16 Flashcards
where are chylomicrons derived from
diet
where are chylomicrons packaged
in the intestine to liver lipids to various tissues
what apo is associated with chylomicrons
apo B48
what activates lipoprotein lipase
apoC-II
why is lipoprotein lipase activated
to release free FA for fuel in adipose tissue, heart, and skeletal muscle
what happens when fats are depleted with respect to chylomicrons
chylomicron rememnrants go to the liver for absorption via apoE-mediated endocytosis
where are VLDL packaged
in the liver from diet dervied de novo synthesized lipids
what apo is associated with VLDL
apoB100
what happens with free FA released by lipoprotein lipase in VLDLs
adipocytes take up free FA and convert to TAGs for storage wich is used by muscle for energy
what does LDL do
deliver cholesterol to various tissues
muscle and adipose tissue have LDL receptors and recognize apoB100 on LDL
what does HDL do
picks up hcolesterol form extra hepatic tissues and retusn to liver (reverse cholesterol transport) where it can be metabolized
blood plasma after a meal
chylomicron rich and cloudy
where is lipoprotein lipase
LPL is anchored tot he cell surface of several tissues that are exposed to the circulation
anchored to sulfate proteoglycans
where is LPL expressed the most
within the heart and adipose tissue
what inhibits LPL
apoC-III
what does LPL do
hydrolyzes the triglycerides carried though circulation by lipoproteins contiaing apoB48 (chylomicrons) and apoB100 (VLDL)
what does the hydrolysis of triglycerides on VLDL by LPL lead to
the formation of smaller more dense lipoprotein within the ciruclation (LDL)
LPL deficiency
is a genetic deficiency causes very high TG levels in circulation and several health complications
fat intake must be restrictedd to less than 20 g a day (5 tsp )
familial hypercholesterolemia
LDL receptor defect
severe accumulation of cholesterol pramarily from LDL in the ciruclation
what could cause hypercholesteolemia without detectable genetic defect
prolonged high saturated fat intake and high cholesterol down regulate LDL-R (LDL receptor)
high LDL cholesterol levels are assocaited with an increased risk of cardiovascular disease
cholesterol uptake by receptor mediated endocytosis steps
- LDL receptor synthesized in rough ER moved to plasma membrane via golgi apparatus
- LDL receptor binds to apoB100 on LDL initiation endocytosis
- LDL in internalized in endosome
- LDL receptor is segregated into vesicles and recycled to surface
- endosome with LDL fuses with lysosome
- lytic enzymes in lysosome degrade apo B100 and cholesteryl esters releasing AA, FA, and cholesterol
process of removing non hepatic cholesterol for delivery to liver and ultimately for excretion from the body such as use for bile acids/ salts synthesis and bile is excreted
reverse cholesterol transport (RCT)
what does RCT require
the transfer of cholesterol and phospholipids from cells to nascent HDL )mostly the protiens verry little lipid) in the circulation
moving cholesterol from cells to HDL
cholesterol efflux
nascent HDL is converted to mature HDL in ciruclation
mature HDL is taken up by the liver (only lipids not apoA-I)
apoA-I can be reused to form more HDL
mature HDL is taken up by the liver (only lipids not apoA-I)
selective uptake
what turns cholesterol elsters to cholesterol
cholesteryl ester hydrolase uses H20 and releases FA
PLTP
phospholipid transffer protein
what does the conversion of nascent HDL to mature HDL require
transfer protein such as LCAT or PLTP
what does LCAT require
apoA-I as a cofactor
what is provided to HDL in the circulation by PLTP
phospholipids
what does PLTP do
transfers excess phospholipids from aboB100 containing lipoprotiens (VLDL, LDL) to HDL
importance of PLTP
provides phospholipid to expand the HDL surface area
provides lecitin or phosphatidyl choline for LCAT activity
contributes to the metabolism of apoB100 containing lipoproteins VLDL into LDL
what does ABCA1 do
effluxes lipids to lipid poo aloA-I
cholesterol efflux regulatory protein
ABCA1
what is the major receptor responsible for selevtive uptake of HDL
scavenger receptor class B type I or SR BI
what increases cholesterol efflux in mice
high dietaty n-3 PUFA
what do bile acids act as
amphipathic detergents that facilitate the enzymatic digestion and absorption of dietary fats in the intestine
what is the principle route by which cholesterol is removed from the body in feces
bile acids/ salts
what are conjugated bile acids called
bile salts
examples of bile salts
taurine and glycine
what are the most important metabolite of cholesterol
bile acids/ bile salts
taurine and glycine feature and function
are acidic which facilitates their detergent properties
where are bile acids formed and where do they go. when does this happen
fomred in liveer and delivered to gallbladder
upon fat intakem they are released into the intestine
percentage of bile salts and where
95% are recycled in enterohepatic circulation
5% are excreted (bile acid binding agents increase excretion)
rate limiting enzyme to convert choleseteerol to bile acids
cholesterol 7 alpha hydroxylase (cyp7)
what are some steroid hormones derived from cholesterol
cortisol, estradiol, aldosterone, mineralocorticoid, progesterone, pregnolone
affects protein and carb metabolism, suppreses immune response, inflamation, and allergic response
cortisol
regulates reabsorption of na, cl, hco3, in kidney
aldosterone
male and female sex hormones. influence secondary sexual characteristics, regulate female reproductive cycle
estradiol
mineralcorticoid
aldosterone
glucocorticoid
cortisol
