disease
 Prevention
• The same healthy lifestyle changes recommended
to treat atherosclerosis also help prevent it. You've
heard it before — stop smoking, eat healthy foods,
exercise regularly, maintain a healthy weight,
drink less alcohol. Just remember to make changes
one step at a time, and keep in mind what lifestyle
changes are manageable for you in the long run.
Fatty liver refers to the deposition of excess
triglycerides in the liver cells.
The normal concentration of lipids in liver is
around 5%.
Liver is not storage organ for fat.
In the normal liver, Kupffer cells contain lipids
in the form of droplets.
In fatty liver, droplets of triacylglycerols are
found in the entire cytoplasm of hepatic cells.
Causes impairment in metabolic functions of
liver.
Fatty liver is associated with fibrotic changes
& cirrhosis.
Causes of fat deposition in liver:
Mobilization of NEFA from adipose tissue.
Excess synthesis of fatty acid from glucose.
Reduced removal of fat from liver:
Toxic injury to liver.
Secretion of VLDL needs synthesis of apo B-100
& apo C.
Decreased oxidation of fat by hepatic cells.
The capacity of liver to take up the fatty acids
from blood, exceeds its capacity for excretion
as VLDL.
This leads to the overproduction of
triacylglycerols & their accumulation in liver.
Fatty liver can occur in diabetes mellitus &
starvation due to increased lipolysis in adipose
tissue.
Alcoholism & high fat diet are associated with
increased mobilization of fatty acids & cause
fatty liver.
Alcohol also inhibits fatty acid oxidation &
promotes fat synthesis & its deposition.
Excess calorie intake:
Excess calories, either carbohydrates or as
fats, are deposited as fat.
Obesity may be accompanied by fatty liver.
In toxic injury to the liver due to poisoning by
compounds like carbon tetrachloride, arsenic,
lead, etc.
Inhibit protein synthesis & causes fatty liver.
lmpaired synthesis of lipoproteins:
The synthesis of very low density lipoproteins
(VLDL) actively takes place in liver.
VLDL formation requires phospholipids &
apoprotein B.
Impaired lipoprotein synthesis may be due to:
Defect in phospholipid synthesis.

A block in apoprotein formation.

A failure in the formation/secretion of
lipoprotein.
Fatty liver due to impairment in phospholipid
synthesis is studied in detail.
Dietary deficiency of lipotropic factors such as
choline, betaine, inositol etc.
Deficiency of essential fatty acids leads to a
decreased formation of phospholipids.
Lipoprotein synthesis & their secretion require
ATP.
Decrease in the availability of ATP.
Pyridoxine & pantothenic acid deficiency also
impairs lipoprotein formation.
Deficiency of vitamin Eis associated with fatty
liver.
Selenium acts as a protective in nature.
Certain hormones like ACTH, insulin, thyroid
hormones, adrenocorticoids promote
deposition of fat in liver.
NAFLD is the most common liver disease,
where fat is accumulated in hepatocytes.
High fat diet & uncontrolled diabetes mellitus
are the most common causes.
As the disease progresses, inflammatory
reaction occurs, which is termed as NASH.
Fat molecules infiltrate the cytoplasm of the cell
(fatty infiltration).
These are seen as fat droplets in the cytoplasm
The nucleus is pushed to a side of the cell.
Ultimately the hepatic cell is lysed.
As a healing process, fibrous tissue is laid
down, causing fibrosis of liver or cirrhosis.
These are the substances required for the
normal mobilisation of fat from liver.
The deficiency of these factors may result in
fatty liver.
Important lipotropic factors:
Choline, Betaine, Methionine & Inositol.
Folic acid, vitamin B12, glycine & serine also
serve as lipotropic factors.
Choline & inositol are components of
phospholipids & required for their synthesis.
The other lipotropic factors are concerned
with transmethylation reactions & ultimately,
the synthesis of choline.
Severe protein deficiency (e.g.kwashiorkor)
causes fatty liver.
Due to a defect in the synthesis of choline as a
result of insufficient amino acid (methionine)
supply.
Vitamin E& selenium give protection due to
their anti-oxidant effect.
Omega 3fatty acids have a protective effect
against fatty liver.
Decreased phospholipid synthesis.
Impaired formation of lipoprotein membrane.
Reduced synthesis of carnitine due to
insufficient supply of methyl groups.

