Exam 2: Notes Flashcards

(39 cards)

1
Q

lipids are the building blocks of _____ _____

A

fatty acids

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2
Q

what affects the physical properties of fatty acids

A

length and saturation

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3
Q

16:0 vs. 16:1

A

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

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4
Q

lipids are stored as…

A

triglycerol

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5
Q

purposes of fat

A

energy storage–more energy/atom, not hydrated (hydrophobic, reduces weight)

insulation

membranes

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6
Q

hydrogenation of fats makes ____ double bonds

A

trans

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7
Q

plant cell lipid adaptation

A

use galactose (galactolipids)

sulfogalactolipids b/c phosphate is limited in soil

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8
Q

archae

A

unique membrane structure

long chain monolayer of fatty ethers (ether bond to glycerol)

ether bonds are less reactive so archae can live at extremes

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9
Q

monolayer purpose vs. bilayer

A

heat to monolayer does not cause peeling

heat + bilayer causes separation/peeling away

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10
Q

neg polar head group purpose

A

prevent loss of DNA from inside of cells

protect cell from attack (RNA/DNA has neg charges)

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11
Q

sphingolipids

A

cell-cell recognition

fatty acid attached to sphingosine by an amide bond

versatile head group (usually sugars)

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12
Q

things to know about fatty acid metabolism

A

activated with CoASH

degraded in 4 step process

fatty acid activation followed by beta-oxidation

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13
Q

products of lipid metabolism and how many you get

A

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)

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14
Q

oxidation of MFA

A

activated with CoASH, B-ox normally until db reached

isomerase makes db trans then continue as normal

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15
Q

products of MFA oxidation compared to saturated

A

16:1

8 acetyl CoA

7 NADH

6 FADH2 (double bond already present)

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16
Q

PFA oxidation

A

methylene group btw dbs

activation and b-ox normal until db

isomerase makes 1st db trans

reduce 2nd db with NADPH, H+ –> NADP (hydrogenase)

17
Q

products of PFA oxidation compared to saturated

A

16:2

8 acetyl CoA

6 NADH (1 NADPH needed to turn 2db –> 1db)

6 FADH2

18
Q

B-ox of odd # of FA ex. 15C

A

proceeds normally until the end

produces propionyl CoA

too small for enzymes of B-ox pathway

converted to TCA intermediate succinyl CoA

19
Q

enzymes used in B-ox of odd # FA

A

carboxylase w/ biotin (HCO3- + ATP –> H+, ADP, Pi)

isomerase w/ B12

20
Q

acetyl CoA can also form…

A

ketone bodies

21
Q

ketone bodies

A

used to export acetyl units w/e CoA b/c its limited

produced in diabetes and starvation (both activate gluconeogenesis)

22
Q

why do diabetes + starvation activate gluconeogenesis

A

brains prefer glucose as energy

siphons off oxaloacetate from TCA

keeps acetyl CoA from entering TCA, and diverts to ketone bodies

23
Q

lipid biosynthesis

A

not reverse of B-ox

uses acetyl CoA, NADPH, ATP

coordinately regulated (not happening at same time)

unique intermediate malonyl CoA

24
Q

purpose of malonyl CoA

A

elongates lipid 2C at a time

loses CO2 in process

25
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
26
lipid biosynthesis steps
6 step process loss of CoASH
27
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)
28
unsat FA synthesis
lipid and NADPH are oxidized O2 reduced to H2O uses 4e-; 2 from NADPH, 2 from lipid mixed function oxidase
29
mixed function oxidase
FAD, cyt cofactors O2, H+, NADPH --> 2 H2O, NADP needed for prostaglandin synthesis
30
prostaglandins
hormones that cause fever, pain, and inflammation
31
aspirin + ibuprofen
inhibit prostaglandin synthesis prevent pain and swelling suicide inhibitors (irreversible covalent modification to key catalytic aa in active site)
32
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
33
COX-1 & COX-2 are quite similar in structure
COX-2 involved in prostaglandin synthesis COX-2 specific drug kills people (Vioxx)
34
cholesterol syn has how many steps
4 3 acetyl CoA --> mevalonate mevalonate --> isoprene several isoprenes --> squalene squalene --> cholesterol
35
weird hydrogenase in cholesterol syn (HMG-reductase)
HMG-CoA, 2 NADPH, 2H+ --> CoASH, 2 NADP, mevalonate
36
mevalonate
critical intermediate in cholesterol biosynthesis
37
HMG-CoA reducatase
major regulatory point of cholesterol biosyn (makes mevalonate from HMG-CoA)
38
statins
mevalonate analogs inhibit HMG-CoA reductase (lovastatin, zocor) isoprene used to make cholesterol instead
39
isoprene
precursor for many compounds must take supplements to replace compounds since used to make cholesterol now uses carbocation