Dislipedeamia Flashcards
what is a lipid
organic molecule, poorly souble in water
carbon containing, few oxygen molecules
hygrophilic head, hydrophobic tail
what is a TAG
3 FA attached to a glycerol
less O2
more hydrophobic
what is cholestrol ester (CE)
cholestrol and FA
no oxygen
why do we need fat
energy cell membrane protection of organs thermal insulation neural insulation
why do we need cholestrol
acts as a membrane stiffner present between TAG tails uses in - steriods - vit D - bile acid
what is the role of lipoproteins
make cholestrol and TAG souble
has a hydrophobic core made up of TAG and cholestrol
hydrophilic outside
what is the only way the body can get rid of cholestrol
through excretion
name the 4 lipoproteins
chylomicrons
VLDL
LDL
HDL
describe chylomicrons in terms of lipid, protein and density
high lipid
low protein
low density
describe VLDL in terms of lipid, protein and density
high ish density
lowish protein
low ish lipid
describe LDL in terms of lipid, protein and density
low ish lipid
highish protein
highish density
describe HDL in terms of lipid, protein and density
high protein
low lipid
high density
how do short and medium chain Fats enter the blood
TAG and CE broken down in FA and glycerol in the intestinal lumen
enter portal vien
Postprandial
what does HDL donate to Chylomicron
Apo protein C2 and Apo E
Postprandial
how does the chylomicron bind to the tissue
via Apo C2 and lipoprotein lipase
TAG absorbed
Postprandial
what is produced after chylomicron binds
a chylomicron remant
more cholestrol dense, less TAG
Postprandial
what happens to the chylomicron remant
ApoC2 goes back to HDL
ApoE binds to receptor on liver
chlyomicron remnant stored in liver
Fasted
how much of the VLDL remant bind to the liver
50%
Fasted
what happens to VLDL
leaves the liver
recieves ApoC2 and ApoE
binds to tissue via ApoC2 and lipoprotein lipase
what is produced after VLDL binds to tissue
VLDL remant
what happens to other 50% of VLDL
LDL synethsis
docks to hepatic lipase - removes any TAG left
new LDL
LDL taken up by cell
what is the problem of LDL
half life of a couple of days so spends longer in the blood exposing it to free radicals and toxins
gets unfavourably modified
what happens to unfavourably modifide LDL
macrophages do not recognize it
- express SR-a Receptor
- takes up LDL
- macrophage has no internal feedback, so has a build up of C
- becomes a foam cell
- atherosclerosis
phamaological treatments for cholestrol
treat underlying disease if appropriate (diabetes)
lifestyle modifications - diet, smoking, exercise
Drugs
- statins
- resins
- exetimibe
how do statins work
statins stop cell producing its own C
upregulates expression of LDL receptors
how do resins work
prevents recycling of bile acids
so you lose more C
express more receptors
how do exetimbe work
knocks out C transporter in SI
prevents C getting into the system
effect of high fat diet on chylomicrons
high fat diet
high fat = more chylomicrons
describe the interaction between chylomicrons and LDL
high fat diet
chylomicron exchanges some C for fat from LDL via CET
produces chylomicorn with more cholestrol in it
LDL with small amount of fat in it
what is the effect of TAG rich chylomicrons from high fat diet
(high fat diet)
leads to oxidative stress
causes endothelial to stop working
LDL can get through endothelial wall and settle in wall
what happens to the small LDL after interacting with Chylomicron
(high fat diet)
binds to hepatic liapse, pass on small amount of TAG to become a smaller LDL remant
what is the effect of small LDL remant
high fat diet
easier for it to be damaged
macrophages collect
endothelial wall damaged so macrophage can pass through
what happens to HDL following high fat diet
high fat diet
same thing as LDL
takes some TAG from VLDL
binds to liver and delivers TAG
becomes a smaller HDL remant
what happens to smaller HDL remant
high fat diet
more rapidly removed from the blood
less HDL to give ApoC2 and ApoE to chylomicron
leads to impaired clearence of TAG
oxidative stress happening at the same time
what is the relationship between HDL and chlyomicrons
inversely proportinate
possible dietary inverventions
reducing dietary C reduce fat intake reduce salt fat increase fibre intake limit sugar consumption limit alcohol
effect of increasing fibre
increases C loss through gut
effect of limiting alcohol
decreased VLDL
80% of alcohol metabolised by the liver
up to 31% of an alcohol bolus ends up as VLDL
leads to fatty liver
effects during exercise
increase delivery and use of TAG
- reduce TAG blood pool
effects post exercise
increase HDL production increase lPLase expression and activity increase hepatic fatty acid oxidation increase size of VLDL improves endothelial function improves redox state
effect of increase HDL production
increase ApoC2 and ApoE availibilty
effect of increase lPLase expression and activity
enchances TAG clearence
effect of increase hepatic fatty acid oxidation
decrease hepatic TAG output
effect of increase size of VLDL
VLDL TAG hydrolysed more quickly
effect of improved endothelial function
preventing infiltraion of lipoprotein/macrophages into the sub endothelial space
ACSM guidelines for improving blood lipid profile
start 3 days a week, increase to 5-7
40-80% age predicited HRmax
11-24 RPE
150-300 mins a week
