Classification of Lipoproteins

with Clinical Significance

Submitted By
Muhammad Asad Ullah
#14488

Submitted To
Dr. Salman Khan
Biochemistry

Doctor of Physical Therapy

ABASYN UNIVERSITY PESHAWAR
4TH Semester – Spring 2020
Sr. No Contents
1 Introduction to Lipoproteins
2 Structure of Lipoproteins
3 Classification of Lipoproteins
Based on Density
Based on Electrophoretic Mobilities
Based on Nature of Apo-Protein Content
4 Clinical Significance of Lipoproteins
coronary heart disease
Fatty Liver
 Introduction to Lipoproteins
 Lipids absorbed from the diet and these are synthesized by the liver and adipose tissue
must be transported between various cells and organs for utilization and storage.
 Lipids are insoluble in water, the problem of transportation in the aqueous plasma is
solved by associating nonpolar lipids (triacylglycerols and cholesteryl esters) with
amphipathic lipids (phospholipids and cholesterol) and proteins to produce water-
miscible lipoproteins.
 Lipoproteins are the biochemical combination of both lipids and proteins. Many
enzymes, transporter, antigens and toxins are Lipoproteins.

Structure of Lipoproteins

 Lipoproteins consist of a nonpolar core and a single surface layer of amphipathic lipids
 The nonpolar lipid core consists of mainly triacylglycerol and cholesteryl ester and is
surrounded by a single surface layer of amphipathic phospholipid and cholesterol
molecules
 Lipoproteins are oriented so that their polar groups face outward to the aqueous medium.

Classification of Lipoproteins
Based on Density
There are five different types of lipoproteins in the blood, classified according to their
density. The main types of lipoproteins that are analyzed in a lipid panel includes

 very low-density lipoproteins (VLDS)

 low-density lipoproteins (LDL)
 high-density lipoproteins (HDL)
 Chylomicrons
 Intermediate Density Lipoprotein (IDL)

 very low-density lipoproteins (VLDS)

These lipoproteins consist of main triglycerides, some cholesterol molecules, and less protein. A
lot of fat a conjugated protein contains, the less density it has. during this case, very low-density
lipoprotein is a smaller amount dense than most lipoproteins due to its high lipoid composition.
Very low-density lipoprotein is formed within the liver and is liable for delivering triglycerides
to cells within the body, that is required for cellular processes. As triglycerides get delivered to
cells, very low-density lipoprotein is formed up less of fat and a lot of macromolecule, feat
steroid alcohol on the molecule. As this method happens, VLDL will eventually become an LDL
molecule
  low-density lipoproteins (LDL)

LDL consists of additional cholesterol than triglycerides and proteins as it contains less lipid and
additional protein compared to very low-density lipoprotein, its density is greater. LDL is
accountable for carrying cholesterol to cells that require it. Elevated LDL levels area Associated
with high risk of cardiovascular disorders. Certain forms of LDL—specifically smaller dense
LDL (Sd LDL) and oxidized LDL (ox LDL)—have been related to promoting the formation of
atherosclerosis by depositing fats on the walls of arteries within the body. as a result of increased
levels of LDL are associated with development of cardiovascular disorders, LDL is additionally
referred to as the “bad” cholesterol.

 high-density lipoproteins (HDL)

Compared to LDL, HDL consists of less cholesterol and more protein, making these lipoproteins
the densest. HDL is made in the liver and in the intestines. It is responsible for containing
cholesterol from cells back to the liver. Because of this, HDL is also considered the “good”
cholesterol.
There are also some other lipoproteins that also function in transporting fats to cells, but
are not commonly measured in a routine lipid panel. These include:

 Chylomicrons
These lipoproteins are the least dense out of all of the lipoproteins. These molecules are primarily
composed of triglycerides and a small amount of protein. Chylomicrons are responsible for transporting
lipids from the intestinal path to cells in the body.

