CLINICAL CASES
323
VLDL
Lipoprotein
lipase
capillary
" wall
Adipose and
muscle
Cell
FFA-albumin
♦ Glycerol
VLDL
remnants
Cholesterol
Hepatic
Lysosome
Synthesis
H i IM ■)
CE>TG
LDL receptors
Liver Cell
LDL receptors
( Lysosome )
Peripheral Cells
Figure 35-2. Formation of VLDL and metabolism into LDL. (Abbreviations
are as used in Figure 35-1.)
secreted from liver and is tethered to the external surfaces of liver cells by
heparan sulfate. LDL is taken up by receptor-mediated endocytosis upon bind-
ing to the LDL receptor in liver and peripheral tissues.
Elevated serum TG levels can occur due to a number of factors.
Hypertriglyceridemia can be the result of a genetic disorder in one of the pro-
teins involved in lipoprotein metabolism, or it can arise secondarily to a num-
ber of other disorders, including diabetes mellitus, obesity, and alcohol abuse,
and as a side effect of some medications such as P-blockers, oral estrogens,
and some diuretics. Genetic deficiencies in LPL, apoC-II, or HL can give rise
to elevations in circulating TG, as can over production of apoB-100 or
increased apoE2 levels. ApoE2 has a decreased affinity for hepatic receptors
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