Impairment in fatty acid oxidation.

LIPID STORAGE DISEASES
 Lipid storage diseases
 Lipid storage diseases, or lipidoses, are a group of
inherited metabolic disorders in which harmful amounts
of fatty materials called lipids accumulate in some of the
body's cells and tissues. People with these disorders
either do not produce enough of one of the enzymes
needed to metabolize lipids, or they produce enzymes
that do not work properly. Over time, this excessive
storage of fats can cause permanent cellular and tissue
damage, particularly in the brain, peripheral nervous
system, liver, spleen, and bone marrow.
 Inheritance
 Lipid storage diseases can be inherited two
ways
 1.Autosomal recessive inheritance occurs when
both parents carry and pass on a copy of the faulty
but none of the parents show symptoms of disease.
 2.X-linked recessive (or sex linked) inheritance
occurs when the mother carries the affected gene
on the X chromosome that determines the child’s
gender and passes it to her son.
 Pathophysiology
 Because glycosphingolipids are essential components of
all cell membranes, inability to degrade these substances
and their subsequent accumulation results in physiologic
and morphologic alterations of specific tissues and
organs that lead to characteristic clinical manifestations.
In particular, progressive lysosomal accumulation of
glycosphingolipids in the central nervous system can lead
to a neurodegenerative course; whereas, storage in
visceral cells can lead to organomegaly, skeletal
abnormalities, bone marrow dysfunction, pulmonary
infiltration, and other manifestations.
 Types of lipid storage
diseases
 Niemann pick disease
 Fabry disease
 Farbers disease
 Gangliosidosis
 Krabbe disease
 Metachromatic leukodystrophy
 Wolmans disease
 Gaucher disease
 most common of the lipid storage diseases
 Cause
 caused by a deficiency of the enzyme glucocerebrosidase.
 Resulting in accumulation of glucocereboside in spleen
,liver, kidneys,lungs,brain and bone marrow.
 CLINICAL FEATURES
 Type 1 (non neuropathic form)
May be asymptomatic.
 Begin early in life
 Bruise easily
 Fatigue
  Hepatomegally
 Spleenomegally
 Brain not affected
Type 2 (acute infantile neuropathic)
 Begins within three months of birth.
 Poor ability to suck and swallow.
 Abnormal eye movements.
 Extensive and progressive brain damage.
 Spasticity, Seizures and Limb rigidity.
 Hepatomegally and Splenomegally.
Type 3 (chronic neuropathic )
 Can begin at any time in child hood or
even inadult hood but milder neurologic
symptoms as compared to type two.
 Respiratory problems.

 Anemia.

 Skeletal problems.

Treatment
 For type 1 and most type 3 patients, enzyme
replacement treatment given
 intravenously every two weeks can dramatically
decrease liver and spleen size, reduce skeletal
abnormalities and other manifestations.
 bone marrow transplantation cures the non-
neurological manifestations.
 Blood transfusion for anemia.
 Splenectomy (rarely )
 No effective treatment for brain damage.
Prognosis
 Type 1: may live well into adulthood.
 Type 2: usuallyo teen age die before age two.
 Type 3: live to teen age.
 Niemann-Pick disease
Cause
 Niemann-Pick types A and B result from
accumulation of the fatty substance called
sphingomyelin, due to deficiency of an enzyme
called sphingomyelinase.
 Resulting in accumulation of
sphingomyelin in liver,spleen, bone
marrow,lungs and in some patients in
brain.
Type A
 Infants are normal at birth but at age of six
years develop:
 Splenomegally
 Hepatomegally
 Swollen lymph nodes
 Profound brain damage
(atraxia,spasticity,slurred speech,loss of muscle
tone )
 Anemia
 Susceptible to recurrent infections.
Type B
 enlargement of the liver and spleen
characteristically occurs in the pre-teen years.
Most
patients also develop ataxia, peripheral
neuropathy, and pulmonary difficulties progress
with age.
Brain is generally not affected.
Treatment
 There is currently no cure for Niemann-Pick
disease. Treatment is supportive.
 FABRY DISEASE
 The only X-linked lipid storage disease.
 Predominantly affecting males.

