class of lipoprotein _ biochemistry

1. Kathiravan Kaniasan (kathi_darkknight@ymail.com)
Fikri Abdullah Zawawi ( fikriaz_1331@yahoo.com)
Salsabiila Solahuddin (salsabiila4392@gmail.com )
Mohd Amil Abd Latiff (Mohdamil2310@yahoo.com )
Doc. Ing. Jan Vacek, Ph.D.

2.  WHAT IS LIPOPROTEIN?
 Spherical macromolecular complexes of lipids and specific protein.
 This is because our body’s lipids ( triglycerides & cholesterol ) are insoluble in
circulating plasma (blood)
 So, those lipids must be packaged with protein to make them dissolve in plasma
and can be transport to peripheral tissues.
CLASSES OF LIPOPROTEIN & THEIR ROLE IN
TRANSPORT CHOLESTEROL
Source : http://www.docstoc.com
* in general, as density of lipoprotein
increases, the size of the particles
decreases
Apolipoprotein =
1. specific lipid binding protein
attach to the surface .
2. Intracellular recognition for
exocytosis of the nascent particle
after synthesis.
3. Activation oflipid processing
enzymes in bloodstream.

3. 
 There are 5 main classes :
1. Chylomicrons (CM)
 Produced in intestinal epithelial cells from dietary fat
 Carries triacylglycerol in blood.
2. Very Low Density Lipoprotein (VLDL)
 Prodeuced in liver, mainly from dietary carbohydrate
 Carries triacylglycerol in blood
3. Intermediate Density Lipoprotein (IDL)
 Produced in blood (remnant of VLDL after triacylglycerol digestion)
 Endocytosed by liver or converted to LDL
4. Low Density Lipoprotein (LDL)
 Produced in blood (remnant of IDL after triacylglycerol digestion-end product of VLDL)
 Contain high concentration of cholesterol and cholesteryl esters
 Endocytosed by liver and peripheral tissues
5. High Density Lipoprotein (HDL)
 produced in liver and intestine.
 Exchange protein and lipids with other lipoproteins.
 Funtion in return of cholesterol from peripheral tissues to liver.
CLASSIFICATIONS OF LIPOPROTEINS

4. 
Source : www.intechopen.com

5. 
 Keep their component lipids soluble as they transport them in plasma.
 Provide efficient mechanism for transporting their lipid contents to
tissue.
 Maintaining cholesterol homeostasis, transporting molecule from site
to site and lastly to liver for excretion.
WHAT ARE THEIR FUNCTIONS ?

6. 
 WHAT IS CETP?
 Cholesteryl ester tranfer protein.
 CETP facilitates the transport of cholesteryl ester and triglycerides
between lipoproteins.
 It collects triglycerides from VLDL or LDL and exchanges them for
cholesteryl esters from HDL and vice versa.
 CETP can be both antiartherogenic or proartherogenic.
FUNCTION OF CETP & LCAT IN
CHOLESTEROL METABOLISM

7. 
Source :
http://content.onlinejacc.org/article.aspx?articleid=1137247

8. 
 WHAT IS LCAT ?
 Lecithin-cholesterol acyltransferase.
 Also called PCAT (Phosphotidylcholine-cholesterol acyltranferase)
 Synthesised by liver.
 Is an enzyme that converts free cholesterol into cholesteryl esters
( more hydrophobic form of cholesterol ) which is then
sequestered into the core of lipoprotein.
 The enzyme is bound to high-density lipoproteins (HDLs) and
low-density lipoproteins (LDLs) in the blood plasma.
 Causes the cholesteryl ester-poor HDL3 to turn into cholesteryl
ester-rich HDL2.
 It then carries these esters to liver.

9. 
Source : www.pace-cme.org

10.  Cholestrol is insoluble in water, so it is transported
in the blood plasma by lipoproteins.
 2 types of lipoprotein – LDL and HDL.
 LDL transport cholestrol from the liver to the tissues
including the artery walls.
 HDL therefore help to protect arteries against
atherosclerosis.
THE RELATIONSHIP OF OXIDISED LDL &
DYSFUNCTIONAL HDL TO
ATHEROSCLEROSIS

11. 
 VLDL  LDL by lipoprotein lipase
 transported across the intact Endothelium and
becomes trapped in the ECM (Extracellular Matrix)
of the subendothelial space oxidation (Oxidized
LDL).  goes directly within the inner-lining
endothelium of any artery in the body 
macrophages, and platelets at the site of the vessel,
forming a plaque that begins to grow thicker 
atherosclerosis
Production of LDL

