Question on lipid/cholesterol transport

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Daitong

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Hey all,

I'm a bit confused as to why* mature HDLs transfer CEs to VLDL/IDL/LDL in exchange for TGs, aren't VLDL/LDL/IDLs only supposed to have cholesterol, not cholesterol esters? What is the purpose of doing this, and why would the HDL want TGs in return?

P.s. why is Niacin the most effective antilipid for elevating serum HDL levels? Why does it elevate it at all?

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So this is a topic I hate and don't understand 100%, but I'll try to look it up and work it out, it will be good for both of us..

First:
Hey all,
P.s. why is Niacin the most effective antilipid for elevating serum HDL levels? Why does it elevate it at all?
It's a relative value. Niacin is picking up any cholesterol in the body, pushing it to the liver, so the net result is the serum cholesterol is lower, having a higher proportion of HDL compared to to LDL.

Then:
I'm a bit confused as to why* mature HDLs transfer CEs to VLDL/IDL/LDL in exchange for TGs, aren't VLDL/LDL/IDLs only supposed to have cholesterol, not cholesterol esters? What is the purpose of doing this, and why would the HDL want TGs in return?

So it's not a question of exchanging HDL and TGs, it's a sequence of products being broken down and a certain proportion of triglycerides/cholesterol being carried.

HDL produces cholinesterase II(CII) as the "password" for chylomicrons to enter the liver. Then a breakdown product of the liver is VLDL which is 95% triglycerides/5% cholesterol -> then broken down and enters the adipose tissue using CII as the password -> then broken down again to IDL is 95% triglyceride/5% cholesterol with CII as the password -> then the final breakdown product LDL which is 5% cholesterol only which returns to the liver

The whole point is to move short and long free fatty acids absorbed from the intestine to liver. Short and long free fatty acids get converted to chylomicrons, then converted to lacteals (lymphatic channels for fat only), where 75% sticks to the endothelium and 25% goes to the liver and the sequence above starts to produce more HDL(I think?) and VLDL.

Extra points:
Total cholesterol = HDL + LDL + Triglycerides

HDL is the "good guy" because it uses APOE enzyme to activate its own enzyme LCAT to wrap two water soluble molecules around triglycerides to transport it through the blood vessel (which is 95% water). It is constantly recycling CII and APOE to allow access to the liver and adipose tissue.

LDL "bad guy" because it is the only one carrying cholesterol

Statins work because they are inhibiting HMG CoA reductase enzyme, decrease LDL, AND enhance Lipoprotein lipase activity (whose normal function is store away triglycerides)
 
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