Master exam 1 Flashcards
precursor of prostaglandins, thromboxanes and leukotrienes
arachidonic acid
generic structure of phospholipid
2 fa
glycerol backbond
phosphate
alcohol
diffrent sites wheree phospholipids components can vary
fatty acids - different chain lenghts, saturated vs unsaturated
head groups- different alcohols
More or less phosphate groups
local hormone
localized close to a cell or just within the tissue they were secreted in
not circulation
short halflives
do not build up to high levels in circulation
property of prostaglandins that make them a local hormone
?
why are local hormones more likely to have pleitoropic effects
different tissues can have different receptors for the same hormone so it can have multiple effects that dont interfere since its only acting within one type
citrate lyase role in cholesterol and fatty acid syn
both are made in cytosol acetyl coa comes from mitochondria but cant get out on its own. so it leaves as citrate which gets cut apart by the lyase
rate limiting and regulated step of fatty acid synthesis
acetyl coa via acetyl coa carboxylase to malonyl coa
ACAT
acts on a cell to allow storage of free cholesterol to take from hdl?
LCAT
converts free cholesterol to cholesterol esters in the HDL changins shape
essentrial features of steriod hormone receptor
nuclear receptor transactivation domain DNA binding domain hinge ligand binding domain NLS transcription factor
essential features of non steriodal hormone receptors
d
aspartate + alpha ketoglutarate
glutamate
oxaloacetate
enzyme: aspartate aminotransferase
coenzyme: PLP
homocystein genaration
methionine is metabolized to homocysteine by Met condensing with ATP to form SAM. the methyl group from SAM can be transferred to a variety of acceptors causing SAM to SAHwhich becomes adenosine and homocysteine
Hcy low level control
remethylation to Met via THF and B12
or transulfuration to cystvia VOMIT coenzyme and PLP
sphingolipids vs phospholipids
sphingo have serine backbone`
phospholipids have glycerol
pancreatic
hormone senstivie
lipoprotein
lipases
cleaves dietary TAG into fa and monag to get through membranes
frees TAG into fa to leave adipose
cleaves TAG to enter adipose and muscle
prostaglandin
RL
arachidonic acid to prostaglandin to prostaglandins, protacclin, thromboxanes
PGHS turns aa to PH2 then other enzymes depending on tissue decide what it becomes
COX1 vs COX2
types of PGHS
1 is hosukepping, constitutive
2 is highly regulated, transient and pro inflammatory, mRNA up and down regulated
what can be activated first in lipid biosynthesis
either phosphatidic acid or alcohol
sources of lipid diversity
different fatty acyl chains
different head groups
PL vs ether lipids vs sphingolipds
diverstiy in glycosylation pattern
NSAIDs
d
RL of FA synthesis
acetyl coA + CO2 via acetyl coa carboxylase and biotin make malonyl coA \+ citrate \+dephosphorylation -end product -phosph
fatty acid synthase
condense reduce dehydrate reduce to keep adding acetyl co a to malonyl until palmitic acid using NADPH
configuration needed for beta oxidation
trans but cis is normal so use isomerase
4 steps of beta oxidatino
dehydrogenate (FAD)
hydrate
dehydrogenate (NAD)
thiolysis
RL beta oxidation
transport to mitochondria
carnitine shuttle where acetyl coa swaps with carneitine to get in
malonyl co a inhibits CPT 1
ketone bodies
made in liver cuz HMG coa lyase, but liver cant use it
cis vs trans fatty acids
cis has kink and is nateural
trans is no kink from processsed and packs weird
where do FA elongation and desaturation happen
er
FA synthase
Very long chain fatty acids
have to start in peroxisomes