 Intermediate Density Lipoprotein (IDL)

These lipoproteins are less dense than LDL molecules but denser than VLDL particles. As the
triglycerides on VLDL are broken down by the cells that need it, the particle becomes denser due to the
change in the lipid to protein ratio. This results in VLDL being changed into IDL. As triglycerides and
cholesterol are delivered to more cells in the body, IDL will gradually be converted into LDL
 Based on Electrophoretic Mobilities

 Lipoproteins may be separated according to their electrophoretic properties into α, pre β, β,

and broad beta lipoproteins.
 The mobility of a lipoprotein is mainly dependent upon protein content.
 Those with higher protein content will move faster towards the anode and those with
minimum protein content will have minimum mobility.
 HDL are -α, VLDL pre- β, LDL-β, and IDL are broad beta lipoproteins.
 Free fatty acid and albumin complex although not a lipoprotein is an important lipid fraction
in serum and is the fastest moving fraction.
 Chylomicrons remain at the origin since they have more lipid content.

Based on Nature of Apo-Protein Content

 One or more apolipoproteins (proteins or polypeptides) are present in each lipoprotein.
 he major apolipoproteins of HDL (α-lipoprotein) are designated A.
 The main apolipoprotein of LDL (β -lipoprotein) is apolipoprotein B (B100), which is found
also in VLDL.
 Chylomicrons contain a truncated form of apo B (B-48) that is synthesized in the intestine,
while B-100 is synthesized in the liver.
 Apo E is found in VLDL, HDL, Chylomicrons, and chylomicron remnants
 They can form part of the structure of the lipoprotein, e.g. apo B, structural component of
VLDL and Chylomicrons
 They are enzyme cofactors, e.g. C-II for lipoprotein lipase, A-I for lecithin: cholesterol acyl
transferase (LCAT), or enzyme inhibitors, e.g., apo A-II and apo CIII for lipoprotein lipase,
apo C-I for cholesteryl ester transfer protein
 They act as ligands for interaction with lipoprotein receptors in tissues, e.g. apo B-100 and
apo E for the LDL receptor, apo A-I for the HDL receptor.
 Clinical Significance of Lipoproteins

coronary heart disease

There is a correlation between coronary heart disease and lipoprotein size and composition is
present. Within the low-density lipoprotein (LDL) family the small LDL particles are associated
with increased risk of coronary heart disease. These particles also have increased apolipoprotein
(apo) B content. The appearance of these small LDL particles is the manifestation of complex
alteration of plasma lipoprotein metabolism. The LDL size is influenced by genetic, endocrine,
and environmental factors. Within the high-density lipoprotein (HDL) family the decrease of
larger HDL2 particles is associated with coronary heart disease. HDLs can also be separated
according to their apoprotein composition into particles containing lipoprotein (Lp)A-I only and
particles containing LpA-I and LpA-II. Most studies have shown that the concentration of LpA-
I-only particles decreases in coronary heart disease. HDLs are remodeled in the circulation and
this remodeling continues in vitro after the blood is taken. Therefore, adequate preservation of
blood samples is necessary

Fatty Liver

 It is an abnormal accumulation of certain fats (triglycerides) inside liver cells. Fatty livers
fall into two main categories-
 Hepatic triacylglycerol synthesis provides the immediate stimulus for the formation and
secretion of VLDL.
 Impaired VLDL formation or secretion leads to no mobilization of lipid components
from the liver, results in fatty liver.

More synthesis of Triglycerides

 High carbohydrate diet

 High fat feeding
 Starvation
 Diabetes mellitus
High carbohydrate diet stimulates de novo fatty acid synthesis by providing excess of Acetyl
CoA and high fat feeding provides more flux of fatty acids from the diet that can be esterifies to
provide excess triglycerides

Defective VLDL synthesis

The second type of fatty liver is usually due to a metabolic block in the production of plasma
lipoproteins, thus allowing triacylglycerol to accumulate. The lesion may be due to –
 A block in apolipoproteins synthesis
 Protein energy Malnutrition
 Impaired absorption
 Presence of inhibitors of endogenous protein synthesis