ATHEROSCLEROSIS AND CORONARY HEART DISEASE

ATHEROSCLEROSIS AND CORONARY HEART DISEASE


Robbins and Angell (1976) define atherosclerosis as follows : “ Basically, the disorder comprises the development of focal atheromas, within the intima and inner portion of the media. As the disorder advances, the atheromas undergo a variety of complications calcification, internal hemorrhages, ulceratin, and sometimes superimposed thrombosis” [1]. Atherosclerosis (ath-er-o-skler-O-sis) is a disease in which plaque (plak) builds up on the insides of your arteries. [See images].

Arteries are blood vessels that carry oxygen-rich blood to your heart and other parts of your body. Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. Over time, plaque hardens and narrows your arteries. The flow of oxygen-rich blood to your organs and other parts of your body is reduced. This can lead to serious problems, including heart attack, stroke, or even death. Some people with atherosclerosis have no signs or symptoms. They may not be diagnosed until after a heart attack or stroke.

Atherosclerosis can affect any artery in the body, including arteries in the heart, brain, arms, legs, and pelvis. As a result, different diseases may develop based on which arteries are affected [2].

1. Coronary artery disease (CAD). This is when plaque builds up in the coronary arteries. These arteries supply oxygen-rich blood to your heart. When blood flow to your heart is reduced or blocked, it can lead to chest pain and heart attack. CAD also is called heart disease, and it's the leading cause of death in the United States.
2. Carotid (ka-ROT-id) artery disease. This happens when plaque builds up in the carotid arteries. These arteries supply oxygen-rich blood to your brain. When blood flow to your brain is reduced or blocked, it can lead to stroke.
3. Peripheral arterial disease (PAD). This occurs when plaque builds up in the major arteries that supply oxygen-rich blood to the legs, arms, and pelvis. When blood flow to these parts of your body is reduced or blocked, it can lead to numbness, pain, and sometimes dangerous infections.

In about 99 % of cases, coronary artery disease is due to atherosclerotic changes. Atherosclerotic vascular disease, in particular, coronary heart disease (CHD), is a major cause of human morbidity and mortality in both industrialised and developing countries. These results support the proposal that early control of risk factors is likely to prevent or delay progression of atherosclerosis and prevent or delay the onset of CHD. [1,3]. The CHD risk factors are associated with lipids in arterial tissue just as they are associated with gross and microscopic lesions [4,5,6,7].

The Incidence of CHD

In the UK, for example, nearly 170,000 people die each year as a result of CHD (25% of all deaths). Similarly, in the USA, CHD causes around 700,000 (40% of) deaths each year. However, there are very wide variations in the incidence of CHD worldwide. For instance, data from the World Health Organization (WHO) MONItoring of trends and determinants in CArdiovascular disease (MONICA) study assessing CHD and risk factors in 38 populations from 21 countries show that age-standardised annual cardiovascular event (fatal and non-fatal) rates (during 1985–1987) in men ranged from 76/100,000 in Beijing, China to 915/100,000 in North Karelia, Finland, and in women, from 30/100,000 in Catalonia, Spain to 256/100,000 in Glasgow, UK. Also, while CHD mortality rates in many industrialised countries have fallen over the past 20–30 years (e.g. by 50–60% in Australia, Canada, Japan and the USA), there have been striking increases in the rates in eastern/central Europe (e.g. 25–35% rises in Romania and Poland) and in developing countries. [8]

Prevention

Medical priorities [9]; In the context of a comprehensive population strategy— to reduce tobacco use, encourage healthy food choices and increase physical activity for the whole population — the medical priority is to focus on those who have developed symptoms of coronary heart disease or other major atherosclerotic disease, and those who are at high risk of developing such diseases in the future.

The priorities for preventive cardiology are:

1. Patients with established coronary heart disease or other atherosclerotic disease.
2. Healthy individuals who are at high risk of developing coronary heart disease or other atherosclerotic disease, because of a combination of risk factors—including smoking, raised blood pressure, lipids (raised total cholesterol and low density lipoprotein (LDL)-cholesterol, low high density lipoprotein (HDL)-cholesterol and raised triglycerides) raised blood glucose, family history of premature coronary disease—or who have severe hypercholesterolaemia or other forms of dyslipidaemia, hypertension or diabetes.
3. Close relatives of patients with early onset coronary heart disease or other atherosclerotic disease, and of healthy individuals at particularly high risk.
4. Other individuals met in connection with ordinary clinical practice.

