Exam 2: Notes Flashcards
lipids are the building blocks of _____ _____
fatty acids
what affects the physical properties of fatty acids
length and saturation
16:0 vs. 16:1
16: 0… higher MP, good packing, max van der waals interactions
16: 1… low MP, kink in chain prevents good packing (mostly cis), fewer van der waals interactions
lipids are stored as…
triglycerol
purposes of fat
energy storage–more energy/atom, not hydrated (hydrophobic, reduces weight)
insulation
membranes
hydrogenation of fats makes ____ double bonds
trans
plant cell lipid adaptation
use galactose (galactolipids)
sulfogalactolipids b/c phosphate is limited in soil
archae
unique membrane structure
long chain monolayer of fatty ethers (ether bond to glycerol)
ether bonds are less reactive so archae can live at extremes
monolayer purpose vs. bilayer
heat to monolayer does not cause peeling
heat + bilayer causes separation/peeling away
neg polar head group purpose
prevent loss of DNA from inside of cells
protect cell from attack (RNA/DNA has neg charges)
sphingolipids
cell-cell recognition
fatty acid attached to sphingosine by an amide bond
versatile head group (usually sugars)
things to know about fatty acid metabolism
activated with CoASH
degraded in 4 step process
fatty acid activation followed by beta-oxidation
products of lipid metabolism and how many you get
FADH2, NADH, acetyl CoA
acetyl CoA = 1/2 # of carbons (16:0 = 8 CoA)
NADH = 1 less than # of CoA (16:0 = 7 NADH)
FADH2 = 1 less than # of CoA (16:0 = 7 FADH2)
oxidation of MFA
activated with CoASH, B-ox normally until db reached
isomerase makes db trans then continue as normal
products of MFA oxidation compared to saturated
16:1
8 acetyl CoA
7 NADH
6 FADH2 (double bond already present)
PFA oxidation
methylene group btw dbs
activation and b-ox normal until db
isomerase makes 1st db trans
reduce 2nd db with NADPH, H+ –> NADP (hydrogenase)
products of PFA oxidation compared to saturated
16:2
8 acetyl CoA
6 NADH (1 NADPH needed to turn 2db –> 1db)
6 FADH2
B-ox of odd # of FA ex. 15C
proceeds normally until the end
produces propionyl CoA
too small for enzymes of B-ox pathway
converted to TCA intermediate succinyl CoA
enzymes used in B-ox of odd # FA
carboxylase w/ biotin (HCO3- + ATP –> H+, ADP, Pi)
isomerase w/ B12
acetyl CoA can also form…
ketone bodies
ketone bodies
used to export acetyl units w/e CoA b/c its limited
produced in diabetes and starvation (both activate gluconeogenesis)
why do diabetes + starvation activate gluconeogenesis
brains prefer glucose as energy
siphons off oxaloacetate from TCA
keeps acetyl CoA from entering TCA, and diverts to ketone bodies
lipid biosynthesis
not reverse of B-ox
uses acetyl CoA, NADPH, ATP
coordinately regulated (not happening at same time)
unique intermediate malonyl CoA
purpose of malonyl CoA
elongates lipid 2C at a time
loses CO2 in process
fatty acid synthase
complex (7 subunits) used to construct lipids
in humans 1 pp
in bacteria 7 separate pps
charged w/ acetyl CoA + malonyl CoA
lipid biosynthesis steps
6 step process
loss of CoASH
regulation of FA synthesis
each 2C elongation requires ATP + 2 NADPH
palmitoyl CoA inhibits carboxylase b/c end product
citrate from TCA activates b/c shows you have a lot of acetyl CoA
phosphorylation (post-translational modification)
gene expression (whether or not you make the enzyme)
unsat FA synthesis
lipid and NADPH are oxidized
O2 reduced to H2O
uses 4e-; 2 from NADPH, 2 from lipid
mixed function oxidase
mixed function oxidase
FAD, cyt cofactors
O2, H+, NADPH –> 2 H2O, NADP
needed for prostaglandin synthesis
prostaglandins
hormones that cause fever, pain, and inflammation
aspirin + ibuprofen
inhibit prostaglandin synthesis
prevent pain and swelling
suicide inhibitors (irreversible covalent modification to key catalytic aa in active site)
COX-cyclooxygenase
2 isozymes COX-1 & COX-2
aspirin inhibits both forms
COX-1 inhibition causes stomach irritation
COX-2 inhibition relieves pain and fever
COX-1 & COX-2 are quite similar in structure
COX-2 involved in prostaglandin synthesis
COX-2 specific drug kills people (Vioxx)
cholesterol syn has how many steps
4
3 acetyl CoA –> mevalonate
mevalonate –> isoprene
several isoprenes –> squalene
squalene –> cholesterol
weird hydrogenase in cholesterol syn (HMG-reductase)
HMG-CoA, 2 NADPH, 2H+ –> CoASH, 2 NADP, mevalonate
mevalonate
critical intermediate in cholesterol biosynthesis
HMG-CoA reducatase
major regulatory point of cholesterol biosyn (makes mevalonate from HMG-CoA)
statins
mevalonate analogs inhibit HMG-CoA reductase (lovastatin, zocor)
isoprene used to make cholesterol instead
isoprene
precursor for many compounds
must take supplements to replace compounds since used to make cholesterol now
uses carbocation
