Lipoprotein (a)

What is Lipoprotein (a)

Lipoprotein (a)  (also called Lp(a)) is a type of lipoprotein. A lipoprotein is a biochemical assembly that contains both proteins and lipids, bound to the proteins, which allow fats to move through the water inside and outside cells. The proteins serve to emulsify the lipid (otherwise called fat) molecules.

Many enzymes, transporters, structural proteins, antigens, adhesins, and toxins are lipoproteins.

Examples include the plasma lipoprotein particles classified under high-density (HDL) and low-density (LDL) lipoproteins, which enable fats to be carried in the blood stream, the transmembrane proteins of the mitochondrion and the chloropast, and bacterial lipoproteins.

Genetic studies and numerous epidemiologic studies have identified Lp(a) as a risk factor for atherosclerotic diseases such as coronary heart disease and stroke.

Discovery of lipoprotein (a)

Lipoprotein(a) was discovered in 1963 by kare Berg  and the human gene encoding apolipoprotein(a) was cloned in 1987. Though it was known it was known that it is a risk factor for heart disease. But now evidence for lp(a) as an emerging risk factor is mounting in the literature.

Structure of lipoprotein (a)

Lipoprotein (a) [Lp(a)] consists of an LDL-like particle attached to an additional protein molecule called as apolipoprotein(a) [apo(a)], which is covalently bound to the apoB of the LDL like particle. Lp(a) plasma concentrations are highly heritable and mainly controlled by the apolipoprotein(a) gene [LPA] located on chromosome 6q26-27.

Apo(a) proteins vary in size due to a size polymorphism [KIV-2 VNTR], which is caused by a variable number of so-called kringle IV repeats in the LPA gene. This size variation at the gene level is expressed on the protein level as well, resulting in apo(a) proteins with 10 to > 50 kringle IV repeats (each of the variable kringle IV consists of 114 amino acids). These variable apo(a) sizes are known as “apo(a) isoforms”. There is a general inverse correlation between the size of the apo(a) isoform and the Lp(a) plasma concentration. One theory for the size/plasma level correlation involves difference rates of protein synthesis. There appears to be a relationship between the number of kringle repeats and the processing time of the precursor apo (a) protein. That is, the larger the isoform, the more apo(a) precursor protein accummulates intracellularly in the endoplasmic reticulum. Lipoprotein (a) is not fully synthesized until the precursor protein is released from the cell, so the slower rate of production for the larger isoforms limits the plasma concentration.

Apo(a) is expressed by liver cells (hepatocytes), and the assembly of apo(a) and LDL particles seems to take place at the outer hepatocyte surface. The half-life of Lp(a) in the circulation is about 3 to 4 days.

The key to optimal health is providing all the nutrients to the body in adequate amount, exercise and eating an alkaline diet menu plan, which maintains the body pH slightly on the alkaline side.


1)  Wikipedia, “Lipoprotein (a)”,accessed on 19th May2013,

2)  Nordestgaard BG, Chapman MJ, Ray K, Borén J, Andreotti F, Watts GF, Ginsberg H, Amarenco P, Catapano A, Descamps OS, Fisher E, Kovanen PT, Kuivenhoven JA, Lesnik P, Masana L, Reiner Z, Taskinen MR, Tokgözoglu L, Tybjærg-Hansen A (December 2010). “Lipoprotein(a) as a cardiovascular risk factor: current status”. Eur. Heart J. 31 (23): 2844–53.

3) Kamstrup PR, Tybjærg-Hansen A, Nordestgaard BG (April 2011). “Lipoprotein(a) and risk of myocardial infarction–genetic epidemiologic evidence of causality”. Scand. J. Clin. Lab. Invest. 71 (2): 87–93.

4)  Danesh J, Collins R, Peto R (2000). “Lipoprotein(a) and coronary heart disease. Meta-analysis of prospective studies”. Circulation 102 (10): 1082–5.

5)  Smolders B, Lemmens R, Thijs V (2007). “Lipoprotein (a) and stroke: a meta-analysis of observational studies”. Stroke 38 (6): 1959–66.

6)  Schreiner PJ, Morrisett JD, Sharrett AR, Patsch W, Tyroler HA, Wu K, Heiss G (1993). “Lipoprotein(a) as a risk factor for preclinical atherosclerosis”. Arterioscler. Thromb. 13 (6): 826–33

7)  Berg K (1963). “A new serum type system in man – the Lp system”. Acta Pathol Microbiol Scand 59 (3): 369–82.



Lipoprotein (a)

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