19- Cholesterol and Triglycerides Flashcards
fat is present as ______ in adipose tissue
triacylglycerol
___ releases FFA into blood from adipose cell surface
HSL hormone-sensitive lipase
HSL is inhibited by ____
insulin
we aren’t releasing FFA in well fed state
FFA in the blood bind to ____
albumin
“well fed state lipids”
lipoprtns
for transport of dietary lipids
chylomicrons
for transport of endogenous lipids
VLDL
for reverse lipid transport/excretion
HDL
entry apoprtn
ApoA
structural support Apoprtn
ApoB
exit Apoprtn
ApoC
interaction w/ receptors apoprtn
ApoE
activators of LCAT. Extract lipids from membranes for reverse transport
ApoA
structural prtns, interact with lipoprtn receptors and mediate the uptake of particle into target cells
ApoB
Modulate lipoprtn lipase activitiy, liberate FFA and glycerol from lipoprtns
ApoC
bind to receptors to allow removal of remnant particles from the circulation
ApoE
what happens when there is too much LDL in the system..
LDL is bound by cells that are not normally part of the system such as macrophages –? upatke oxidized LDLs leading to plaques and atherosclerosis (foam cells)
how is cholesterol added to VLDLs to make them IDL
via CETP the CE jump from HDL to the VLDL
Friedewald Formula
LDL cholesterol calculation
LDL = total cholesterol - HDL - 20% triglycerides
type I dyslipidemia
increase chylomicrons
increased cholesterol
and increased triglycerides
increased LDL and increased cholesterol and NO increased triglycerides
type IIa dyslipidemia
increased VLDL and LDL and increased cholesterol and triglycerides
type IIb dyslipidemia
increased IDL and cholesterol and triglycerides
type III dyslipidemia
increased VLDL and tiglycerides but no increased cholesterol
type IV dyslipidemia
type V dyslipidemia
incrased VLDL and chylomicrons and cholesterol and tiglycerides
defect in lipoprtn metabolism itself
primary dyslipidemia
familial hypercholesterolemia
- defects in ApoE/B LDL receptor
- autosomal codominant
- dyslipidemia IIa or IIb
Familial defective ApoB100
defective ApoB100 prevents binding of LDL to receptor
disturbance in lipid profile with no actual changes in metabolism
secondary dyslipidemia