Exam 2: Notes Flashcards

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
Q

fatty acid synthase

A

complex (7 subunits) used to construct lipids

in humans 1 pp

in bacteria 7 separate pps

charged w/ acetyl CoA + malonyl CoA

26
Q

lipid biosynthesis steps

A

6 step process

loss of CoASH

27
Q

regulation of FA synthesis

A

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
Q

unsat FA synthesis

A

lipid and NADPH are oxidized

O2 reduced to H2O

uses 4e-; 2 from NADPH, 2 from lipid

mixed function oxidase

29
Q

mixed function oxidase

A

FAD, cyt cofactors

O2, H+, NADPH –> 2 H2O, NADP

needed for prostaglandin synthesis

30
Q

prostaglandins

A

hormones that cause fever, pain, and inflammation

31
Q

aspirin + ibuprofen

A

inhibit prostaglandin synthesis

prevent pain and swelling

suicide inhibitors (irreversible covalent modification to key catalytic aa in active site)

32
Q

COX-cyclooxygenase

A

2 isozymes COX-1 & COX-2

aspirin inhibits both forms

COX-1 inhibition causes stomach irritation

COX-2 inhibition relieves pain and fever

33
Q

COX-1 & COX-2 are quite similar in structure

A

COX-2 involved in prostaglandin synthesis

COX-2 specific drug kills people (Vioxx)

34
Q

cholesterol syn has how many steps

A

4

3 acetyl CoA –> mevalonate

mevalonate –> isoprene

several isoprenes –> squalene

squalene –> cholesterol

35
Q

weird hydrogenase in cholesterol syn (HMG-reductase)

A

HMG-CoA, 2 NADPH, 2H+ –> CoASH, 2 NADP, mevalonate

36
Q

mevalonate

A

critical intermediate in cholesterol biosynthesis

37
Q

HMG-CoA reducatase

A

major regulatory point of cholesterol biosyn (makes mevalonate from HMG-CoA)

38
Q

statins

A

mevalonate analogs inhibit HMG-CoA reductase (lovastatin, zocor)

isoprene used to make cholesterol instead

39
Q

isoprene

A

precursor for many compounds

must take supplements to replace compounds since used to make cholesterol now

uses carbocation