Secondary prevention [9]; Patients with coronary heart disease or other atherosclerotic disease :
Lifestyle; Lifestyle changes depend on the readiness of coronary and other high risk patients to modify their behaviour. When patients develop symptoms of coronary heart disease, or are found to be at high risk, this is an ideal opportunity to review lifestyle. Many will consider making appropriate changes and, with professional and family support, can do so for life.

Stop smoking tobacco; Patients should be professionally encouraged and supported to stop smoking all forms of tobacco for life.

Make healthy food choices; For a patient with atherosclerotic disease the dietetic goals are:

1. To reduce total fat intake to 30% or less of total energy intake, the intake of saturated fat to no more than one third of total fat intake, and the intake of cholesterol to less than 300 mg per day.
2. To achieve the reduction in saturated fats by replacing them in part with monounsaturated and polyunsaturated fats from both vegetable and marine sources, as well as with complex carbohydrates.
3. To increase the intake of fresh fruits, cereals and vegetables.
4. To reduce total calorie intake when weight reduction is needed.
5. To reduce salt and alcohol use when blood pressure is elevated.

Increase physical activity; All patients should be professionally encouraged and supported to increase their physical activity safely to a level associated with the lowest risk of vascular disease.

Treatment of Atherosclerosis and CHD

The main treatment for atherosclerosis and CHD is lifestyle changes. You also may need medicines and medical procedures. These, along with ongoing medical care, can help you live a healthier life. You must consult to your pharmacist and doctor for drugs (medicines) treatment. Your pharmacist and doctor can help decide which type of drug is best for you.

Andi Surya Amal
Email : suryaamal88@gmail.com

Reference :

1. Sokolow M, Mcllroy (1979), Clinical Cardiology, Lange Medical Publications-California,124125
2. Healthscout’s site; Description of Atherosclerosis
3. Malcoma T.G., McMahanb C.A., et al, (2009) Associations of Arterial Tissue Lipids with Coronary Heart Disease Risk Factors in Young People, Atherosclerosis Journal, Vol. 203-2; 515-521.
4. Gupta S and Camm A.J.(1999), Developments in Cardiovascular Medicine; Chronic Infection, Chlamydia And Coronary Heart Disease, Springer Netherlands Publisher. Vol. 218, 1
5. Wood D, Backer G.D. et.al. (1998), Prevention of coronary heart disease in clinical practice, Recommendations of the Second Joint Task Force of European and other Societies on Coronary Prevention, European Heart Journal 19, 1434–1503
6. Mangion D.M and Roy S.S,(1993), Serum lipids and coronary heart disease in British elderly, Postgrad Med J 69, 609 – 614
7. Wierzbicki A.S, Mikhailidis D.P, (2002), The Relationship Between HDL-C, Atherosclerosis and Coronary Heart Disease, Librapharm Limited, Curr Med Res Opin;18(1)
8. Ingelsson E, Schaefer E. J.(2007) Clinical Utility of Different Lipid Measures for Prediction of Coronary Heart Disease in Men and Women, JAMA;298:776-785
9. Moshides, J. (1987), High Density Lipoprotein Free Cholesterol and Other Lipids in Coronary Heart Disease, Journal of The American Heart Association; Arterioscler Thromb Vasc Biol ;7;262-266

TREATING HIGH CHOLESTEROL

Treating High Cholesterol

The main goal of cholesterol-lowering treatment is to lower your LDL level enough to reduce your risk of developing heart disease or having a heart attack. The higher your risk, the lower your LDL goal will be. The following of Adult Treatment Panel (ATP) III; there are two main ways to lower your cholesterol:

1. Therapeutic Lifestyle Changes (TLC)–includes a cholesterol-lowering diet (called the TLC diet), physical activity, and weight management. TLC is for anyone whose LDL is above goal.
2. Drug Treatment–if cholesterol-lowering drugs are needed, they are used together with TLC treatment to help lower your LDL.

To find your LDL goal (the following of ATP III guidelines); the main parts of your risk category below.

Category I, Highest Risk, your LDL goal is less than 100 mg/dL. If your LDL is 100 or above, you will need to begin the TLC diet. If your LDL is 130 or higher, you will need to start drug treatment at the same time as the TLC diet. If your LDL is 100 to 129, you may also need to start drug treatment together with the TLC diet. Even if your LDL is below 100, you should follow the TLC diet on your own to keep your LDL as low as possible.

