agestora.

ge
FAFSFORNGfhhshon as men
If excess energy is consumed than is
requited thenit'sstored as fatfor
met a
AND.FR
tNSPORIndhnanopontt usuallysynthesised
in liter
carbohydrates are stored as glycogen
Thebodystoreof fat is not limited
can't have guts sugars circulating around bloodstream heart
disease diabetes
Fat is stored as a Long term
fuel at Macylglycerol ITAG
Most of the fat we eat it TAG
coming from our diet the1meatthighs
small
TAG coming in from
intestine can be stored in adipose
tissue or given up to cells for gutty
acid oxidation
FATTY ACIDSYNTHESIS LEAD acids aresynthesisedinitiallyfrom
Fattybreakdown
the of glycogen glucose
process is stimulated by insulin which
is theonly anabolic hormone whereas
glucagon is catabolic
Glucoseundergoes glycolysis to produce
pyruvate
decarboxylated ro acetylCoA
during wink reaction in
AcetylOoA and
oxaloacetate combine
mitochondria I
to form citrate AAhh CoAleaves
Excessclimate mitochondria as
that can'tenter the FASoccurs in
TCAcycleleaves the mitochondria cytosol
and enters the cytosol where it
splitsup back into AWhp CoA t oxaloacetate
MECHANISM can't form glucose in
gluconeogenesis
coASynthesis
Malonyt AcetylCoA and NCO5 react MalonylCoA
pathway is catalyzed by AcetylWA carboxylase
which is activated by insulin cratelimiting
ATPsupplies energy Apptpi
MalonylCoA inhibits carnitinetransferase
preventsgathy acid from enteringmitochondria
foroxidation
NADPHneededforFAS providedby hexose
monophosphate used as reducingagent to
synthesise the FA
ForFAS always add malonylCoA andremove
a core so net addition of carbon is 2
 FATTY ACID SY NTMASE
A multi enzyme protein
that catalyses fatty
acid synthase
Not asingleenzyme
but a wholeenigmatic
system which catalyses
7 different reactions
where 2 carbonatoms
from malonyl CoA are linked together to
form PatmitourCoA
Overallsynthesis of palmitate from
acetylCoA requires 14 NADPH and 7ATP
LTAG is synthesised from 3 FA's and Gp

FATTYACID ORGANISATION
insoluble so to preventthem from accumulating in blood streams must
be put into anothergown
Apoproteins react with TAG phospholipids to form lipoproteins
Apolipoprotein bind lipids to form lipoproteins which can
then be transportedthrough the lymphatic circulatorysystem
This lipoprotein is known as a very low density lipoprotein LUDD
Triaoyrglycerol synthesis
Glycerol 3 phosphate accepts a FA from fatty
the enzyme glycerol 3 phosphate
acyl CoA by CRATE
acyltransferase LIMITIN
Forms Vysophosphatidic acid which accepts
another fatty acid to form phosphatidic
acid
converted into
diacylglycerol
using phosphatidic acid phosphorylase
d
converted into TAG by
diacylglycerol acyltransferase
 LIPOPROTEINS
structuralrole act as receptors
activate lipaseenzymes
INNER CORE triglycerides
cholesterolesters
OUTERSHELL single Layer of phospholipids
cholesterol
apoproteins
Types of lipoproteins
Chinomicrons Largest Low density carry
mainly dietary fats LTAa
VLDL mainly the fat we synthesise in the liver containing the
highest amount of TAGS
LDL Low Density lipoproteins which carries mainly cholesterol
tohissues Highlevels are bad
HDL High Density lipoproteins carry cholesterol from tissues to river
high levels are more favoured TRANSPORT OF EXOGENOUS
FAT LDIETARY FAT
Following digestion in small intestine
lipasescause lipids TAGS
to
combinewith
Apo B 48 into Chinomicrons
which enter circulation
HDL is involved in shuttling apoprotein
so they aren't always degraded
Po A E t Apro CHcombinewith TAGS
and Apo B 48
Apoprotein c is needed to activate lipoprotein lipase which
catalyses hydrolyses TAGS FAT glycerol continues to wirer
enter adiposehistualcomorped
is then back
returned toHDL into TAas
Apoprotein E is importantas they're recognisedby receptors on the liver
whichremoves the chemomicron from circulation
Chiyomicron remnant is taken up byApoE orApo B 48 receptor on the
liver
TRANSPORT OF ENDOGENOUS FATS
Transport of lipids from Vitor
VLDL in viverconsists of TAGS bound
with Apoprotein B100 which leaves liver
HDL transfers Apoprotein E and CH to
this cheapomicron
goes throughcapillary
where Apoprotein c activates Lpl
which hydrolyses the TAGS
into free fatty acids glycerol
turned into
TAGS and
chipo microns wave capillary as stored in adipose
an intermediate density lipoprotein tissuewhilst glycerol
halt the Chinomicron can be returns tothe liver
returned to the liver by the help
of Apoprorein E on the chylemicron
t now only contains
Hemm to Wbl Apoprotein BIO becomes
LDL
Mutations in the B100 receptorI Half goes backto
B100proteinpreventuptake of liver other half goes to
LDL leading toLDL accumulation peripheral tissue via
in theblood Btoo receptor
ROLEOFHDL 1N CHOLESTEROL TRANSPORT
HDLis synthesised in liver and small
intestine Chinomicron with ApoproteuriA 1
attached to it
cholesterolcomes from peripheral
tissue
Apoprotein A 1 activates an enzyme
known as lecithincholesterol Acm
Transferase UCAT
WAT takes a fatty acid chain from
phosphatidylcholine and reacts with
hydroxyl group of cholesterol
forms cholesterol
As it increases in size ester
it is able to transfer more stored
cholesterol to VLDL
esters in HDL
HDL is then taken up
bythe liver via SR B1 receptor
CHOLESTEROL SYNTHESIS

react to
tomythe
catalyses the rate vomitingstep in
synthesis of mevalonate
forms
inhibits cholesterol
cholesterol
synthesis
cholesterolitself can enter cells by endocytosis and is taken up by
Uffosomes which then release the cholesterol which alters gene
expression affecting cholesterol synthesis

VDL RECEPTORS
Receptors onthe liver CB100receptors responsibleto remove LDL from
the circulation via receptor mediator endocytosis
Familial hypercholesterolemia is a genetic disorder in chromosome
19 Thebody is unable to remove LDL from the body
This leads to A body cholesterol levels
Premature death from atherosclerosis
HYPERLIPIDAEMIA lHyperlipoproteinaemias
Hypercholesterolemia geneticdisorderwherethe liver is unable
to uptakeLDL
Hypertriglycerideemia geneticdisorder high levels of triglycerides
in the blood
othersinclude deficiency of C H protein1 apoproteins involved in
remnant uptake
lipoprotein A competes with plasminogen during clotting showing
the process
s OBESITY DIETARYSATURATED AND
fgfktk.FRRSJDp TYPE2 DIABETES UNSATURATED FATTYACIDS
DIETARY CHOLESTEROL ALCOHOLISM
ATHEROSCLEROSIS
The accumulation of fattydeposits which narrow arteryvwmen can
beidentified as plaque Involved inflammation proliferation of
the smooth muscle in arterywww
contains CT and poolof cholesterol richlipid
starts as a fattystreakfrom the accumulation of foamcells
macrophagesfilled withWpial mainly cholesterol
modifiedLDL is not recognised bythe B100 Receptor instead is
takenup by scavengerreceptors on the foam cells