12.  HDL particles are formed by the addition of lipif to
apo-A1 ( an apolipoprotein made by liver and
intestine secreted into bloddstream.
 How HDL become dysfunction?
 When specific site on apo-A1 is oxidised.
 It will exerted a proinflammatory effect on endothelial cells.
 Dysfunctional HDL also increased redox activity and reduced
antioxidant properties.
 When it loss its function, it no longer can carry
cholesterol away from vessels to liver for removal –
cholesterol will accumulate in vessels – narrowing
the vessels.
Dysfunctional HDL to Atherosclerosis

13. 
 WHAT IS DYSLIPOPROTEINEMIAS ?
 The presence of abnormal concentrations of lipoproteins or
abnormal lipoproteins in the blood.
1. Hyperlipoproteinemia
2. Hypolipoproteinemia
DIAGNOSIS & MODERN TREATMENT OF
DYSLIPOPROTEINEMIAS

14. 
 In clinical routine, patient are screened for dyslipoproteinemia
by a standard lipid profile.
 Included in a lipid profile profile is the measurement of total
cholesterol, triglycerides, and the cholesterol of high density
lipoproteins (HDL-C).
 Occasionally, the exact diagnosis requires further testing, such
as measurement of apolipoprotein composition or
measurement of LDL particle size.
 For practical, clinical reasons dyslipoproteinemias are
commonly divided into hypercholesterolemia,
hypertriglyceridemia, mixed hyperlipidemia, and low HDL
cholesterol disorder.
Diagnosis of Dyslipoproteinemia

15. 
Source : www.telegraphindia.com

16. 
 Treatments depend on type of dyslipoproteinemia
1. Low-saturated-fat and low-choleterol diet
2. Cholestyramine, Colestipol, Lovastatin, Nicotinic
acid, Neomycin
3. Intestinal bypass
4. Carbohydrate restriction
5. Alcohol restriction
Treatment of dyslipoproteinemia

17. 
 1 in 5 men and 1 in 7 women die from CHD.
 There are 94,000 deaths from CHD in the UK each year.
 Death rates from CHD have fallen by 45% for people aged under 65
years in the last 10 years. This fall is fastest in those aged 55 years and
over. It is largely due to a reduction in major risk factors (mostly
smoking) and improvement in treatment and secondary prevention.
The fall is not as high as that in some other countries such as Australia
(48%) and Norway (54%).
 Death rates from CHD are highest in Scotland, and the North of
England, and lowest in the South of England. For more than 25 years
these rates have been consistently highest in Scotland.
EPIDEMIOLOGY

18. 
 Age
 CHD increases with age. This is a non-modifiable risk factor.
 Alcohol
 1 to 2 units of alcohol per day reduce the risk of CHD. Alcohol
increases HDL cholesterol and reduces thrombotic risk. Higher
levels of consumption increase risks from other causes.
 The World Health Report in 2002 estimated that 2% of CHD in
men in developed countries is due to excessive alcohol
consumption.
 Cholesterol
 The INTERHEART study suggested that 45% of heart attacks in
Western Europe are due to abnormal blood lipids.
 People with low levels of HDL cholesterol have an increased risk
of CHD and a worse prognosis after a myocardial infarction.
 In the UK, it is suggested that the target cholesterol is < 4 mmol/L
for people with diabetes or established CVD or for people at high
risk of developing CVD. People with HDL cholesterol <1 mmol/L
should also be considered for treatment.
Risk factor

19.  Richard A.Harvey Lippincott’s Illustrated Reviews
Biochemistry – 2011 –pages=173-219
 Dawn B.Marks, Allan D.Marks, Collen M.Smith- Basic Medical
Biochemistry- 1996- pages=487-540
 Prof Philip J. Barter, The Heart Research Institute,
http://atvb.ahajournals.org/content/23/2/160.full -
Arteriosclerosis, Thrombosis, and Vascular Biology. 2003; 23:
160-167
 Dayuan Li and Jawahar L. Mehta,
http://cardiovascres.oxfordjournals.org/content/68/3/353.full
, Oxidized LDL, a critical factor in atherogenesis -Oxford
JournalsMedicine Cardiovascular Research Volume 68, Issue
3Pp. 353-354
 Peter O. KwiterovichJr, title= diagnosis and Management of
Familial Dyslipoproteinemias, 2013, current cardiology report -
read 18th march 2014
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