Category II, Next Highest Risk, your LDL goal is less than 130 mg/dL. If your LDL is 130 mg/dL or above, you will need to begin treatment with the TLC diet. If your LDL is 130 mg/dL or more after 3 months on the TLC diet, you may need drug treatment along with the TLC diet. If your LDL is less than 130 mg/dL, you will need to follow the heart-healthy diet for all Americans, which allows a little more saturated fat and cholesterol than the TLC diet.

Category III, Moderate Risk, your LDL goal is less than 130 mg/dL. If your LDL is 130 mg/dL or above, you will need to begin the TLC diet. If your LDL is 160 mg/dL or more after you have tried the TLC diet for 3 months, you may need drug treatment along with the TLC diet. If your LDL is less than 130 mg/dL, you will need to follow the heart-healthy diet for all Americans.

Category IV, Low-to-Moderate Risk, your LDL goal is less than 160 mg/dL. If your LDL is 160 mg/dL or above, you will need to begin the TLC diet. If your LDL is still 160 mg/dL or more after 3 months on the TLC diet, you may need drug treatment along with the TLC diet to lower your LDL, especially if your LDL is 190 mg/dL or more. If your LDL is less than 160 mg/dL, you will need to follow the heart-healthy diet for all Americans. To reduce your risk for heart disease or keep it low, it is very important to control any other risk factors you may have such as high blood pressure and smoking.

Writer’s note; you must consult to your doctor for drug treatment. Self medication may be can cause new problem include side effect and drugs interaction if you are to take other drugs. Your doctor can help decide which type of drug is best for you. But, Therapeutic Lifestyle Changes (TLC) is a set of things you can do to help lower your LDL cholesterol. The main parts of TLC are: The TLC Diet, Weight Management and Physical Activity.

Because you already have heart disease or are at high risk for developing it, you should start on the TLC Diet right away. The TLC Diet is a low saturated fat, low cholesterol diet that will help to reduce your blood cholesterol level to decrease your chance of developing heart disease, future heart attacks, and other heart disease complications. Just enough calories to achieve or maintain a healthy weight and reduce your blood cholesterol level. (Ask your doctor or registered dietitian what is a reasonable calorie level for you.)[see also in nhlbi.nih]

The information shown in Table 1-2 may be helpful for the physician both for dietary and lifestyle assessment and for guidance of the patient adopting TLC recommendations. The table is compiled from current ATP III dietary recommendations, Dietary Guidelines for Americans (2000), Obesity Education Initiative (OEI) guidelines for weight reduction, and the Surgeon General’s Report on Physical Activity. See in tables below.




Weight reduction of even a few pounds will reduce LDL levels regardless of the nutrient composition of the weight loss diet, but weight reduction achieved through a calorie-controlled diet low in saturated fatty acids and cholesterol will enhance and sustain LDL cholesterol lowering.

Weight loss through reduced caloric intake and increased levels of physical activity should be encouraged in all overweight persons. Prevention of weight gain also should be emphasized for all person.

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THE PRINCIPAL CHOLESTEROL DISORDERS

THE PRINCIPAL CHOLESTEROL DISORDERS


Cholesterol is a fat-like substance (lipid) that is present in cell membranes and is a precursor of bile acids and steroid hormones. Cholesterol travels in the blood in distinct particles containing both lipid and proteins (lipoproteins). Three major classes of lipoproteins are found in the serum of a fasting individual: low density lipoproteins (LDL), high density lipoproteins (HDL), and very low density lipoproteins (VLDL). Another lipoprotein class, intermediate density lipoprotein (IDL), resides between VLDL and LDL; in clinical practice, IDL is included in the LDL measurement.

Each class contains differing proportions of fat and protein. VLDL consist of five-sixths triglycerides and one-sixths cholesterol. While circulating in the blood, VLDL is transformed first to intermediate-density lipoprotein (IDL), which is 30% cholesterol and 40% triglycerides, and then to low-density lipoprotein (LDL), which carries from 60% to 75% of the total blood cholesterol. High levels of LDL-cholesterol are associated statistically with an increased risk of coronary heart disease (CHD) – the higher the level, the higher the risk.

