It is an irony, we paint the lipids as chief villains in the genesis of atherosclerosis and CAD. The fact of the matter is, it is the protein component that hides among the lipid jelly, with multiple folds and stinging tails, that ultimately help the LDL to penetrate the intact endothelium . These are called , apo-lipoprtiens. The fate of lipid molecules is determined by these apparently humble looking proteins .It must also be noted the even the goodness of HDL vanish if its apo-liprotein fails to co-operate . The Apo proteins are labeled differently in each sub fraction of lipids. Its Apo A 1 in HDL Apo B 100, in LDL and Apo C in VLDL.
Playing with English Alphabet A
Scientists can be casual , though not intentional when naming newly detected molecules. The major nomenclature issues are with Apo A , Apo a , Lip a These three entirely separate proteins with nearly identical names, should not be confused with. A subtle shift between a lowercase letter and a capital letter completely changes the meaning, taking us from a highly dangerous cardiovascular risk factor to a healthy, protective one.
Apolipoprotein A : This is a highly beneficial protein that defines the HDL function.(Ofcourse one must remember too much of HDL can be toxic as well .In fact when it exceeds 60 mg ,it will become dysfunctional, rather harmful.This is the U curve phenomenon of HDL)
Apolipoprotein(a) : This is the sticky, genetically fixed protein tail found only on Lipoprotein(a). It promotes blood clotting and triggers arterial inflammation.
Lp(a) : It is formed when a single Apo(a) protein tail binds to the Apolipoprotein B-100 (ApoB) wrapper of a standard LDL like particle. Because of this hybrid structure, Lp(a) possesses dual pathogenic properties. LDL core delivers cholesterol into the arterial wall, while the attached Apo(a) tail promotes localized inflammation and thrombosis . Lp(a) plasma levels are strictly determined by inheritance and remain highly stable throughout an individual’s life.
Lipoprotein(a) structure. Lp(a) is composed of two parts: one part is low-density lipoprotein (LDL)-like particles with apolipoprotein B100 (apo-B100), and the other part is the stinging tail apolipoprotein a [apo(a)]
Among the above three molecules, lipoprotein(a) is the celebrated one kept in the limelight. It is strongly determined by genetics and is a predictor; rather, we can call it a marker of LDL virility (like Apo B 100). It is entirely produced in the liver, its level is claimed to be static lifelong. Obviously, it cannot be true, as it would heavily dependent on liver function. Further, different vendors have come into the market with this, and they have different normal ranges.
Final message
When reading the lipid molecules, please focus on the English . A capital A vs. small a makes a huge difference between harming and healing the patient. Of course, we must be thankful, as of now, we have don’t have no small b or small c Apolipoproteins in lipidology.
Reference
Lipid particle science
Dr.S.Venkatesan MD 