Cholesterol Flashcards

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1
Q

why is most atp made in mitochondria

A

where most acetyl-coA is made

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2
Q

what are the primary sources of fat

A

diet
de novo synthesis in the liver
storage depots in adipose

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3
Q

properties of bile salts

A

made in liver, stored in gall bladder
emulsify fats + fat soluble vitamins ADEK
have hydrophobic and hydrophillic sides

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4
Q

orlistat

A

inhibits pancreatic + gastric lipase which reduces fat absorption = weight loss
derivative of lipstatin

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5
Q

side effects of orlistat

A

abdominal pain
urgency to defecate
increased flatus
steatorrhoea

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6
Q

what do lipoproteins do

A

transport lipids in plasma

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7
Q

how are chylomicrons made

A

after enterocytes absorb digestion products in small intestine brush border, triglycerides are resynthesised in golgi and form CMs

need apoproteins from HDL in bloodstream

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8
Q

function of chylomicrons

A

dietary fat transport

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9
Q

chylomicron journey

A

intestinal lacteal => thoracic duct => left subclavian vein => BS

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10
Q

what is lipoprotein lipase and what does it do

A

breaks down triglycerides carried by CMs, allowing fatty acids + glycerol to enter tissues

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11
Q

what happens to fatty acids and glycerol

A

FA: B-ox
G: liver => gluconeogenesis

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12
Q

where is lipoprotein lipase found

A

capillary endothelium lining: adipose/heart/skeletal muscle

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13
Q

cholesterol properties

A

steroid/basis of all steroids

increases/decreases membrane fluidity depending on temp + membrane nature

supplied by liver via de novo synthesis

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14
Q

3 main stages of cholesterol formation

A
  1. synthesis of isopententyl pyrophosphate
  2. condensation of IPP to form squalene
  3. cyclisation and demethylation of squalene to form cholesterol
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15
Q

how are bile salts synthesised
(+ name 2 primary bile salts)

A

cholesterol is broken down by series of reactions

glycholate + taurocholate

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16
Q

structure, function + types of lipoproteins

A

phospholipid monolayer surrounding cholesterol esters and triglycerides

transports hydrophobic lipids in aqueous environment

VLDL, LDL, IDL, HDL

17
Q

formation of cholesterol esters

A

made in plasma from cholesterol + acyl chain of phosphatidyl-choline

18
Q

HDL

A

‘good’
cholesterol from tissue to liver for use/disposal (reverse cholesterol transport)
reduces blood cholesterol levels

5% Tg, 20% CE, 30% PL, 8% FreeChol

19
Q

LDL

A

‘bad’
cholesterol from liver to tissue
increases tissue cholesterol

6% Tg, 42% CE, 22% PL, 8% FreeChol

20
Q

what is familial hypercholesterolaemia

A

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

21
Q

what are xanthomas

A

bumps on skin due to deposition of plasma LDL derived cholesterol to macrophages of skin (familial hypercholesterolaemia)

22
Q

FH and fibroblasts

A

new research: FH = fibroblasts = no functional receptors due to mutates genes
LDL cant be up taken into cytosol so its left in serum

23
Q

what do statins do

A

inhibit HMG-CoA reductase in step 3 of cholesterol formation

e.g lovastatin

24
Q

what do resins do

A

binds/sequesters bile acid-cholesterol complexes to prevent reabsorption in intestine
lowers LDL + increases HDL

e.g cholestryamine