HDL carries less than 25% of the total blood cholesterol. It is thought to assist with the removal of LDL-cholesterol from the blood and body tissues. High levels of HDL-cholesterol appear to be protective against coronary heart disease – the higher the LDL level, the lower the risk.

The principal cholesterol disorders are classified into 5 mayor types according to the nature of the lipoprotein abnormality and associated clinical features. Type I and V are not associated with the development of atherosclerosis. Type II, III and IV are associated with the atherosclerotic process that causes coronary heart disease and peripheral vascular disorders. The lipoprotein features of these classes are as follows :
Type IIa: increased total cholesterol and LDL-cholesterol; normal triglycerides.
Type IIb: increased total cholesterol, LDL-cholesterol and VLDL; moderately increased triglycerides.
Type III: increased IDL-cholesterol (abnormal form); increased triglycerides.
Type IV: normal total cholesterol, increased VLDL, decreased HDL-cholesterol; increased triglycerides.

See also on the classification of lipoprotein abnormality according to Frederickson-WHO in the table below.


Cholesterol Management Program
Peoples who might benefit from evaluation at the Center include :

1. Diabetics with low HDL (“good”) cholesterol and high triglycerides
2. Any people with total cholesterol > 220 AND triglycerides > 200
3. Markedly elevated LDL (“bad”) cholesterol > 200
4. Isolated low HDL cholesterol (normal total cholesterol and triglycerides)
5. Strong family history of early heart disease (males < 55 years old, females < 65 years old)
6. Need for combination therapy (2 or more cholesterol drugs)
7. Peoples with prior heart attack, stroke, or revascularization procedure (bypass or angioplasty) who are having evidence of disease progression despite treatment
8. Intolerant of cholesterol drugs, especially “statins” like Lipitor, Crestor, Zocor, Pravachol, Lescol, Mevacor, and Vytorin

It is also important to lose weight if you are overweight, to be physically active, and to not smoke. Discuss your treatment plan with your doctor.


Reference :

1. NCEP; Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) – Final Report, NIH Publication No. 02.5215, September 2002
2. Long JW, The Essential Guide to Prescription Drugs, HarpersCollins Publisher, Inc. 1993 Edition, 50-52
3. Wormser H (PhD,Professor of Medical Chemistry), Lipoprotein Metabolism. Power Point Presentation, PSC 3110 Fall 2004
4. http://www.heartoflouisiana.com/programs.php

CHOLESTEROL DISORDERS

CHOLESTEROL DISORDERS

Other Names :
Dyslipidemia, hypercholesterolemia, hyperlipidemia, hyperlipoproteinema, hypertriglyceridemia, lipid transport disorders, lipoprotein disorders. (The article focused to ‘hyper', although ‘hypo’ like hypocholesterolemia includes cholesterol disorders).

Prevalence

For example in USA : The following statistics relate to the prevalence of High Cholesterol; 19% of adults aged 20–74 in USA 1994 (US Government Statistics). Prevalence statistics by age group with high cholesterol in the US 1999-2000 (Health United States, 2003, NCHS) :

1. Age group for men : [11% of men aged 20-34], [21.1% of men aged 35-44], [22.9% of men aged 45-54], [16.5% of men aged 55-64], [19.2% of men aged 65-74], [10.1% of men aged over 75].
2. Age group for women : [9.3% of women aged 20-34], [12.8% of women aged 35-44], [23.7% of women aged 45-54], [26.2% of women aged 55-64], [37.4% of women aged 65-74], [27.6% of women aged over 75].

Lipids Abnormality

Abnormal levels of lipids (especially cholesterol) can lead to long-term problems, such as atherosclerosis. Generally, a high total cholesterol level (which includes LDL, HDL, and VLDL cholesterol) or a high level of LDL (the "bad") cholesterol increases the risk of atherosclerosis and thus the risk of heart attack and stroke. However, not all types of cholesterol increase this risk. A high level of HDL (the "good") cholesterol may decrease risk, and conversely, a low level of HDL cholesterol increases risk. The effect of triglyceride levels on the risk of heart attack is less clear-cut. But very high levels of triglycerides (higher than 500 milligrams per deciliter of blood, or mg/dL) can increase the risk of pancreatitis. For people older than 20, levels of total cholesterol, triglycerides, LDL cholesterol, and HDL cholesterol after fasting should be measured at least once every 5 years. Collectively, these measurements are called the fasting lipoprotein profile.

