Cholesterol Flashcards
why is most atp made in mitochondria
where most acetyl-coA is made
what are the primary sources of fat
diet
de novo synthesis in the liver
storage depots in adipose
properties of bile salts
made in liver, stored in gall bladder
emulsify fats + fat soluble vitamins ADEK
have hydrophobic and hydrophillic sides
orlistat
inhibits pancreatic + gastric lipase which reduces fat absorption = weight loss
derivative of lipstatin
side effects of orlistat
abdominal pain
urgency to defecate
increased flatus
steatorrhoea
what do lipoproteins do
transport lipids in plasma
how are chylomicrons made
after enterocytes absorb digestion products in small intestine brush border, triglycerides are resynthesised in golgi and form CMs
need apoproteins from HDL in bloodstream
function of chylomicrons
dietary fat transport
chylomicron journey
intestinal lacteal => thoracic duct => left subclavian vein => BS
what is lipoprotein lipase and what does it do
breaks down triglycerides carried by CMs, allowing fatty acids + glycerol to enter tissues
what happens to fatty acids and glycerol
FA: B-ox
G: liver => gluconeogenesis
where is lipoprotein lipase found
capillary endothelium lining: adipose/heart/skeletal muscle
cholesterol properties
steroid/basis of all steroids
increases/decreases membrane fluidity depending on temp + membrane nature
supplied by liver via de novo synthesis
3 main stages of cholesterol formation
- synthesis of isopententyl pyrophosphate
- condensation of IPP to form squalene
- cyclisation and demethylation of squalene to form cholesterol
how are bile salts synthesised
(+ name 2 primary bile salts)
cholesterol is broken down by series of reactions
glycholate + taurocholate
structure, function + types of lipoproteins
phospholipid monolayer surrounding cholesterol esters and triglycerides
transports hydrophobic lipids in aqueous environment
VLDL, LDL, IDL, HDL
formation of cholesterol esters
made in plasma from cholesterol + acyl chain of phosphatidyl-choline
HDL
‘good’
cholesterol from tissue to liver for use/disposal (reverse cholesterol transport)
reduces blood cholesterol levels
5% Tg, 20% CE, 30% PL, 8% FreeChol
LDL
‘bad’
cholesterol from liver to tissue
increases tissue cholesterol
6% Tg, 42% CE, 22% PL, 8% FreeChol
what is familial hypercholesterolaemia
monogenic dominant condition in which serum cholesterol is increased
single mutation = 2-3x = atherosclerosis in middle age
double = 5x = severe atherosclerosis + coronary infarcts in adolesence
what are xanthomas
bumps on skin due to deposition of plasma LDL derived cholesterol to macrophages of skin (familial hypercholesterolaemia)
FH and fibroblasts
new research: FH = fibroblasts = no functional receptors due to mutates genes
LDL cant be up taken into cytosol so its left in serum
what do statins do
inhibit HMG-CoA reductase in step 3 of cholesterol formation
e.g lovastatin
what do resins do
binds/sequesters bile acid-cholesterol complexes to prevent reabsorption in intestine
lowers LDL + increases HDL
e.g cholestryamine
