6.18 Blood Lipoproteins Flashcards
Atherosclerosis
narrowing of blood vessels that can be the result of plaque formation from lipid deposition
Type 1 hyperlipoproteinemia or familial LPL deficiency
caused by a deficiency of LPL or ApoC-11. Results in accumulation of chylomicron TAG, increased risk of pancreatitis
Nonalcoholic (hepatic steatosis)
caused by imbalance between TAG synthesis and secretion of VDL
Familial Hypercholesterolemia
results from point mutations in the LDL receptor gene
Dyslipoproteinemia (dyslipidemia)
presence of abnormal concentrations of lipoproteins or abnormal lipoproteins in the blood. major risk factor for atherosclerosis and coronary artery disease. Requires the use of a standard fasting lipid panel
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Lipoprotein complexes include (name 5)
chylomicrons, very low density lipoproteins (VLDL), intermediate density lipoproteins (IDL), low density lipoproteins (LDL), high density lipoproteins (HDL)
Structure of Lipoproteins
Inner core of triacylglycerols and cholesterol esters, phospholipid outer layer with apolipoproteins and unesterified cholesterol
Rank blood lipoproteins by size and density (protein to lipid ratio, so high ratio means high % of protein)
Size: HDL < LDL, VLDL < Chylomicrons
Density: Chylomicrons < VLDL < LDL < HDL
Functions of apoliproteins
recognition sites for cell surface receptors, activates lipoprotein metabolism enzymes, structural components of the lipoprotein
Chylomicron pathway (where is it made, how is it metabolized?)
Made in the intestinal mucosal cells, released into the lymphatic system, moves to the capillaries, releases contents with the help of lipoprotein lipase, remnants taken up by the liver
VLDL pathway (where is it made, how is it metabolized?)
Produced by the liver, secreted into the blood, degraded by lipoprotein lipases, turns into LDL, endocytosed by extrahepatic tissues (skeletal muscle) and the liver.
Function of Cholesterol Ester Transfer Protein (CETF)
catalyzes the exchange of TAG from VLDL with Cholesterol Ester from HDL. Basically allows VLDL to exchange a TG for a CE with HDL.
Oversupply of Cholesterol inhibits
both synthesis of LDL receptors and synthesis of cholesterol
What is the function of LDL particles?
provide cholesterol to peripheral tissues and return to liver
What are LDL receptors?
expressed on cells, allows binding and uptake of LDL particles, synthesis and expression inhibited by oversupply of cholesterol
How is cholesterol ester made and why do we need to make it?
Synthesized from cholesterol by ACAT (acyl CoA cholesterol acyl transferase), allows storage of cholesterol in cells, stimulated by excess cholesterol.
The six regions/domains of the LDL Receptor
LDL binding domain, Epidermal growth factor like domain, N-linked oligosaccharide domain, O-linked oligosaccharide domain, Transmembrane domain, Intracellular (cytosolic) domain
Metabolism of HDL
Formed in the blood, take up cholesterol from peripheral tissues to return to liver as cholesterol esters
What are scavenger receptor activity (SR-A)?
causes endocytosis of modified LDL (result of endothelial injury) where the lipid or apo B have undergone oxidative damage
What are foam cells?
What macrophages turn into when they consume excess modified (oxidized) lipoprotein
