lipoprotein metabolism Flashcards
fatty acids
hydrophobic long carbon chains - saturated, monounsaturated, polyunsatuarted, cholesterol, triglycerides = esters w fatty acids
cholesterol balance
intestinal absorption of dietary. and biliary cholesterol and cholesterol biosynthesis in the liver and intestine
cholesterol function
most vital lipid, required for fluidity of membrane, affects receptors GPCR, adrenergic, required to make hormones, obtained from diet and synthesized de novo from acetyl-coa
can lead to atherosclerosis, low density. lipoprotein
lipids in the blood
fatty. acid - bound to albumin
cholesterol triglycerides and phospholipids - transported by lipoproteins
LDL lipids
transport cholesterol
binds to LDL receptors and LDL particle taken up to cell, endocytose, taken to lysozome, C123, mutations –> too much cholesterol and disease niemann pick
transported to mitochondria to make more things like steroids
SREBP
activates when there is low cholesterol by driving transcription of cholesterol or making more LDL receptors
SREBP and SCAP
usually stay in ER but if levels fall –> golgi wher eenzymes help cleave protein
hmgcoa reductase can synthesize cholesterol
anatomy of lipoprotein
layer of phospholipid, cholesterol in membrane, some charge inside, insoluable material inside and proteins that do a lot of things like binding to LDL receptors (e.g. apo B)
apolipoproteins
structural determinants of lipoproteins, enzyme foacts, ligands for bidning to lipoprotein receptors
LDL has apoB100 (recognized by LDLr)
they only have this protein
chylomicrons
cholesterol packaged / lipoprotein
VLDL
important lipoprotein
lipoprotein trnasport
cholesterol comes in - transport lipids thru capillaries - tryglyceride turns into glyceorl and fatty acids for energy - VLDL particles from liver ! –> LDL particles w apoB100 protein, HDL particles pick up cholesterol from different tissues
apob48
microsomal triglycide transfer protein - adds tricglyceride and then goes to blood
apob100
made in liver, generated in rough er, vldl particles, then blood
HDL and apoc2 interact
coenzyme, cofactor
triglyceride degrading enzymes
LPL (lipoprotein lipase)
triglyceride into fatty acids see before slide
cholesterol can decrease transcription of
LDL proteins
coronary atherosclerosis
blockage or coronary blood vessels
left coronary artery - LAD, LCx
right coronary artery -
bloackage of epicardial coronary vessels in excess of 60% –> ischemia
atherosclerosis
build up of plaque in walls of arteries – can lead to MI/heart attack where heart muscle dies
LDL is a major risk factor
stress test
treadmill test to see how well heart handles workload
stressing agent
contraindications -
angina pectoris
partial blockage of blood vessel
free radical formation
in heart disease free radicals are released in artery linbing and oxidize LDL (low density lipoproteins)
dyslipidemias e.g. atherosclerosis
native LDL particles, undergo into subendothelial space, free radicals oxidize them, monocytes take them and form foam cells that just burst
role of macrophage inflammation of the artery
stuff from before, release protease –> inflammation
statins have anti inflam properties
