lipids Flashcards

1
Q

what are the main classes of lipids

A
fatty acids 
phospholipids
triacylglycerol TAG
steroids
glycolipids
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2
Q

what is a lipid?

A

an organic, hydrophobic molecule

fat

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3
Q

Where are lipids found?

A

in cell membranes
in the blood
in droplets in adipose tissue

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4
Q

function of lipids?

A
structural component of membranes
energy stores
enzyme co-factors (g-proteins)
signalling molecules
hormones
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5
Q

How are FA’s released from TAGs

A

so when the ephinephrine adrenaline levels increase (sympathetic) energy is required so need to release FA’s from stores in adipose tissue
this increase causes kinases to activate lipases which hyrdolyse TAGs and release FAs into the circulation

in the blood unesterified FA’s are carried by albumin proteins and esterified FA’s are carried by lipoprotein like chylomicrons to other organs or tissues

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6
Q

starvation and ketosis

A

when in periods of starvation or energy deprivation ketosis occurs
low glucose and energy levels
Fatty acids produce acetyl CoA- so if the levels of CoA are too high then it inhibits pyruvate dehydrogenase and activates pyruvate carboxylase which causes oxaloacetate to be diverted for gluconeogenesis

if acetyl CoA can no longer feed into C.A.C and bind with oxaloacetate then ketosis occurs and it’s turned into ketone bodies

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7
Q

what can ketone bodies be used for in the body?

A

skeletal and cardiac muscle can use them for fuel/energy
also the brain
the liver cannot use them

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8
Q

how can excess ketone bodies be harmful?

A

they can cause the body to become very acidic

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9
Q

how is it identified in a patient that they may be producing ketone bodies? and which patients are likely to have this problem?

A

a fruity odour on their breath
diabetic patients as they don’t produce enough insulin so without this they break down fat for energy… so increase in acetyl CoA etc

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10
Q

breakdown of TAG process

A

starts in the mouth with amylase
then broken down in the small intestine by the action of bile salts and pancreatic lipases creating monoglycerol and 2 fatty acid chains
After digestion, monoglycerides and fatty acids associate with bile salts and phopholipids to form micelles. Micelles transport these molecules to the enterocyte (cells) to be absorbed (only the monoglycerides and fatty acids can pass through the membrane)

in the enterocyte- they are re-synthesised into TAG and then they get taken up by protein to move into the circulation.

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11
Q

Fatty acid synthesis key points:-
where?
start and end product?
what energy does it use up?

A

occurs in the cytosol in the liver, lactating mammary gland or adipose tissue
starts with acetyl CoA and ends with palmitic acid (fatty acid)
uses ATP and 14 NADPH

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12
Q

Citrate shuttle

A

acetyl CoA is split to form citrate which then moves through the mitochondrial membrane
once through CoA is added back on producing oxaloacetate
oxaloacetate is then turned into malate (NADH used)
malate is turned into pyruvate (which can shuttle back across the membrane) NADPH used
now we have acetyl CoA in the cytosol.

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13
Q

what shuttle is needed to move from mitochondria to cytosol?

A

citrate shuttle

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14
Q

what shuttle is needed to move from cytosol to mitochondria?

A

carnitine

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15
Q

Process of fatty acid synthesis after citrate shuttle?

A
acetylCoA carboxylase (activated in high levels of citrate) is needed to turn acetyl CoA into malonyl CoA
lots of steps but overall 8 acetyl CoA make 1 palmitate

then multi-functional fatty acid synthase (a massive 7 enzyme structure) is used
has an ACP arm that moves substrate from one active site to the next along chain
it synthesises fatty acid 2 carbons at a time
makes palmitic acid (a common fatty acid)

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16
Q
fatty acid breakdown key points:- 
where?
start and end product?
process name?
what is needed for the start of this process?
A

occurs in the mitochondria
starts with fatty acid and makes acetyl CoA
beta oxidation (3 steps- activation, transport and degradation)
CoA is needed for activation
CPT-1 is inhibited by malonyl CoA

17
Q

Fatty acid oxidation/breakdown process

A

fatty acid is activated by adding CoA to it to make fattyacylCoA
then the carnitine shuttle is needed to move it from the cytosol to the mitochondria

once fattyacylCoA is in the mitochondria final degradation step can occur (2 carbon atoms at a time)
there are 4 stages
dehyrdogenation produces FADH2
hydrolysis
dehydrogenation produces NADH and ATP
thiolysis - cleaved to produce acetyl CoA which then feeds into C.A.C

18
Q

Carnitine shuttle process

A

fattyacylCoA can move through outer membrane
carnitine palmitoyl-transferase 1 then converts fattyacylCoA into fattyacylcarnitine and CoA returns

fattyacylcarnitine can now get through inner membrane after this, carnitine palmitoyl-transferase II will take CoA and add it on in replacement for carnitine so it is fattyacylCoA again but now in the mitochondria

carnitine shuffles back into intermembrane space

19
Q

Which process- glucose or fatty acid breakdown produces more energy?

A

fatty acid oxidation

20
Q

Common lipoproteins

A

chylomicrons- TAG rich- taken from intestine/adipose tissue
VLDL- very low density lipoprotein TAG rich
LDL- smaller still - mainly carry cholesterol
HDL- smallest- also carry cholesterol

21
Q

where are bile salts formed? what are their function? what are they derived from?

A

in the gallbladder
act like detegrent- dispersion of lipids so they don’t all clump together
derived from cholesterol like HDL