Exam 2 -- questions

Question 1

where does heme synthesis occur

Answer 1

partly in mitochondria, partly in cytosol of liver and bone marrow

Question 2

where does fa degradation occur

Answer 2

cytosol–>mitochondria

Question 3

where does gluconeogenesis occur

Answer 3

first part in mitochondria, then in cytosol. (last step only possible in liver)

Question 4

where does PPP occur

Answer 4

liver, adrenal cortex, lactating tissues, RBCs

Question 5

PTL vs LPL vs HSL

Answer 5

PTL: dietary TG to MAG and glycerol
LPL: TGs in CMs to MAG and glycerol for adipocyte take up
HSL: hydrolyzes adipocyte TG to free fa’s

Question 6

CM vs VLDL vs LDL vs HDL

Answer 6

CM: dietary TGs in small intestine–>tissues
VLDL: endogenous TGs in liver –> tissues
LDL: made from depleted CM/VLDL, goes to tissues, only one that enters cells (receptor mediated endocytosis)
HDL: returns tissue chol to liver for degradation

Question 7

how are odd chain fa broken down?

Answer 7

propionyl CoA (3C) –> succinyl CoA. uses cofactors biotin and B12. Uses ATP.

Question 8

how much energy is obtained in ONE round of beta-oxidation?

Answer 8

make 1 FAD --> 2 ATP
make 1 NAD --> 3 ATP
make 1 ACoA --> 12 ATP
lose 2 ATP in making acyl-CoA
  total= 15 ATP

Question 9

what are the lipogenic enzymes:

Answer 9

1. ACoA carboxylase
2. fa synthesis
3. citrate lyase
4. malic enzyme
5. dehydrogenase in PPP

Question 10

how/where does fa chain elongation occur?

Answer 10

• ER membrane

- acyl-Coa donates 2C units to carboxy terminus of malonyl CoA

Question 11

how/where are double bonds added into fa’s?

Answer 11

• ER membrane

- accomplished by desaturases (9, 6, 5)

Question 12

sphingolipid synthesis pathway

Answer 12

All derived from sphingosine.
Sphingosine
(+fa) = ceramide
(+phosphotidyl choline) = sphingomyelin

OR ceramide + carb = glycosphingolipid

(Kaiser 5)

Question 13

cellular control of chol synthesis?

Answer 13

inc chol activates protease, protease releases SREBP from ER, goes to nucleus to activate SRE. SRE now activates HMGCoa and LDL receptor production

Question 14

KB synthesis pathway

Answer 14

2 ACoA –> acetoacetyl CoA –>3-hydroxy-3-methyl-glutaryl CoA –>acetoacetate–>acetone or 3-hydroxybutyrate

Question 15

leptin vs ghrelin

Answer 15

leptin: produced by adipocytes, dec appetite, inc caloric expenditure
ghrelin: produced by stomach, inc appetite

Question 16

10 essential aa’s

Answer 16

PVT TIM HALL

phe, val, thr, trp, ile, met, his, arg, lys, leu

Question 17

negative vs positive N balance

Answer 17

Positive : taking in more than you’re excreting, growing/healing etc

Question 18

CPS I vs CPS II

Answer 18

Both make CP
CPS I in mito during urea cycle
CPS II in cytosol during pyrimidine synthesis

Question 19

how does NH4 get transported into bloodstream/liver for degradation?

Answer 19

1. most is glutamine

2. from muscles as alanine (pyr + NH3)

Question 20

which are the 2 ONLY ketogenic aa’s

Answer 20

Leu and Lys

Question 21

how is THF made

Answer 21

folate to dihydrofolate to THF. Both steps need DHFR (dihydrofolate reductase). This is what methotrexate blocks!

Question 22

how are dNTPs made from NTPs? ie how to make deoxyribose nt’s from ribose nt’s?

Answer 22

ribonucleotide reductase. Blocked by binding of dATP (adenosine deaminase deficiency)

Question 23

Complex carb: proteoglycan. where is it made

Answer 23

protein w long repeating dissacharide units (GAG)
“slippery,” has shell of water
made in golgi
form ECM, or found in synovial fluid, eye, cartilage, mucous

Question 24

complex carb: glycoprotein. where is it made

Answer 24

protein with shorter oligosaccharide, usually branched
made in RER and golgi
found in ECM, cell surface, functions for cell recognition, antigenicity, globular proteins of human plasma

Question 25

direct reversal of DNA damage

Answer 25

photolyase- e coli / plants. undoes uv damage

and

AGT (or MGMT)- not in plants, directly removes methyl group that was the mutation

Question 26

MMR

Answer 26

identify methylated (older/parental) strand and fix errors on daughter strand according to old

Question 27

BER

Answer 27

repairs base alteration or loss. glcosylase recognizes/removes error leaving AP site. Filled in by AP-endonuclease

Question 28

NER. what are diseases assoc?

Answer 28

UV specific endonuclease, recognizes thymine dimers and cuts it out via “double incisions”.
**XP, Cockayne’s, Trichothiodystrophy

Question 29

HR (also called recombination repair). what disease is assoc w this?

Answer 29

used to repair ds breaks.dna repaired from undamaged sister xsome. strands joined via holliday junction, branch migration and resolution.
**BRCA

Question 30

Nonhomologous end-joining (NHEJ)

Answer 30

used to repair ds breaks. dna ends processed and ligase joins the 4 ends, more error prone, some dna lost

Question 31

catecholamine synthesis pathway? what deactivates these/or inactivates the deactivation (drug)?

Answer 31

tyr–>dopa–>dopamine–>norepi–>epi. MAO inactivates, MAO inhibitor will increase life of NT

Question 32

serotonin synthesis

Answer 32

try–>5-hydroxytryptophan–>serotonin.

Question 33

define heritability

Answer 33

proportion of observable diff in trait bw individuals within population due to genetic differences

Question 34

allelic vs locus heterogeneity

Answer 34

allelic: different mutations at some locus/gene cause disease
locus: multiple genes w mutations lead to “same” disease