High blood cholesterol itself does not cause symptoms, so many people are unaware that their cholesterol level is too high. It is important to find out what your cholesterol numbers are because lowering cholesterol levels that are too high lessens the risk for developing heart disease and reduces the chance of a heart attack or dying of heart disease, even if you already have it. Cholesterol lowering is important for everyone–younger, middle age, and older adults; women and men; and people with or without heart disease.

Causes

The major cholesterol disorders are primarily hereditary (familial) and therefore genetically determined. Secondary causes can contribute to congenital lipid disorders or can independently account for abnormalities of blood lipid metabolism. Among the secondary causes are the following conditions: Hypothyroidism, biliary cirrhosis, nephrosis, anorexia nervosa and acute intermittent porphyria can cause significant increases in blood cholesterol levels. Diabetes, chronic alcoholism, chronic kidney failure and acute hepatitis can cause significant increase in blood triglyceride levels. However, the most apparent secondary cause of lipid disorders is the high dietary cholesterol and fat content consumed by the American public.

There are drugs that can cause this disorders. The following drug have been reported to cause abnormal increase in cholesterol blood levels: anabolic (malehormonelike) steroid, chenodiol, disopyramide, thyazide diuretics, trimeprazine. The following drugs have been reported to cause abnormal increases in triglyceride blood levels: cortisonelike drugs, estrogens, isotretinoin, oral contraceptives, thiazide diuretics, timolol.

Detection and Evaluation

Adult Treatment Panel (ATP) III recognizes that detection of cholesterol disorders and other coronary heart disease (CHD) risk factors occurs primarily through clinical case finding. Risk factors can be detected and evaluated as part of a person’s work-up for any medical problem. Alternatively, public screening programs can identify risk factors, provided that affected individuals are appropriately referred for physician attention.

The identification of cholesterol disorders in the setting of a medical examination has the advantage that other cardiovascular risk factors—including prior CHD, PVD, stroke, age, gender, family history, cigarette smoking, high blood pressure, diabetes mellitus, obesity, physical inactivity—co-morbidities, and other factors can be assessed and considered prior to treatment. At the time of physician evaluation, the person’s overall risk status is assessed. Thus, detection and evaluation of cholesterol and lipoprotein problems should proceed in parallel with risk assessment for CHD.


Reference:

1. Long JW, The Essential Guide to Prescription Drugs, HarperCollins Publisher, Inc. 1993 Edition, New York, 50-53
2. Salinas CAS, Olaiz G, et all, High prevalence of low HDL cholesterol concentrations and mixed hyperlipidemia in a Mexican nationwide survey Journal of Lipid Research, Vol. 42, 1298-1307, August 2001
3. http://www.wrongdiagnosis.com/c/cholesterol/stats.htm
4. http://www.merck.com/mmhe/sec12/ch157/ch157a.html
5. http://www.nhlbi.nih.gov/guidelines/cholesterol/atglance.htm
6. Grundy S.M, Cleeman J.I et al, Implications of Recent Clinical Trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines, NCEP Report, (Circulation. 2004;110:227-239.)
7. NIH, Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III), National Cholesterol Education Program National Heart, Lung, and Blood Institute National Institutes of Health NIH Publication No. 02-5215 September 2002

LIPOPROTEIN METABOLISM

Lipoprotein Metabolism

ENZYMES, RESEPTORS, ANTIOXIDANTS AND LIPID

ENZYMES, RESEPTORS, ANTIOXIDANTS AND LIPIDS

Enzymes

Lipoprotein lipase (LPL), found in muscle and adipose tissue capillaries, hydrolyses lipoprotein triglycerides. Hepatic lipase also hydrolyses lipoprotein triglyceride and is involved in the conversion of IDL to LDL. Cholesterol synthesis is controlled by 3-hydroxy-3methylglutaryl coenzyme A reductase (HMG-CoA reductase). Non-hepatic cells receive most of their cholesterol from LDL not from endogenous synthesis. A fall in cell cholesterol up regulates HMG-CoA reductase. A great deal of the lipoprotein-cholesterol that is secreted subsequently returns to the liver, either on LDL or from reverse transport on HDL.

Lecithin cholesterol acyltransferase (LCAT), which accompanies HDL, esterifies free cholesterol, the ester moving to the HDL core. HDL3 becomes the larger HDL2; this process may be reversed by hepatic lipase. LCAT aids the removal of phospholipids and free cholesterol from VLDL during catabolism, and also their passage to HDL.

