Lipid Chemistry and Applications to Health
(9-24-20) because the latter is polar.
I. Overview and Chemistry of Lipids
 Lipids have long hydrocarbon
composition
 Biomolecules are polymers
 Not all lipids molecules are comprised
of fatty acid. Only SOME. Steroid is an
example.
 Fatty acids have functional groups in
the form of carboxylic acid (-COOH)
 Fatty acids have functional groups in
the form of carboxylic acid
(-COOH_
 Biological wax have ester groups
 Basic unit is 4 hydrocarbon ring forms
 Phosphate can interact with water
 Most phospholipids have hydrocarbons
Five Categories of Lipids based on function.
 Bond breakage releases energy.
Longer hydrocarbon chain = greater
energy. 2X energy in lipids than
carbohydrates.
 Carbohydrate = short-term. Lipids long
= term
 Energy Use of lipids has ketone
byproducts. Ketone can lend to cellular
damage.
 Triglyceride most common and it is a
storage forms of fats.
 Cholesterol doesn’t have fatty acids.
 Non-polar lipids are insoluble in H2O
 Lipids are digested through emulsifiers
in the form of bile acids.
 Bile acids disperse the fats into smaller
particles for digestion.
 Long hydrocarbon chain renders the
-COOH functional group weaker in
effect.
 Smaller fragments = greater exposure
to -COOH = Water soluble.
 Protective coating lipids helps in the
protection against water.
Types of Fatty Acids
A. Saturated
 Contains the maximum number of
hydrogen atom bound to carbon in a
single bond.
 Linearity = greater vander waal’s forces
= greater stacking capability due to
regularity of shape = tend to solidify in
room temp.
 BAD FOR HEALTH; can deposit in
blood vessels.
B. Unsaturated
- Monounsaturated
 Double bonds are electrophylic
 One double bond
- Polyunsaturated
 Many double bond.
-Trans Unsaturated fatty acid
 Becomes linear due to trans-isomerism
 Different orientation of -H
 Linearity lend by structure = greater
vander waal’s forces = greater stacking
capability due to regularity of shape =
tend to solidify in room temp.
 BAD FOR HEALTH; can deposit in
blood vessels.
-Cis Unsaturated fatty acid
 Becomes kinked due to cis-isomerism
 Same orientation of -H
 Bends/Kinks = weaker vander waal’s
forces = weaker stacking capability due
to irregularity of shape = tend to liquefy
in room temp.
 HEALTHY; will be released
Nomenclature

Delta Method
 “[carbon atoms]:[double bonds](Delta
sign and double bond location in
superscript)”
Omega method
 Same but counting starts at the
opposite of -COOH and instead of delta
use Omega
 Found in fishes. It is healthy.
Water Solubility and Melting Point of Fatty
Acids
 Greater hydrocarbon chain = lower
solubility = greater melting point
 Double bond = liquid fatty acids
(trans-fact exception)
 Greater degree of unsaturation =
greater double bonds = lower melting
point
 Carboxylic acid group are NOT included
in the double-bond counting.
II. Triaglycerol or Triglyceride
 Dehydration process (reaction between
hydroxyl group and fatty acid group) will
lead to ester functional group to join
glycerol and fatty acids, creating
triglyceride and H2O.
 Fats are saturated or trans fats. Solid at
room temperature.
 Oils are bent. Inhibits stacking of fatty
acids, hence they are liquid at room
temperature.
 Both are triglycerides. The difference is
in the saturation.
Hydrolysis
 Hydrolysis can be used to remove
triglyceride into glycerol and fatty acids.
E.g., lipase.
Hydrogenation
 Example of electrophilic addition
 Double-bond turns into single bond.
 Example is peanut oil. Hydrogenation
will cause the oil to become a butter
due to the stacking capability from the
single bonds.
Saponification

Acetyl-coenzyme A will add 2 carbon atoms

 Produce glycerol and fatty acids with ALWAYS. Odd numbers are uncommon in
salts. normal conditions.
 Has greater polarity = greater H2O III. Membrane Lipids
affinity.
 Grease can bind to the tail of the COOH
salt.
 Non-polar tail binds to grease; polar
head binds to H2O.

1. Phospholipid
 2 Fatty acids and 1 phosphate group

 Grease becomes a ligand around the

micelle, promoting stain removal.

 Short-chain aldehydes are created

through oxidation.
 Lack of anti-oxidants can promote
rancidity and a change in smell.
Anti-oxidants promote greater shelf-life
among cans.
 Free radicals - substance with high EN.
E.g., H2O2, O2- (produced in the
human body in limited concentrations).
They can promote oxidation.
 Free-radicals are unstable due to
unpaired electrons. Free radicals will
steal electrons from stable molecules.
This loss of electron will change the
structure, causing tissue damage.
 To prevent free-radicals, anti-oxidants  Cholesterol is also a membrane lipids.
like vitamin E must be consumed to Made up of ring forms with 27 C atoms.
give free electrons. Important in lending rigidity of the
Classification of Fatty Acids membrane. Can also be converted into
bile acids (cholic acids, chuchu, and
eme).
 Made up of hydrocarbon rings.  Protein part = apoprotein/apolipoprotein
 All originated from cholesterol. = polar
 Side-chains make them different.

 Associated with hydrocarbon chain

 Mineralocorticoid- regulates Na and K.  Greatest denisty is HDL
 Cortisol - metabolism of glucose.  HDL = great density = more proteins
 Cortisone and prednisolone - used with  Proteins are important in transpo.
anti-inflammatory drugs.
 They are non-polar, meaning they can
enter the cell membrane.

 HDL is good because it will be the one

 Essential fatty acids
 All came from arachidonic acid.
 Prostoglandin causes vasodilation and
inflammaton.
 Leukotene - for inflammation
 Thromboxane - for blood clotting.
 Aspiring inhibits thromboxane, can lead
to abnormal clotting.
to store cholesterols in the liver.
 LDL is bad because it will be the one to
release cholesterol from liver.
 Despite being ring-forms, cholesterol
are linear, causing deposition.
V. Pathogenesis

 Formation int tunica intima

IV. Lipoproteins
 Proteins + lipids
 Used for transportation
 Blood has O2. Oxidation will cause
tissue damage from agents. Oxidants
will steal electrons. Atherosclerosis can
also cause tissue damage. Tissue
damage will cause cholesterol to go into
deeper layers aka tunica.
 Macrophage will control the
accumulation of lipids by eating the
cholesterol. This will create foam cells.
Foam cells can die if too much
cholesterol is ingested. Inflammatory
substances will then be released
causing accumulation of different
substances.

 Ruptured foam cells will release

engulfed cholesterol = causes
inflammation, recruiting more
substances into the site = accumulation
of cholesterol in the blood vessel =
vasoconstriction = leads to clotting from
thrombus preventing blood flow.