Cholesterol presents in dietary fat.
Palmitic acid is an example of Triglycerides
Body can synthesize essential FAs .
Management of hypercholesterolemia reduces CVD mortality.
VLDL has a less mean diameter than LDL .
Circulating lipoproteins are static process
Apolipoprotein E can be exist in IDL
IDL has a higher density than HDL
Hepatic triglyceride lipase inhibited by A-|| at high concentration .
Mobilizing lipase activated by the decrease glucagon and insulin
CMs transfer apoA to HDL & acquire apoC & apoE from HDL.
VLDL remnants are called IDL
Not all LDL is formed from VLDL
The number of LDL-apoB receptors on the cell surface regulated by cholesterol pool
C-|| inhibits clearance CM and VLDL remnant particles
All VLDL are formed from TGs synthesized in the liver (endogenous VLDL)
There is no effect after menopause regarding to plasma lipoproteins
Increasing risk of acute pancreatitis when plasma TG concentration > 10 m mol/L
High P/S ratio increase LDL cholesterol
Small dense TG-rich LDL particles related to the third type of LDL
Cholestasis has no significant effect on LDL
Hypothyroidism increase LDL cholesterol in circulation
Antiretroviral drugs prevent exacerbate hyperlipidemia
After overnight fasting time, if CMs cleared ,there may be a pathological disturbance.
Homozygotes familial hypercholesterolemia develop CHD in childhood.
Disfunction of apoE and change in their structure impaired IDL uptake by liver
We use TGs with medium chain-length FAs to management the Familial hyperalphalipoproteinemia
Familial defective apoB-100 is a Familial hypercholesterolemia
Nicotinic acid bind with bile acids in the gut prevent their absorption
Statins (HMG-CoA reductase inhibitors ) are the main treatment for hypertriglyceridemia:
Tangier disease reduced HDL levels.
CM, VLDL & LDL are absent from the plasma in Hypobetalipoproteinemia
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