Lipids exchange between lipoproteins and there is active enzyme-mediated transfer. Cholesterol ester transfer proteins (CETP) pass HDL cholesterol ester to VLDL with reverse movement of triglycerides: this limits the accumulation of cholesterol ester in HDL, However, excess cholesterol ester in VLDL may not be physiologically appropriate.

Receptors

Lipoproteins are recognizes apoB100, and IDL apoE, taking up cholesterol into the cell. Higher cholesterol levels in the cell lead to :
1. Increased acyl cholesterol acyltransferase (ACAT) activity with cholesterol re-esterification.
2. Inhibition of HMG-CoA reductase and cholesterol synthesis.
3. Decreased new LDL-receptor synthesis and membrane insertion.
LRP binds multiple apoE copies on chylomicron remnants, facilitating their hepatic removal.

Atherosclerotic plaques are an inflammatory response to vessel wall injury; they contain macrophages and T lymphocytes, and have cytokine and growth factor expression. Endothelium modifies LDL, with phospholipid peroxidation and apoB degradation.

Activated macrophage with acetyl-LDL or oxidized-LDL receptors avidly remove modified LDL. Macrophage uptake may be a helpful scavenging mechanism, but in excess macrophage become lipid-laden foam cells of the fatty streak, which have a pivotal role in atherogenesis.

Antioxidants

Antioxidants may protect LDL from oxidative damage, and may be anti-atherogenic. The antioxidants vitamin E and β-carotene are carried on LDL. Changes in diabetic metabolism that predispose to lipoprotein oxidation may accelerate atherogenesis.


See images as description on the links below :
1.Lipid (cholesterol); transport, penetration, and balance
2.Forming of The Mixed micelle
3.Helical wheel projection of a portion of ApoA-I

STRUCTURE AND FUNCTIONS OF LIPOPROTEINS

STRUCTURE AND FUNCTIONS OF LIPOPROTEINS


Lipids are transported in blood as large macromolecules; these are complexes with proteins. Free fatty acids are the exception, mainly binding to albumin. Hydrophobic lipids, triglycerides and phospholipids are within the lipoprotein core, with the polar portions of phospholipids and the water-soluble alcohol portion of free cholesterol projecting into the aqueous environment, causing solubilization of the lipoprotein.

Types of lipoproteins are chylomicrons, very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), Low-density lipoprotein (LDL) and High-density lipoprotein (HDL). Lipoprotein classes can be separated physicochemically, either by electrophoresis wich uses surface charge or by ultracentrifugation which uses relative density.


Chylomicrons are the largest, lightest lipoproteins, they carry dietary triglycerides to be hydrolysed by peripheral tissues lipoprotein lipase (LPL). Fatty acids either provide energy or are stored as triglycerides. Whereas VLDL carry triglycerides synthesized in the liver also to the periphery. LDL are the main cholesterol carriers, delivering cholesterol to peripheral tissues, or back to the liver, through LDL receptors. IDL normally undergo rapid conversion to LDL or are removed by the liver.

As triglycerides are removed, chylomicrons and VLDL shrink in size, and are further catabolized as remnants. Chylomicron remnants are removed by a liver chylomicron remnant receptor, known as LRP (LDL receptor-related protein) or the α2-macroglobulin receptor, VLDL remnants, intermediate-density lipoproteins (IDL), are acted on by hepatic lipase, removed by the liver or converted to low-density lipoproteins (LDL).

Apolipoproteins

The apoliporoteins are major components of lipoproteins. Apolipoproteins have structural and functional roles; stabilization of the molecule; receptor-recognition peptides for cell lipoprotein uptake; or coenzimes for lipid metabolism. Types of apolipoproreins are apoprotein B (apoB48 and apoB100), apoprotein C (apoC-I, apoC-II and apoC-III; the last has three isoforms: C-III0, C-III1 and C-III2), apoprotein E, apoprotein A (apoA-I, apoAII) and apoprotein (a).

Lipoprotein Structure

Generalized structure of a plasma lipoprotein is shown on the figure below.


The similarities with the structure of the plasma membrane are to be noted. A small amount of cholesterol ester are triacylglycerol are to be found in the surface layer and little free cholesterol in the core.