BMW3010 – Multimorbiditeit in Obesitas – Case 5
HOW DOES NORMAL FAT /HORMONAL -METABOLISM IN THE LIVER FUNCTION ?
Exogenous pathway
Dietary lipids are emulsified by bile acids, then hydrolyzed, absorbed and packaged into
chylomicrons, which are released into lymphatic vessels. At this moment, the
chylomicrons contain:
Cholesteryl esters
Phospholipids
Triglycerides
ApoB48
In the blood stream, the chylomicrons acquire ApoC2 and ApoE from HDLs, resulting in
formation of their mature shape. After LPL-mediated hydrolysis in the capillaries of adipose
and muscle tissue, CRs residuals re-enter into the bloodstream to be taken up by the
liver (receptor mediated, LDLR), where the lipid content is further hydrolyzed and used for
the synthesis of VLDLs, or otherwise used in the beta-oxidation.
Endogenous pathway
VLDLs contain ApoB100 with a small amount of triglycerides, phospholipids and cholesteryl
esters. In the bloodstream, they acquire ApoC2 and ApoE from HDLs, and release free
FAs to muscle and adipose tissue after LPL activation. VLDLs now transform into
intermediate density lipoproteins, which are removed by the liver (1) or, after further
lipase activity, become low-density lipoproteins (LDL) (2). The uptake of all
lipoproteins is mediated by the LDL Receptor (LDLR).
HOW DOES NORMAL FAT /HORMONAL -METABOLISM IN THE LIVER FUNCTION ?
Exogenous pathway
Dietary lipids are emulsified by bile acids, then hydrolyzed, absorbed and packaged into
chylomicrons, which are released into lymphatic vessels. At this moment, the
chylomicrons contain:
Cholesteryl esters
Phospholipids
Triglycerides
ApoB48
In the blood stream, the chylomicrons acquire ApoC2 and ApoE from HDLs, resulting in
formation of their mature shape. After LPL-mediated hydrolysis in the capillaries of adipose
and muscle tissue, CRs residuals re-enter into the bloodstream to be taken up by the
liver (receptor mediated, LDLR), where the lipid content is further hydrolyzed and used for
the synthesis of VLDLs, or otherwise used in the beta-oxidation.
Endogenous pathway
VLDLs contain ApoB100 with a small amount of triglycerides, phospholipids and cholesteryl
esters. In the bloodstream, they acquire ApoC2 and ApoE from HDLs, and release free
FAs to muscle and adipose tissue after LPL activation. VLDLs now transform into
intermediate density lipoproteins, which are removed by the liver (1) or, after further
lipase activity, become low-density lipoproteins (LDL) (2). The uptake of all
lipoproteins is mediated by the LDL Receptor (LDLR).
