Hepatic lipase function

[ChessMaster3000]

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according to FA the function of hepatic lipase is to remove TGs from IDL to form LDL. This would make sense, except for one thing: we know that LDL is taken up by LDLR on hepatocytes. If the hepatocytes need to take up IDL to transform it into LDL using hepatic lipase, then what is the need for the LDL receptor? Do hepatocytes create LDL, release it into the circulation for some reason (?), and then reuptake it? Or, probably more likely, does IDL also get peripherally converted to LDL with Lipoprotein lipase, which then gets endocytosed by liver cells?

So, I guess the question ultimately becomes, are there two sites of synthesis of LDL--within the hepatocyte itself (from endocytosed IDL), and peripheral nonhepatic conversion to LDL?

On a side note, does anyone know the difference between ACAT and LCAT? They seem to have very similar functions.

 

[AnalisCanalis]

On a side note, does anyone know the difference between ACAT and LCAT? They seem to have very similar functions.

ACAT is present in liver and intestinal mucosa to esterify cholesterol to cholesteryl esters either for storage or transport in VLDL and chylomicrons, whereas LCAT serves a similiar role in peripheral blood where it esterifies cholesterol for retrograde transport in HDL.

 

[ulikedaggers]

according to FA the function of hepatic lipase is to remove TGs from IDL to form LDL. This would make sense, except for one thing: we know that LDL is taken up by LDLR on hepatocytes. If the hepatocytes need to take up IDL to transform it into LDL using hepatic lipase, then what is the need for the LDL receptor? Do hepatocytes create LDL, release it into the circulation for some reason (?), and then reuptake it? Or, probably more likely, does IDL also get peripherally converted to LDL with Lipoprotein lipase, which then gets endocytosed by liver cells?

So, I guess the question ultimately becomes, are there two sites of synthesis of LDL--within the hepatocyte itself (from endocytosed IDL), and peripheral nonhepatic conversion to LDL?

On a side note, does anyone know the difference between ACAT and LCAT? They seem to have very similar functions.

Some IDL is taken up by LDL (they both have ApoB-100). The hepatocyte can use the TG from IDL to make more VLDL. The hepatocyte doesn't release the LDL it just created, it just processes it as if the LDL came from peripheral blood via the LDLR.. at least that's what we learned. The idea is that since some IDL ultimately gets taken up, it's more efficient for the hepatocyte to make LDL rather than be constantly secreting IDL back into the blood.

So yes, two sites, the main one being via LPL in the capillary endothelium.

ACAT and LCAT are the same except for location (LCAT in blood, ACAT in ER) and substrate. Both convert chol to cholE, but ACAT uses an acylCoA substrate and LCAT uses lecithin (phosphatidylcholine).

Edit: I meant some IDL is taken up by the liver, not "by LDL" .

 

[ChessMaster3000]

Some IDL is taken up by LDL (they both have ApoB-100). The hepatocyte can use the TG from IDL to make more VLDL. The hepatocyte doesn't release the LDL it just created, it just processes it as if the LDL came from peripheral blood via the LDLR.. at least that's what we learned. The idea is that since some IDL ultimately gets taken up, it's more efficient for the hepatocyte to make LDL rather than be constantly secreting IDL back into the blood.

So yes, two sites, the main one being via LPL in the capillary endothelium.

ACAT and LCAT are the same except for location (LCAT in blood, ACAT in ER) and substrate. Both convert chol to cholE, but ACAT uses an acylCoA substrate and LCAT uses lecithin (phosphatidylcholine).

And I'm guessing acat doesnt require apoA activation, while lcat does? Is ACAT in SMOOTH er?

 

[ulikedaggers]

And I'm guessing acat doesnt require apoA activation, while lcat does? Is ACAT in SMOOTH er?

Not completely sure, but I think yes for both.

Also I think ApoE is actually responsible for hepatic IDL uptake, not ApoB-100 (which is for LDL only). This is why in type IV (?) dyslipidemia you have increased VLDL and IDL.

 

[ChessMaster3000]

Not completely sure, but I think yes for both.

Also I think ApoE is actually responsible for hepatic IDL uptake, not ApoB-100 (which is for LDL only). This is why in type IV (?) dyslipidemia you have increased VLDL and IDL.

as a matter of fact, vldl and idl do have apob-100. a way to remember this is the liver synthesizes vldl-->idl-->ldl, so where else would LDL get its b100 from? HDL provides apoc and apoe, but not b100, therefore it must come from vldl

 

[ulikedaggers]

as a matter of fact, vldl and idl do have apob-100. a way to remember this is the liver synthesizes vldl-->idl-->ldl, so where else would LDL get its b100 from? HDL provides apoc and apoe, but not b100, therefore it must come from vldl

Yeah, they have apob-100, but apoE is necessary for uptake. But I just mixed up VLDL and chylomicrons, so maybe I should just stop trying to help explain all this lol.


Chylomicron and IDL = ApoE for uptake (IDL still has ApoB-100)
LDL = ApoB-100 for uptake.