Cause
 Deficiency of enzyme alpha galactosidase.
 Resulting in accumulation of globosides in nervous
tissue,eyes,kidneysand cardiovascular system.
Clinical features
 Burning pain in arms and legs
 Cardiomegally
 Fever
 Renal impairment
 Angiokeratomas (small,non cancerous, reddish
purple elevated spots on skin ) on lower part of
trunk.
Treatment
 Enzyme replacement therapy
 Phenytoin or carbamazepine for pain
 Dialysis or renal transplant.
Angiokeratomas
 Farber’s disease
Cause
 Deficiency of the enzyme called ceramidase.
 Resulting in accumulation of ceramide in joints , tissues
and central nervous system.
Clinical features
 Dyspnea
 Dysphagia
 Vomiting
 Arthritis
 Horseness
 Xenthemas
 Joint contractures
Treatment
 no specific treatment for Farber’s disease.

 Most children with the disease die by age

2.
 Krabbé disease
Cause
 deficiency of the enzyme beta galactactosidase.
 Resulting in accumulation of galactocerebrosides in
white matter of CNS and peripheral nerves.
Clinical features
 Onset usually before age 6 months
 Hypertonia
 Seizures
 Spasticity
 Irritability
 Optic atrophy and blindness
Diagnosis
 Characteristic grouping of cells into globoid
bodies in white matter of brain.
 Demyelination of nerves and degeneration
and destruction of brain cells.
Treatment
 No specific treatment

 Bone marrow tranasplantation helpful in

some patients.
 Metachromatic
leukodystrophy
Cause
 Due to deficiency of enzyme arylsulfatase A.
 Resulting in accumulation of sulfatides in CNS, peripheral
nerves and kidneys.
Clinical features
 Normal at birth
 Develop difficulty in walking and tendency to fall followed
by intermittent pain in arms and legs.
 Progressive loss of vision leading to blindness.
 Developmental delays.
 Dementia.
Treatment
 Treatment is symptomatic and supportive.
 Bone marrow transplantation may delay
progression of the disease in some casses.
 Gangliosidosis
 Two groups
1. GM 1 Gangliosidosis5
Cause
 Due to deficiency of enzyme beta galactosidase
 Resulting in abnormal storage of acidic lipid
materials particularly in nerve cells of central
and periphel nervous system.
Types
a) Infantile
 Neurodegeration
 Seizures
 Hepatosplenomegally
 Coarsning of fascial features
 Skeletal irregularites
 Distended abdomen
 Deafness
 Blindness
Adult type
 Atrophy
 Dystonia
 Corneal clouding
 Angiokeratomas on lower part of trunk.
2. GM 2 Gangliosidosis
Cause
 Due to deficiency of enzyme beta hexosaminidase.
 Types
1. Tay-Sachs disease
Cause
 Due to deficiency of enzyme beta hexosaminidase A.
 Resulting in accumulation of gangliosides in nerve cells.
 Clinical features
 Initially normal
 Sign and symptoms begin at age of six months
 Rapid and progressive neurodegeneration Cherry red
 spots in retinas
 Dementia
 Deafness
 Blindness
 Seizures
Treatment
 No specific treatment
 Symptomatic and supportive
 Anticonvulsants for seizuress
2. Sandhoff disease
Cause
 Due to deficiency of enzyme beta hexosaminidase
A and B.
 Resulting in accumulation of gangliosides and
globosides in nerve cells.
Clinical features
 Same as Tay-sachs disease plus visceral
involvement i.e hepatosplenomegally.
Treatment
 Same as Tay-sachs disease.
 Diagnosis
 Diagnosis is made through clinical
examination, biopsy, genetic testing,
molecular analysis of cells or tissues, and
enzyme assays (testing a variety of cells or
body fluids for enzyme deficiency). In
some forms of the disorder, a urine
analysis can identify the presence of stored
material.
Vitamin deficiency
 VITAMIN A
NIGHT BLINDNESS
VITAMIN B2
PELLAGRA

VITAMIN C
SCURVY

VITAMIN B12
PERNICIOUS
ANEMIA

VITAMIN B7
ALOPECIA

VITAMIN B1
BERI-BERI
 References
 Lehninger,principles of biochemistry.
 Stryer,biochemistry.s
 Lippincott’s,biochemistry.
 Tietz,clinicil chemistry.
 CMDT by Lawrence.
 Online resources
 http://www.ninds.nih.gov
 http://emedicine.medscape.com
 http://www.sharecare.com
 http://www.britannica.com