BIOCHEMISTRY

LIPIDS
 LECTURE PLAN:
1. Lipids defination.
2. Function of Lipids.
3. Classification of Lipids.
4. Biosynthesis of Triglycerides.
5. Nonglyceride lipids.
6. β-oxidation of fatty acids.
7. Pathology of lipid metabolism.
 • The difference between
saturated and unsaturated fat
lies in the number of double
bonds in the fatty acid chain.
Saturated fatty acids lack
double bonds between the
individual carbon atoms, while
in unsaturated fatty acids there
is at least one double bond in
the fatty acid chain.
• Saturated fats tend to be solid
at room temperature and from
animal sources, while
unsaturated fats are usually
liquid and from plant sources.
 Phospholipids (phosphoglycerides)
compound lipids containing phosphoric acid, in
addition to fatty acids, nitrogenous base and alcohol.
There are two classes of phospholipids:
-(A) glycerophospholipids (phosphoglycerides)
-(B) sphingophospholipides (sphingomyelins)

Principal structure of
phospholipids
(phosphoglyceride)
1.Phosphatidic acid glycerophospholipids (phosphoglycerides)1

-phosphatidic acid – simplest phospholipid, does not occur in

good concentration in the tissues – basically it is an
intermediate in the synthesis of triacylglycerols and
phospholipids
Other glycerophospholipids containing different nitrogeneous bases or other groups
2.Lecitins (phosphatidylcholin)[dipalmitol lecitin;
lysolecitin] glycerophospholipids (phosphoglycerides)2

-lecithins (phosphatidiylecholine) – [λεκιθος – agg yolk]

– storage form of body’s choline [dipalmitoyl lecithin – in
lungs; lysolecithin – is formed by removal of fatty acid either
at C1 or C2 of lecithin]
3.Cephalins (phosphatidylethanolamine)
glycerophospholipids (phosphoglycerides)3

-cephalins (phosphatidylethanolamine) – ethanolamine is

the nitrogenous base present; lecitine and cephaline differ with regard to
the base
4.Phosphatidylinositol glycerophospholipids
(phosphoglycerides)4

-phosphatidylinosotol – important component of cell membranes

– stereoisomer myo-inositol is attached to phosphatidic acid.
5. Phosphatidylserine glycerophospholipids (phosphoglycerides)5

-phosphatidylserine – amino acid serin is present in it

6.Plasmalogens glycerophospholipids (phosphoglycerides)6

-plasmalogens – fatty acid is attached by an ether linkage at C1 of

glycerol in the glycerophospholipids.
(choline, inositol, serin may substitute ethanolamine in plasmalogens)
7.Cardiolipins glycerophospholipids (phosphoglycerides)7

-cardiolipin – first isolated from heart muscle – consists of two

molecules of phosphatidic acid held by an additional glycero through
phoshate group
-sphingophospholipides (sphingomyelins)1 (space-
filling model of molecule)
 Cholesterol (χολε-bile) [C27H46O]
Exclusively found in animals, is the most abundant animal sterol.
Was first isolated from bile.
Cholesterol literally means ‘solid alcohol from bile’
It has one hydroxyl group at C3 and
double bond between C5 and C6.
An 8 carbon aliphatic side chain is attachanded to C17,
it also contains a total 5 methyl groups (C18, C19, C21, C26, C27)
β-oxidation of fatty acids 1 (whole)

In biochemistry and metabolism, beta-oxidation is

the catabolic process by which fatty acid molecules are
broken down[1] in the cytosol in prokaryotes and in
the mitochondria in eukaryotes to generate acetyl-CoA,
which enters the citric acid cycle, and NADH and FADH2,
which are co-enzymes used in the electron transport chain.
It is named as such because the beta carbon of the fatty
acid undergoes oxidation to a carbonyl group. Beta-
oxidation is primarily facilitated by the mitochondrial
trifunctional protein, an enzyme complex associated with
the inner mitochondrial membrane, although very long
chain fatty acids are oxidized in peroxisomes.
β-oxidation of fatty acids (I phase) activation
β-oxidation of fatty acids (II phase)
β-oxidation of fatty acids (III phase)
Beta oxidation
oxidation
hydration
oxidation
cleavage
Pathology of lipid metabolism
Most commonly, the lipid metabolism pathology is manifest as hyperlipemia (elevated concentration of lipids in
blood) and tissue lipidoses (excessive lipid deposition in tissues). Normally, the lipid contents in the blood plasma are:
• total lipids: 4-8 g/L
• triglycerides: 0,5-2,1 mmol/L
• total phospholipids: 2,0-3,5 mmol/L
• total cholesterol: 4,0-9,8 mmol/L (esterified cholesterol accounts for 2/3 of total cholesterol).
Hyperlipemia may manifest itself by an increased concentration of lipids, or certain groups thereof. For example,
hypercholesterolemia and hypertriglyceridemia may be mentioned in this connection. Since practically all the blood plasma
lipids make part of lipoproteins, hyperlipemias may be reduced to one of the hyperlipoproteinemia forms which differ in the
varied rations of plasma lipoproteins of different groups.
Hyperlipoproteinemia is characterized by the enhanced content of chylomicrons in the blood plasma;
simultaneously, the percentage of - and -lipoproteins may be lowered. The triglyceride content is 8-10 times above the
norm, while cholesterol does not exceed the normal level.
Secondary hyperlipoproteinemias, which arise from a disordered lipid tissue metabolism or its impaired control,
are observed in diabetes mellitus, thyroid gland hypofunction, alcoholism, etc.
Tissue lipidoses. Hyperlipoproteinemias may lead to tissue lipidoses and also arise from hereditary defects of the
enzymes involved in the synthesis and breakdown of lipids in the tissues.
Atherosclerosis is a wide-spread pathology, manifested chiefly by the deposition of cholesterol in arterial walls,
which results in the formation of lipids plaques (atheromas). Lipid plaques are specific foreign bodies around which the
connective tissue develops abnormally (this process is called sclerosis). -Lipoproteins and, partly, pre- -lipoproteins
containing much cholesterol exhibit atherogenic properties.
 Ketosis is a pathologic state produced by an excess of ketone bodies in
the organism. Ketosis may be regarded as lipid metabolism pathology with a
certain reserve, since excessive biosynthesis of ketone bodies in the liver is
sequent upon an intensive hepatic oxidation not only of fatty acids, but also of
ketogenic amino acids. The breakdown of carbon frameworks of these amino
acids leads to the formation of acetyl-ScoA and acetoacetyl-ScoA, which are
used in ketogenesis.
The ketosis is accompanied by ketonemia and ketonuria, which is
manifested by the increased concentration of ketone bodies in blood and their
excretion in the urine. In an aggravated form of ketosis, the ketone body
concentration in blood may be as high as 10-20 mmol/L. The ketone bodies
are normally present in the daily urine in trace amounts, while in pathology, 1
to 10 g (or even more) of ketone bodies per day is excreted in the urine.
Most commonly, ketonemia and ketonuria are observed in diabetes
mellitus (the manifest ketosis symptoms are dependent on the extent of
diabetes mellitus), as well as in prolonged starvation or in “steroid” diabetes.
YANA BURMISTROVA